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Experimental Studies of Molybdenum Physiology and Toxicology

SHEEP Molybdenum -Induced Apoptosis of Splenocytes and Thymocytes and Changes of Peripheral Blood in Sheep

To investigate the effects of molybdenum  Mo on apoptosis of lymphocytes and changes of peripheral blood in sheep, a total of 20 5-month-old healthy female sheep were randomly divided into five groups of 4 and orally administered with water containing Na2MoO4.2H2O 0, 5, 10, 20, and 50 mg/kg BW/day for 28 days. Jugular vein blood was taken on the 0th, 7th, 14th, 21st, and 28th day of Mo treatment, respectively. On the 28th day, the spleen and thymus were removed for observing histopathology and apoptosis-related DNA damage by hematoxylin and eosin HE staining and TdT‑mediated dUTP Nick-End Labeling TUNEL staining, respectively. The blood routine indexes were determined by an automatic blood analyzer. Further, the apoptosis of lymphocytes and changes in mitochondrial membrane potential MMP of peripheral blood were analyzed by flow cytometry. Results showed that excessive Mo induced apoptosis-related DNA damage in the splenocytes and thymocytes and significantly increased the apoptosis indexes of the splenocytes and thymocytes P < 0.01. Furthermore, the treatment with excessive Mo significantly decreased the MMP P < 0.01 and promoted apoptosis in peripheral blood lymphocytes P < 0.01. And the number of WBC, Lymph, Gran, and RBC and the indexes of HGB and HCT were also significantly decreased P < 0.05 or P < 0.01, while RDW was significantly increased by excessive Mo P < 0.05 or P < 0.01. In conclusion, excessive Mo-induced DNA damage and apoptosis of the lymphocytes changed the RBC-related indexes of the peripheral blood in sheep.

Cui, Shu-gang, Yu-ling Zhang, Hong-wei Guo, Bian-hua Zhou, Er-jie Tian, Jing Zhao, Lin Lin, and Hong‑wei Wang. Molybdenum-Induced Apoptosis of Splenocytes and Thymocytes and Changes of Peripheral Blood in Sheep." Biological Trace Element Research 2023: 1-11..


RAT Sodium molybdate  dihydrate does not exihibit developmental or reproductive toxicity in Sprague-Dawley rats maintained on a marginal copper diet

Groups of 24 weanling female Sprague-Dawley rats were administered molybdenum  Mo as sodium molybdate  dihydrate SMD in drinking water at target dose levels of 0, 20, or 40mg Mo/kg bw/day and fed a semi-purified marginal copper 6.2 ppm Cu AIN-93G diet for 8 weeks prior to mating, through cohabitation and pregnancy until Gestation Day 21. The objective was to confirm the reproductive and developmental effects of SMD reported by Fungwe et al. 1990 at estimated doses as low as 1.5mg Mo/kg bw/day in a similarly designed study with marginal Cu diet 6.3 ppm. There were no test material-related effects at 20 or 40mg Mo/kg bw/day on mortality, clinical observations, body weight, body weight gain, food consumption, estrous cycling, reproductive performance, maternal macroscopic pathology, ovarian or uterine parameters, litter size, resorptions, fetal sex ratio, fetal weight, or external fetal malformations or variations. Water consumption was increased compared to controls at both dose levels during the pre-mating and gestation periods, with no apparent adverse impact. There was no evidence of copper depletion in serum at any dose level. In conclusion, the no-observed-adverse-effect levels NOAELs for systemic, maternal reproductive, and developmental toxicity in this marginal Cu diet study are 40mg Mo/kg bw/day, consistent with the results of guideline developmental and reproductive toxicity studies of SMD. The results of Fungwe et al. were not replicated, even at higher dose levels of Mo, and their inconsistencies with guideline toxicity studies of Mo are not explained by the marginal dietary Cu level.

J. Murray, L. Aveyard, S. A. Hubbard, A. M. Hoberman, and S. Carey,Sodium molybdate dihydrate does not exihibit developmental or reproductive toxicity in Sprague-Dawley rats maintained on a marginal copper diet, Reproductive toxicology Elmsford, N.Y., 2023, 108442-108442.



RAT OECD 414 Supplementary Prenatal Developmental Toxicity Study of Sodium Molybdate  Dihydrate in the Rat and Benchmark Dose Evaluation

In a continuing investigation of the potential for reproductive and developmental toxicity of molybdenum  Mo, consequent to the previous published OECD studies [1,2] and as directed by the European Chemicals Agency [3], a supplemental rat GLP-compliant Prenatal Developmental Toxicity PNDT study was conducted to investigate higher dose levels of sodium molybdate  dihydrate SMD in an identical study design OECD 414[4] to Murray et al. 2014a [1], at dietary concentrations calculated to provide target Mo levels of 80 and 120mg/kg bw/day the maximum-tolerated dose. There was no effect on post-implantation loss, litter size, sex ratio or the incidence of external, visceral or skeletal fetal malformations or variations. Fetal weight was reduced proportionate to maternal dose. Minimal differences observed in the ossification status of some extremities of fetuses from females receiving 120mg Mo/kg bw/day were confirmed as transient by skeletal examination of PND 21 pups from a further group of females receiving the same dose regime. There was no evidence of copper depletion in serum, placenta or liver. A benchmark dose evaluation using continuous and dichotomous approaches by combining the fetal body weight data from this study and the previous study determined that the BMD05 ranged from 47 to 57mg Mo/kg bw/day, depending on the modelling approach and the BMDL05 estimates ranged from 37 to 47mg Mo/kg bw/day. These levels are considered a more statistically robust point of departure for risk assessment for reproductive effects than the established NOAEL of 40mg Mo/kg bw/day.

Aveyard, F. J. Murray, S. A. Hubbard, A. M. Hoberman, B. C. Allen, and S. Carey,OECD 414 Supplementary Prenatal Developmental Toxicity Study of Sodium Molybdate Dihydrate in the Rat and Benchmark Dose Evaluation, Reproductive toxicology Elmsford, N.Y., 2023, 108443-108443.


MOUSE Comparison of acute phase response in mice after inhalation and intratracheal instillation of molybdenum  disulfide and tungsten particles

Inhalation studies are the gold standard for assessing the toxicity of airborne materials. They require considerable time, special equipment, and large amounts of test material. Intratracheal instillation is considered a screening and hazard assessment tool as it is simple, quick, allows control of the applied dose, and requires less test material. The particle-induced pulmonary inflammation and acute phase response in mice caused by intratracheal instillation or inhalation of molybdenum  disulphide or tungsten particles were compared. End points included neutrophil numbers in bronchoalveolar lavage fluid, Saa3 mRNA levels in lung tissue and Saa1 mRNA levels in liver tissue, and SAA3 plasma protein. Acute phase response was used as a biomarker for the risk of cardiovascular disease. Intratracheal instillation of molybdenum  disulphide or tungsten particles did not produce pulmonary inflammation, while molybdenum  disulphide particles induced pulmonary acute phase response with both exposure methods and systemic acute phase response after intratracheal instillation. Inhalation and intratracheal instillation showed similar dose-response relationships for pulmonary and systemic acute phase response when molybdenum  disulphide was expressed as dosed surface area. Both exposure methods showed similar responses for molybdenum  disulphide and tungsten, suggesting that intratracheal instillation can be used for screening particle-induced acute phase response and thereby particle-induced cardiovascular disease.

T. Gutierrez, C. Loizides, I. Hafez, G. Biskos, K. Loeschner, A. Brostrom, M. Roursgaard, A. T. Saber, P. Moller, J. B. Sorli, N. Hadrup, and U. Vogel,Comparison of acute phase response in mice after inhalation and intratracheal instillation of molybdenum disulphide and tungsten particles, Basic & Clinical Pharmacology & Toxicology, 2023.

03 Comparing the effect of ammonium molybdate versus ammonium molybdate and menbutone on hepatic functions of sheep with subclinical copper poisoning

This study aimed to investigate the effect of using menbutone in addition to ammonium molybdate on liver enzymes in sheep naturally poisoned with copper. Merino lambs (n = 30), naturally poisoned with copper and which also had high liver enzyme levels, were divided into two groups, each with 15 lambs. The AM + MEN group received ammonium molybdate and menbutone and the AM group received only ammonium molybdate solution. Both groups received 1.7% ammonium molybdate solution (1 mL per 10 kg body weight [BW]) subcutaneously on 0, 2nd and 4th days of the study. Menbutone (Genabil (R), Boehringer Ingelheim, Germany) was administered intramuscularly at a dose of 10 mg/kg BW on days 0 and 2, in addition to ammonium molybdate in the AM + MEN group. Blood samples were collected on days 0 and 7, and aspartate aminotransferase (AST), gamma-glutamyltranspeptidase (GGT) and creatinine levels were evaluated. Over 7 days, AST levels decreased from 351.04 +/- 63.50 IU/L to 286.40 +/- 55.68 IU/L in the AM group (P > 0.05) and from 425.00 +/- 119.25 IU/L to 240.83 +/- 29.62 IU/L in the AM + MEN group (P <= 0.05). GGT levels decreased from 121.16 +/- 15.88 IU/L to 110.39 +/- 10.13 IU/L in the AM group (P > 0.05) and 124.52 +/- 15.50 to 98.60 +/- 9.08 IU/L in the AM + MEN group (P <= 0.05). Based on these findings, the use of menbutone, in addition to ammonium molybdate, has significantly reduced the level of liver enzymes.

  1. Kacar, Z. Mecitoglu, and H. Batmaz,Comparing the effect of ammonium molybdate versus ammonium molybdate and menbutone on hepatic functions of sheep with subclinical copper poisoning, Australian Veterinary Journal.



*03R Accumulation of molybdenum in major organs following repeated oral administration of bis-choline tetrathiomolybdate in the Sprague Dawley rat

Molybdenum is an essential dietary trace element required for several critical enzyme systems. High intake is associated with toxicity in ruminants and animal studies. The proposed therapeutic use of molybdenum-based drugs poses a potential risk for accumulation through chronic administration of therapeutic doses of this element. The current experiment was designed to study the effect of daily dosing of a molybdenum compound, bis-choline tetrathiomolybdate (TTM), in Sprague Dawley rats using laser ablation inductively coupled plasma time-of-flight mass spectrometry (LA-ICP-ToF-MS) and two dosing levels of TTM for up to 3 months. To investigate if molybdenum accumulation was associated with tissue toxicity, histopathology, haematology and clinical biochemistry markers of toxicity were incorporated into the study design. There were no behavioural signs of toxicity to the rats, and no clinical or anatomic pathology was associated with treatment. The current data did show a progressive accumulation of molybdenum within the adrenal gland, kidneys, liver, spleen, brain and testes. Although this was not associated with tissue toxicity within the 3-month study design, greater exposure over a longer period of time has the potential for producing adverse pathophysiological cellular function. Tissue toxicity, as a result of local excessive accumulation of molybdenum over time, has clear implications for the therapeutic use of molybdenum in humans and demands sensitive monitoring of tissue molybdenum levels to avoid toxicity. The current study highlights the shortcomings of conventional biomonitoring approaches to detect molybdenum accumulation with the goal of avoiding molybdenum-associated toxicity.

  1. R. Foster, K. Billimoria, M. E. Del Castillo Busto, S. Strekopytov, H. Goenaga-Infante, and T. J. Morley,Accumulation of molybdenum in major organs following repeated oral administration of bis-choline tetrathiomolybdate in the Sprague Dawley rat, J Appl Toxicol, 2022, 42, 1807-1821.


Note TTM description: "The test compound, TTM, is a solid white powder". In fact it is red.

*03R Effects of Chronic Exposure to Molybdate and Tetrathiomolybdate Supplementation of Water on Immature Rats Acutely Infected with Nippostrongylus brasiliensis. 1. Effects on Outcome of Infection and Host Health

Low molybdate (MoO4) exposure via drinking water in mature rats infected with Nippostrongylus brasiliensis raised liver and plasma copper (Cu) concentrations. The possibility that anthelmintic effects were attributable to conversion of MoO4 to tetrathiomolybdate (MoS4) in a non-ruminant species was investigated by giving three groups of 18 immature rats drinking water containing 70 mg Mo l-1 as MoO4 (group A), 5 mg Mo l(-1) as MoS4 (group B) or no supplement (group C), while receiving a commercial cubed diet. After 41 days, 12 rats from each group were inoculated subcutaneously with 2,000 L3-stage N. brasiliensis larvae. Sub-groups were killed 7, 8 or 9 days post infection (dpi), when adult worms are normally expelled, and enzyme markers for the inflammatory response to infection were measured in plasma or liver. Male rats given MoS4 prior to infection grew more slowly than those given MoO4. Eight dpi, females given MoS4 had lost more body -weight than those in group C, while those given MoO4 had gained weight. Mean worm counts at 7 dpi were 160, 65 and 250 +/- 30.6 (SE), respectively, in groups C, A and B, and differed significantly from each other (P < 0.05) but only rats given MoO4 remained infected 9 dpi (mean worm count 52 +/- 16.4): Faecal egg counts followed a broadly similar pattern. Both Mo sources pre-empted increases in liver and duodenal superoxide dismutase activity, induced by infection 7 and 9 dpi, respectively, in group C and enlarged the femur: neither source prevented hypertrophy of the small intestine and a rise in serum mast cell protease concentration caused by infection. Since data for plasma Cu concentration and caeruloplasmin oxidase activity, reported separately, indicated MoO4 was thiolated in vivo, differences between Mo sources may be attributable to differences in the degree of thiolation, extent of thiomolybdate exposure and rates of thiomolybdate degradation at critical times in host or parasite development. Crown Copyright (C) 2022 Published by Elsevier Ltd. All rights reserved.

  1. Sangwan, D. P. Knox, and N. F. Suttle,Effects of Chronic Exposure to Molybdate and Tetrathiomolybdate Supplementation of Water on Immature Rats Acutely Infected with Nippostrongylus brasiliensis. 1. Effects on Outcome of Infection and Host Health, Journal of Comparative Pathology, 2022, 198, 22-28..


*03R Effects of Molybdate and Tetrathiomolybdate Supplementation of Drinking Water on Immature Rats Infected with Nippostrongylus brasiliensis. 2. Copper Status and Tissue Molybdenum Accretion

Molybdate (MoO4) and tetrathiomolybdate (MoS4) supplementation of rats via drinking water had opposite effects on the establishment of Nippostrongylus brasiliensis larvae but both induced hypercupraemia, temporarily inhibited activities of superoxide dismutase in liver and duodenum after infection and enlarged the femoral head. Effects of MoO4 and MoS4 on activities of caeruloplasmin oxidase (CpO) in plasma, erythrocyte super-oxide dismutase (ESOD) and tissue copper (Cu) and molybdenum (Mo) were compared to test the hypothesis that species lacking a rumen can thiolate MoO4. Three groups of 18 immature Wistar rats were given Mo (70 mg/L as MoO4) or MoS4 (5 mg/L) via drinking water or remained untreated; all received a commercial, cubed diet and 12 from each group were infected with larvae of N. brasiliensis. Rats were killed 7-9 days later and liver, kidney, spleen, heart, muscle (quadriceps), brain and bone (femur) removed for Cu and Mo analysis. Plasma Cu was greatly increased by MoO4 and MoS4, without changing CpO activity, but the effect was more variable with MoO4 and accompanied by a smaller decrease in ESOD. Tissue Cu and Mo were increased by MoS4 in all tissues examined except brain and bone, correlating with plasma Cu and with each other; relation-ships were strongest in spleen, followed by kidney. MoO4 also increased soft tissue Cu and Mo but increases were generally smaller than those induced by MoS4 and correlations between the two elements and with plasma Cu generally weaker. Since hypercupraemia and correlated increases in liver and kidney Cu and Mo are characteristic of systemic thiomolybdate (TM) exposure, we conclude that MoO4 was partially thio-lated to give a different TM profile from that produced by MoS4. The pathophysiological significance of sys-temic exposure to di-and tri-TM merits investigation in non-ruminants as agents of chelation therapy and in ruminants as agents of short-lived TM toxicity on Mo-rich pastures.(c) 2022 The Author(s). Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

  1. F. Suttle, N. P. K. Sangwan, and D. P. Knox,Effects of Molybdate and Tetrathiomolybdate Supplementation of Drinking Water on Immature Rats Infected with Nippostrongylus brasiliensis. 2. Copper Status and Tissue Molybdenum Accretion, Journal of Comparative Pathology, 2022, 198, 80-88.

MoS2 nanoparticles induce behavioral alteration and oxidative stress mediated cellular toxicity in the social insect oecophylla smaragdina (asian weaver ant)

The study evaluates molybdenum disulfide (MoS2) nanoparticles (NPs) induced oxidative stress during cellular toxicity in an invertebrate in vivo system, the weaver ant. The lethal concentration was checked and LC50 was obtained as 50 microg/mL. Feeding assay and the photoluminescence activity confirmed the ingestion of MoS2 NPs by the organism. Behavioral assays showed altered grooming behavior in the MoS2 NP fed ants. A drastic decrease in the hemocyte count in the MoS2 NP fed ants revealed the anti-proliferative role of MoS2. This was further confirmed by 5-bromo-2'-deoxyuridine (BrdU) labeling assay. MoS2 NPs induced apoptotic activity was also observed in the hemocytes by acridine orange/ethidium bromide (AO/EB) staining. The level of oxidative stress during cellular toxicity was observed. An increased reactive oxygen species (ROS) level was observed in the MoS2 NP fed ants when compared to the control group. The increased activity of superoxide dismutase (SOD) and the lipid peroxidation (LPO) product were observed. While, the activities of catalase (CAT) and glutathione-s-transferase (GST) and the glutathione content (GSH) were decreased by MoS2 NPs. The transcript levels of SODs, CAT and GST were up regulated in the treated group. Our results suggest that MoS2 NPs induced oxidative stress mediates the cellular toxicity in the foragers of the weaver ant.

S. Cc, A. Anusri, C. Levna, A. Pm, and D. Lekha, Mos2 nanoparticles induce behavioral alteration and oxidative stress mediated cellular toxicity in the social insect oecophylla smaragdina (asian weaver ant), J Hazard Mater, 2020, 385, 121624.

Alterations of mitochondrial antioxidant indexes and apoptosis in duck livers caused by Molybdenum or/and cadmium

Cadmium (Cd) and high Molybdenum (Mo) can lead to adverse reactions on animals, but the co-induced toxicity of Mo and Cd to liver in ducks was not well understood. To investigate the co-induced toxic effects of Mo combined with Cd on mitochondrial oxidative stress and apoptosis in duck livers. 240 healthy 11-day-old ducks were randomly divided into 6 groups (control, LMo group, HMo group, Cd group, LMoCd group and HMoCd group). After being treated for 30, 60, 90 and 120 days, liver mitochondrial antioxidant indexes, ceruloplasmin (CP), metallothionein (MT), Bak-1 and Caspase-3 genes mRNA expression levels, and ultrastructural changes were evaluated. The results showed that total antioxidative capacity (T-AOC), catalase (CAT), superoxide dismutase (SOD) and xanthine oxidase (XOD) activities in experimental groups were decreased, whereas malondialdehyde (MDA) content and nitric oxide synthase (NOS) activity were increased compared with control group, and these changes of co-treated groups were more obvious in the later period of the experiment. The mRNA expression levels of CP, Bak-1 and Caspase-3 were up-regulated in experimental groups compared with control group and showed significant difference between co-treated groups and single treated groups. The mRNA expression level of MT in Cd group was higher than that in co-treated groups. Additionally, ultrastructural changes showed karyopyknosis, mitochondrial swelling, vacuolation and disruption of mitochondrial cristae in co-treated groups. Taken together, it was suggested that dietary Mo and Cd might lead to mitochondrial oxidative stress and apoptosis in duck livers, and it showed a possible synergistic relationship between the two elements.

Dai, X., Xing, C., Cao, H., Luo, J., Wang, T., Liu, P., Guo, X., Hu, G., and Zhang, C.,Alterations of mitochondrial antioxidant indexes and apoptosis in duck livers caused by Molybdenum or/and cadmium, Chemosphere, 2017, 193, 574-580.


Induction of fetal abnormalities and genotoxicity by molybdenum nanoparticles in pregnant female mice and fetuses

Increasing the uses of molybdenum (Mo) nanoparticles in a wide range of applications including food, industry, and medicine, resulted in increased human exposure and necessitated the study of their toxic effects. However, almost no studies are available on their genotoxic effects, especially on pregnant females and their fetuses. Therefore, this study was undertaken to estimate the possible induction of genotoxicity and fetal abnormalities, especially fetal malformations and skeletal abnormalities by Mo nanoparticle administration in mice. Oral administration of Mo nanoparticles resulted in significant decreases in the maternal body weight, the number and length of fetuses as well as skeletal abnormalities mainly less ossification and less chondrification. Administration of Mo nanoparticles also caused DNA damage induction which elevated the expression levels of p53, the vital gene in maintaining the genomic stability and cell differentiation in both maternal and fetus tissues. Similarly, the expression levels of E-Cad and N-Cad genes that control skeleton development have also been increased in the tissues of female mice administered Mo nanoparticles and their fetuses. Thus, we concluded that oral administration of Mo nanoparticles induced genotoxic effects and fetal abnormalities that necessitated further studies on the possible toxic effects of Mo nanoparticles.

H. R. H. Mohamed, R. H. El-Atawy, A. M. Ghoneim, and A. A. El-Ghor,Induction of fetal abnormalities and genotoxicity by molybdenum nanoparticles in pregnant female mice and fetuses, Environmental science and pollution research international, 2020. Environmental Science and Pollution Research https://doi.org/10.1007/s11356-020-08137-0.



Sulfite-induced protein radical formation in LPS aerosol-challenged mice: Implications for sulfite sensitivity in human lung disease

Exposure to bisulfite HSO3-and sulfite SO32- has been shown to induce a wide range of adverse reactions in sensitive individuals. Studies have shown that peroxidase-catalyzed oxidation of bisulfite leads to formation of several reactive free radicals, such as sulfur trioxide anion SO3-, peroxymonosulfate -O3SOO., and especially the sulfate SO4- anion radicals. One such peroxidase in neutrophils is myeloperoxidase (MPO), which has been shown to form protein radicals. Although formation of bisulfite-derived protein radicals is documented in isolated neutrophils, its involvement and role in in vivo inflammatory processes, has not been demonstrated. Therefore, we aimed to investigate bisulfite-derived protein radical formation and its mechanism in LPS aerosol-challenged mice, a model of non-atopic asthma. Using immuno-spin trapping to detect protein radical formation, we show that, in the presence of bisulfite, neutrophils present in bronchoalveolar lavage and in the lung parenchyma exhibit, MPO-catalyzed oxidation of MPO to a protein radical. The absence of radical formation in LPS-challenged MPO- or NADPH oxidase-knockout mice indicates that sulfite-derived radical formation is dependent on both MPO and NADPH oxidase activity. In addition to its oxidation by the MPO-catalyzed pathway, bisulfite is efficiently detoxified to sulfate by the sulfite oxidase (SOX) pathway, which forms sulfate in a two-electron oxidation reaction. Since SOX activity in rodents is much higher than in humans, to better model sulfite toxicity in humans, we induced SOX deficiency in mice by feeding them a low molybdenum diet with tungstate. We found that mice treated with the SOX deficiency diet prior to exposure to bisulfite had much higher protein radical formation than mice with normal SOX activity. Altogether, these results demonstrate the role of MPO and NADPH oxidase in bisulfite-derived protein radical formation and show the involvement of protein radicals in a mouse model of human lung disease.

A. Kumar, M. Triquigneaux, J. Madenspacher, K. Ranguelova, J. J. Bang, M. B. Fessler, and R. P. Mason,Sulfite-induced protein radical formation in LPS aerosol-challenged mice: Implications for sulfite sensitivity in human lung disease, Redox biology, 2018, 15, 327-334.

[LPS Aerosol is an industrial chemical, It is a specialized soft-film spray coating designed to prevent rust and corrosion on steel, aluminum and other metals. It contains mineral spirits and mineral oil which can be irritating to skin.

Neutrophils. A type of immune cell that is one of the first cell types to travel to the site of an infection. Neutrophils help fight infection by ingesting microorganisms and releasing enzymes that kill the microorganisms. A neutrophil is a type of white blood cell, a type of granulocyte, and a type of phagocyte. https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0022058/]





Reproductive toxicity in male mice after exposure to high molybdenum and low copper concentrations

To evaluate the effects of dietary high molybdenum (HMo) and low copper (LCu) concentrations on reproductive toxicity of male mice, 80 mice were divided into 4 groups of 20. These groups were fed with the following: (1) normal control (NC) diet (NC group); (2) NC and HMo diets (HMo group); (3) LCu diet (LCu group); and (4) HMo and LCu diets (HMoLCu group).

On the 50th and 100th day, superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), and total antioxidant capacity (T-AOC) were analyzed to determine oxidative stress states.

Morphological changes in testicular tissue were evaluated with hematoxylin and eosin staining and ultrastructural changes were monitored by transmission electron microscopy.

The results showed that administration of HMo, LCu, and HMoLCu not only decreased sperm density and motility but also increased the rate of teratosperm occurrence.

A significant increase in MDA content and a decrease in SOD, GSH-Px, and T-AOC contents were observed in LCu, HMo, and HMoLCu groups.

Testicular tissues and cells of mice were damaged by HMo and the damages were more serious in the case of Cu deficiency.

Exposure to HMo adversely affected the reproductive system of male mice, and dietary LCu plays key roles in HMo-induced reproductive toxicity.

Wang, H. W., Zhou, B. H., Zhang, S., Guo, H. W., Zhang, J. L., Zhao, J., and Tian, E. J.,Reproductive toxicity in male mice after exposure to high molybdenum and low copper concentrations, Toxicology and industrial health, 2016, 32, 1598-606.


Effect of Molybdenum Nanoparticles on Blood Cells, Liver Enzymes, and Sexual Hormones in Male Rats

Despite an increasing surge in application of nanoparticles in industries, there is a serious lack of information concerning their impact on human health and the environment. The present study investigated effects of molybdenum nanoparticles (Mo NPs) injected intraperitoneally into Sprague-Dawley rats at different doses of Mo NPs (5, 10, and 15 mg/kg BW per day) during a period of 28 days. Hematological and biochemical parameters as well as sexual hormones and histopathological examinations of the liver and testis were assessed and compared with control group.

The results showed that the serum levels of testosterone decreased significantly in both groups of 10 and 15 mg (Mo NPs)/kg BW in comparison with the control group (p < 0.05). However, there were insignificant differences observed in luteinizing hormone (LH) levels and hematological parameters when compared with the control group (p > 0.05). The results of liver enzymes showed that serum levels of aspartate aminotransferase (AST) decreased significantly in both dosage groups of 5 and 10 mg/kg BW (Mo NPs) when compared with the control group (p < 0.05), and significant decrease obtained in lactate dehydrogenase (LDH) levels at dose of 5 mg/kg BW in comparison with the control group (p < 0.05). The histopathological examination of testis showed a decrease in number of Leydig cells. Also, the number of chronic inflammatory cells increased in portal triad and parenchyma in liver tissue of rats exposed to Mo NPs.

Asadi, F., Mohseni, M., Dadashi Noshahr, K., Soleymani, F. H., Jalilvand, A., and Heidari, A.,Effect of Molybdenum Nanoparticles on Blood Cells, Liver Enzymes, and Sexual Hormones in Male Rats, Biological trace element research, 2016.. doi:10.1007/s12011-016-0765-5

Acute Toxicities of Molybdenum Compounds towards Animals

Acute Toxicities of Molybdenum Compounds towards Animalsa,b
LD50/mg/l (mg/kg)
MoO3c guinea pig LD75 400   [1,2]
  rat LD50190   [1,2]
MoO3(pure) rat LD50 273   [3]
    LD50 296-352   [4]
MoO3 (technical) rat LD50 666   [5]
Ammonium molybdated guinea pig LD 2200 LD100 800 [1,2]
  rat   MLD 203 [1,2]
  rabbit LD 1870   [1,2]
  cat LD1600-3200   [1,2]
Sodium molybdate rat MLD 290   [1,2]
    LD 671    
    LD50 503    
  dog   LD 3200  
  cat   LD1600-3200  
      LD50 344 [6]
Molybdate aq solutione chicken   LD100517+/-83 [7]
  dog   LD1001372+/-441  
  pigeon   LD100 607+/-119  
  rat   LD100 413+/-106  
Mo(VI) rat   MLD 223 [8]
Mo(V) + glucose rat   MLD 132 [8]
Mo(V ) + ascorbic acid rat   MLD 1999 [8]
MoS2 rat   LD50 > 15 000 [9]

Notes and references

aThe definition of toxicity is according to the U.S. Federal Hazardous Substances Labelling Act. The toxicity of the molybdenum compounds listed as toxic is "slight" (e.g., compare sodium arsenate, MLD10 for the rat by intraperitoneal injections). Abbreviations: LD, lethal dose for one animal; LDn, dose killing n% of a group of test animals; MLD, minimum lethal dose, i.e., the smallest of a number of doses which killed one or a group of test animals, all in mg/kg body weight.

b In tests of toxicity by skin absorption, skin irritation, and eye irritation (Test carried out for Climax Molybdenum Co. by Scientific Associates and New Drug Institute) the compounds listed were nontoxic except that ammonium and calcium molybdates were slight eye irritants.

c Some reports of high toxicity of MoO3 are based on the results of long term feeding studies wrongly presented as acute single dose studies

(e.g. LD50 125 mg/kg from L. Fairhall, R. Dunn, N. Sharpless, E. Pritchard, The toxicity of molybdenum, US Public Health Bulletin 293, 1945) (G.G. van Riper and J.C. Gilliland , ULLMANN’S ENCYCLOPEDIA OF INDUSTRIAL CHEMISTRY, 1990, A16, Ch. 12 )

d The description "ammonium molybdate" includes the compounds (NH4)2MoO4, (NH4)2Mo2O7 and (NH4)6Mo7O24.4H2O. There is unlikely to be any difference in the behaviour of the various molybdates.

e After a 60 min intravenous infusion.

[1] Saunders, W. B., Handbook of Toxicology, 1956, London.
[2] Fairhall, L. T., Dunn, R. C., Sharpless, N. E. and E. A. Pritchard, The Toxicity of Molybdenum, U.S. Public Health Service, Public Health Bulletin, 1945, 293
[3] Acute oral LD50 assay in rats FDRL-ID:81-0393 for AMAX Inc. Aug. 1981
[4] Food and Drug Research Laboratories Inc. Acute oral LD50 assay in rats for molybdenum trioxide pure grade, 1981, Waverly New York.
[5] Acute oral LD50 assay in rats FDRL-ID:81-0394 for AMAX Inc. Aug. 1981
[6] Irving Sax, N., Dangerous Properties of Industrial Materials, 1984, 6th Ed. Van Nostrand Reinhold Co. New York, 1953.
[7] Caujolle, F. and Changh, P. H., Agressologie, 1967, 8, 265 (Quoted in Lener, J. and Bibr, B., J. Hygiene, Epidemiology, Microbiology and Immunology, 1984, 28, 405).
[8] Lener, J. and Bibr, B., Proc. Int. Conf.: Heavy Metals in the Environment. Amsterdam 1981, 462. (Quoted in Lener, J. and Bibr, B., J. Hygiene, Epidemiology, Microbiology and Immunology, 1984, 28, 405).
[9] Acute oral LD50 assay in rats of MoS2 FDRL-ID 9589A for AMAX Inc. Nov 29 1987.

Inhalation of dusts of molybdenum trioxide

Inhalation of dusts of molybdenum trioxide (Table below) and the more soluble molybdates produced toxic effects. [Fairhall, 1945] The toxic effect of molybdenum trioxide dust was aggravated by silica [Mogilevskaya, 1961]. Precautions should be taken against the inhalation of dusts of molybdenum trioxide and the more soluble molybdates; maximum permissible concentrations in air recommended by the American Industrial Hygiene Association are 5 mg Mo/m3 (cf. Be, 0.002; V, 0.5; arsine, 0.3) over an eight-hour period. The World Health Organisation recommended in 1969 a "safe concentration zone" of molybdenum as 4-5 mg/m3.

Fairhall, L. T., Dunn, R. C., Sharpless, N. E. and Pritchard, E. A., The Toxicity of Molybdenum, U. S. Public Health Service, Public Health Bulletin, 1945, 293.

Mogilevskaya, O. Ya., Gig. Sanit., 1961, 26, 18.

Effects of MoO3 inhalation on mice and rats compared with controls
ObservableMice, maleMice, femaleRats, maleRats, female
Survival 0 0 0 0
Mean body weights 0 0 0 0
Blood Mo (b) + + + +
Mo toxicity symptoms (c) 0 0 0 0
Bone density or curvature 0 0 0 0
Nasal and larynx lesions + + + +
Chronic inflammation in lungs 0 0 +(d) +(d)
Lung carcinoma + + 0?(e) 0 (e)

(a) Groups of 50 male and 50 femaleF344/N rats and B6C3F1 mice were exposed to MoO3 by inhalation at 0, 10, 30, or 100 mg/m3, 6 h/day, 5 days/week, for 2 years. Controls were not exposed. Plus (+) means a positive effect compared with the controls which increases with the level of exposure. Zero (0) means no effect.
(b) Mo concentrations (mg/g): male mice <0.10 (no MoO3) to 0.77 (highest MoO3), female mice 0.04 to 0.52, male rats 0.22 to 6.0, female rats,0.06 to 2.4
(c) e.g. diarrhoea, alopecia, dermatosis, anaemia.
(d) At highest exposures.
(e) For 1/50 animals.

Chan, P.C., Herbert, R.A., Roycroft, J.H., Haseman, J.K., Grumbein, S.L., Miller, R.A., Chou, B.J., Lung tumor induction by inhalation exposure to molybdenum trioxide in rats and mice, Toxicological Sciences, 1998, 45, 58-65.

Molybdenum trioxide inhalation studies in male rats

The following is a detailed summary of a recent study by K. Ozaki et al.

Correlations between non-neoplastic chronic pulmonary lesions and adrenal pheochromocytoma in 9 recent NTP, 2 year particulate inhalation studies in male F344 rats have been investigated. The re-evaluation of other lesions revealed significant associations of pheochromocytoma only with the severity of inflammation and fibrosis. The particulates investigated were all metal compounds and included molybdenum trioxide.

Pheochromocytomas are benign or malignant tumours which give a yellow-brown colour when stained with chromates. These tumours arise as a result of the increased production of catecholamines, such as dopamine, epinephrine and norepinephrine (adrenaline and noradrenaline) in the adrenal medulla in response to a stress which can be an environmental insult. (Catecholamines are synthesised in chromaffin cells.)

Generally exogenous agents that induce adrenal medullary neoplasia do not cause DNA damage so a carcinogenic response is due to an indirect mechanism.

Mammalian tissues are primarily aerobic and hence dependent upon a continuous supply of oxygen. Inadequate O2 delivery results in hypoxemia. Reduction in arterial O2 tension leads to the release of dopamine and other catecholamines. Activity of tyrosine hydroxlyase, the rate limiting step in the biosynthesis of catecholamines is enhanced in the carotid body and the adrenal gland during hypoxemia.

The hypothesis is that the area of lung tissue damaged by the inhalation of certain particulates is correlated positively with the degree of hypoxemia which leads to the pathological increase in tyrosine hydroxylase activity and the production of catecholamines.

The results of the studies relating to MoO3 are given in the following Table.

Results from the re-evaluation of 9 inhalation studies of the particulate compound MoO3 as reported by NTP.

MoO3 inhalation study
0 mg m-3
10 mg m-3
30 mg m-3
100 mg m-3
Proteinosis 0/50 0/50 0/50 0/50
Fibrosis, interstitium 5/50 2.0 4/50 1.0 7/50 1.0 45/50 1.8
Inflammation, chronic active 10/50 1.8 7/50 1.6 37/50 1.2 48/50 2.1
Alveolar epithelium hyperplasia 12/50 1.8 14/50 1.6 16/50 1.2 7/50 1.3
Metaplasia, squamous epithelium 2/50 1.0 0/50 2/50 1.0 27/50 1.1
HistiocytosisIncrease in cells associatedwith inflammation 11/50 1.9 13/50 1.3 35/50 1.3 46/50 1.7
Alveolar/bronchial adenoma 0/50 0/50 0/50 3/50
Alveolar/bronchial carcinoma 0/50 1/50 1/50 1/50
Adrenal Medulla        
PheochromocytomaBenign + malignant 15/50 13/50 18/50 18/50
Hyperplasia 32/50 2.1 27/50 2.1 28/50 2.1 29/50 2.5

Second number in each cell indicate the mean grade of severity

0 no involvement
1 min. up to 5 small lesions 10% of area
2 mild 10 - 25 % of area
3 moderate 26 - 50% of area
4 marked 51 - 75% of area
5 severe > 75% of area.

Terms used in the Table:

Proteinosis: Aggregates of homogeneous to granular material which stains with eosin within alveolar lumina.
Fibrosis: Dense fibrous tissue - thickening and scaring of connective tissue. This is considered secondary to inflammation.
Hyperplasia: Enlargement of an organ or tissue arising from the increased production of cells. In the case of the adrenal medulla in this study this is related to the increase in the production of catecholamines.
Metaplasia: Abnormal change in tissue.
Histiocytosis: Accumulation of alveolar macrophages with foamy cytoplasm and occasional multinucleated giant cells but few neutrophils. (Macrophages and neutrophils are associated with inflammation).
Adenoma: A gland-like benign tumour.
Carcinoma: A cancer.


General: In the controls inflammation with a smaller contribution from fibrosis was associated significantly (p<0.01) with the occurrence of pheochromocytomas.

None of the other non-neoplastic lung lesions were significantly correlated with the incidence of adrenal pheochromocytomas.

Molybdenum trioxide showed no dose related increase in pheochromocytoma incidence but the correlation between the incidence of pheochromocytoma and the severities of fibrosis and inflammation was highly significant (p < 0.01) and the strongest correlation was with inflammation.

Molybdenum trioxide showed one of the strongest correlations with inflammation of most test compounds. However, it was not understood why the increase in the incidence of pheochromocytomas did not follow the treatment-related increase in the severity of inflammation and fibrosis.

Pheochromocytomas can also be related to aging or in response to a wide variety of xenobiotic agents BUT these lesions are rare in humans and other animal species. They occur more frequently in male than female rats.

Ozaki, K., Haseman, J. K., Hailey, J. R., Maronpot, R. R., and Nyska, A., Association of adrenal pheochromocytoma and lung pathology in inhalation studies with particulate compounds in the male F344 rat - The national toxicology program experience, Toxicologic Pathology, 2002, 30, 263-270.

International Molybdenum Association toxicology testing programme

Toxicology Testing Programme: Rats
SubstanceLD50 or LC50/ mg/l
Acute oralaAcute inhalationbAcute dermalc
LD50 ratsLC50 ratsLD50 rats
Molybdenum trioxide (pure) 3260 > 5.84 > 2000
Molybdenum trioxide (tech) > 5000 > 3.93 > 2000
Ammonium dimolybdate 3883 > 2.08 > 2000
Sodium molybdate 4233 > 1.93 > 2000
Molybdenum disulfide >2000 > 2.82 > 2000
Risk phrase required if:d <2000 < 5 < 2000


a Acute oral is representative of relative toxicity by ingestion. Various doses were administered to rats (10/dose) by infusion into the stomach. Animals were observed for 14 days. For pure molybdenum trioxide there was a statistically significant difference between the oral LD50 in male and female rats: (male, 2689; female, 3830 mg/kg). The value given above is an average and is likely a low estimate.

b Acute inhalation is representative of relative toxicity by inhalation. Dust administered to rats (10) for 4 hours. Animals observed for 14 days.

cAcute dermal is representative of relative toxicity due to skin absorption. Various concentrations adminstered topically to rats (10). Animals observed for 14 days.

Skin irritation: Material applied to rabbit (6) skin for 4 hours. Animals observed for erythema and oedema daily for 4 days.

Eye irritation: Material applied to rabbit (6) eyes (100 mg). Animals observed for 7 days.

Skin sensitization: Guinea pigs exposed to material intradermally and topically twice (induction and challenge).

d All acute oral and dermal results were well above the level that requires a harmful classification and precautionary labelling. In the case of inhalation, in some cases it was not possible to generate a dust cloud of 5 mg/l. However, even at the highest concentrations generated there were no animal deaths and there is no basis to assume that labelling of these materials is indicated.

Toxicological studies on MoS2

Acute inhalation study in rats

The inhalation hazard associated with acute exposure to MoS2is low.
The LC50 (4 hour) of MoS2is > 2.82 mg/l in air.
Labelling of MoS2with the risk phrase R20 Harmful by inhalation is not indicated.

MoS2was administered as a particulate aerosol at a concentration of 2.82 mg/l of air for 4 h. The rats were observed for 14 d post exposure.

There were no deaths. No clinical signs and no changes of bodyweight compared with controls. Food and water consumption was similar to that of controls.

The ratio lung/body weight was similar to the ratio found for controls.
A grey appearance of the lungs was noted for all rats post mortem.

Acute oral toxicity to the rat

The acute lethal oral dose to rats of molybdenum disulphide was demonstrated to be greater than 2000 mg/kg bodyweight.

Molybdenum disulphide will not require labelling with the risk phrase R22, "Harmful if swallowed", in accordance with Commission Directive 93/2 I/EEC.

A group of ten fasted rats (five males and five females) received a single oral gavage dose of MoS2formulated in 1% w/v aqueous methylcellulose and administered at a dose level of 2000 mg/kg bodyweight.

There were no deaths. Clinical signs of reaction to treatment in the main study, comprised piloerection, hunched posture and ungroomed appearance observed in all rats. There were no other clinical signs and recovery was complete in all instances by Day 4.

All rats were considered to have achieved satisfactory bodyweight gains throughout the study.
All animals were killed and examined macroscopically on Day 15, the end of the observation period. This examination revealed no abnormalities.

Eye irritation to rabbits

Molybdenum disulfide is not irritating to the eyes.
100 mg of MoS2was instilled into the eyes of three rabbits. The animals were observed for three days. The MoS2caused very slight conjunctaval irritation.

Acute dermal toxicity to the rat

Molybdenum disulfide will not require labelling with the risk phrase R21 (EU Commission Directive 93/21/EEC: ‘Harmful in contact with skin.’

The acute lethal dermal dose to rats of MoS2> 2000 mg/kg bodyweight.
Ten rats received a topical application of MoS2in 1% w/v aqueous methylcelulose, 2000mg/kg bodyweight.
There was no systemic response to MoS2.
Four rats showed some dermal irritation which had disappeared 4 d after exposue was stopped.

Skin sensitisation in the guinea-pig

Molybdenum disulphide did not produce evidence of skin sensitisation (delayed contact hypersensitivity) in any of the ten test animals.

Molybdenum disulphide does not require labelling with the risk phrase R43 "May cause sensitisation by skin contact in accordance with Commission Directive 93/21/EEC.

The following dose levels were selected:
Intradermal injection:
10% w/v in Alembicol D
Topical application:
70% w/v in Alembicol D
Challenge application:
70 and 35% w1/v in Alembicol D
Ten test and five control guinea-pigs were used in this study.

Skin irritation to the rabbit

No dermal reactions were observed following a single, semi-occlusive application of molybdenurn disulphide to intact rabbit skin for four hours.

Molybdenum disulphide will not require labelling with the risk phrase R38 ‘Irritating to skin', in accordance with Commission Directive 93/21 /EEC.

Three rabbits were each administered a single dermal dose of 0.5 g of MoS2and observed for four days.

Huntingdon Life Sciences Ltd Research Laboratory March 1998

Molybdenum metal and metal powder

As with other fine powders inhalation of quantities of molybdenum dust can be dangerous. Safety precautions have been described [Lamprey and Ripley, 1962]. Molybdenum metal as such and in alloys is not toxic and has been incorporated in stainless steels used in bone and joint surgery where resistance to corrosion by body fluids is required [Bechtol et al., 1959]. Molybdenum alloyed with cobalt and chromium has been used for some 40 years for surgical implants, dental prostheses etc. As with the stainless steel, molybdenum confers corrosion resistance.

Lamprey H. and Ripley, R. L., J. of the Electrochemical Soc., 1962, 109, 713.
Bechtol, C. O., Ferguson, B. and Laing, P. G., Metals and Engineering in Bone and Joint Surgery, The Williams and Wilkins Co., Baltimore, 1959.

Workers handling metals in welding and steelmaking are expected to have higher levels of trace metals. Interpretation of levels requires some knowledge of the toxicokinetics of a metal and the preferred medium for analysis for each: serum, whole blood or urine (preferably a 24-hour collection). Trends are often more informative than concentrations at one time. Molybdenum and vanadium are often found to be elevated among workers exposed to metals who show no evidence of clinical illness. The Mo level in the general population not occupationally exposed to Mo (the whole blood Mo reference range) is 5 - 50 nmol/l as used by the Trace Element and Environmental Toxicology Laboratory at the University of Alberta Hospitals. Mo is described as having 'very low toxicity' [Guidotti et al., 1997.]

Guidotti, T.L., Audette, R.J., Martin, C.J., Interpretation of the trace metal analysis profile for patients occupationally exposed to metals, Occupational Medicine-Oxford, 1997, 47 , 497-503.

Molybdenum carbide and silicide

Aqueous suspensions of MoC and MoSi2 administered intraperitoneally to mice in doses of 3000 mg/kg did not cause death [Chem. Abs., 1969]. Intratracheal administration of suspensions of these compounds to rats in doses of 50 mg/animal had pathological effects derived from the fibrogenic nature of the compounds. Maximum permissible concentrations in air are recommended as 6 mg Mo/m3

Chem. Abs., 1969, 71, 68977v.
Brakhnova, I. T. and Samsonov, G. V., Gig. Sanit., 1970, 35, 42.

Molybdenum pentachloride

Molybdenum pentachloride has a marked irritant effect on the tissues of rats [Spiridonova and Surorov, 1967]. The toxicity is due to hydrochloric acid produced during hydrolysis of the compound and not to molybdenum. Molybdenum pentachloride is a hazardous chemical and, if proper precautions are not taken, its industrial use involves danger of acute intoxication. There were no health problems in the production of MoCl5 at the former Climax Langeloth refinery and the Ann Arbor Laboratory.

Spiridonova, V. S. and Suvorov, S. V., Gig. Sanit., 1967, 32, 79.

Molybdenum pentachloride should be considered as a non-immunotoxic and a weak, nonspecific contact irritant. Immunotoxicity was studied in sheep by a 14 day subchronic exposure to MoCl5 at 1- 100 ppm in food. Contact hypersensitivity was determined by topical ear exposure to MoCl5 [Abdouh et al., 1995].

Abdouh, M., Krzystyniak, K., Flipo, D., Therien, H.M., Fournier, M., Cytometric Profile Of Molybdenum-Induced Contact Sensitization Versus A Strong Allergen Reaction To Oxazolone In Murine Auricular Lymph-Node (Aln) Test, International Journal Of Immunopharmacology, 1995, 17, 545-554.

Molybdenum hexacarbonyl and organomolybdenum compounds

Molybdenum hexacarbonyl is a solid which may be handled in the laboratory without special precautions. It is less toxic than the more volatile iron and nickel carbonyls. However, little is known about the toxic effects of molybdenum hexacarbonyl and organomolybdenum compounds [Vignoli and Defretin, 1963] and it is wise to assume that they are likely to be more toxic than MoO3 and molybdates and they should be handled in such a way that there is no danger of absorption through the skin or inhalation of their dusts and vapours.

Vignoli, L. and Defretin, J. P., Biologie medicale, 1963, 52, 319.

Volatile Mo(CO)6 and W(CO)6 are present in landfill gas from three different municipal waste deposits in concentrations of about 0.2-0.3 microg of Mo/m3 and 0.005-0.01 microg of W/m3. The chemical reactions which give rise to these carbonyls under landfill site conditions are not known. Because volatile metal carbonyls are toxic, questions about the occupational health of workers on landfills needs to be addressed [Feldmann and Cullen, 1997].

Feldmann, J., Cullen, W.R..,Occurrence of volatile transition metal compounds in landfill gas: Synthesis of molybdenum and Tungsten carbonyls in the environment, Environmental Science & Technology, 1997, 31, 2125-2129.

Comparative effects of molybdenum and other elements

In comparative toxicity studies with rats and mice sodium molybdate (LD50 1.45 m mol/kg body weight) was less toxic than sodium tungstate, sodium chromate and sodium vanadate [Pham Huu Chanh, 1965]. The irritant effect of sodium molybdate on skin, mucous membranes, and eyes was much smaller than that of sodium dichromate (an extreme irritant) [Climax Molybdenum Test].

Pham-Huu-Chanh, Arch. Intern. Pharmacodyn., 1965, 154, 243.

The ecotoxicological effects expressed as effect on respiratory rate and chlorophyll a content of the freshwater, algaScenedesmus quadricauda and the bioaccumulation of six ions (Cu2+, Cu+, MoO42-, Mn2+, VO43-, Ni2+) and their associations were determined in comparison with a control [Fargasova, 1998]. The ion concentrations were equal to their EC50 concentrations: for Mo, ammonium heptamolybdate at 2.5 mg l-1. The pH’s of the solutions were not reported. Molybdate had no effect on the respiratory rate; the other ions caused the rate to increase. Combination of moybdate with nickel and copper decreased the rate (but not with manganese). Molybdate and the other ions caused the content of chlorophyll a to decrease. Bioaccumulation of molybdate was negligible MoO42- (< 0.2 %). Molybdate greatly decreased the uptake of Mn, Ni and Cu although these ions had no effect on the uptake of Mo.

Fargasova, A, Accumulation and toxic effects of Cu2+, Cu+, MoO42-, Mn2+, VO43-, Ni2+ and their associations: influence on respiratory rate and chlorophyll (a) content of the green alga Scenedesmus quadricauda, Journal Of Trace And Microprobe Techniques, 1998, 16, 481-490.

Users of the Database should be aware that inclusion of an abstract in the Database does not imply any IMOA endorsement of the accuracy or reliability of the reported data or the quality of a publication.