Toxic Effects Of Hexavalent Chromium Research Articles

Quantitative assessment of Nigella sativa and conjugated silver nanoparticles against hexavalent chromium toxic effects on sperm function

BackgroundInfertility has been observed as one of the major issues in humans, one known risk factor is heavy metals. MethodsThe main focus of the present research was to assess the toxic effect of hexavalent chromium (Cr (VI)) on sperm and its mitigation by Nigella sativa seed extract (NS) and its conjugated silver nanoparticles (NS + NP). In the present study, we administered 1.5 mg/kg body of Cr (VI) orally in mice for 60 days routinely, to induce toxicity in testes and effect on sperm production and motility in male mice. NS and NS + NP (50 mg/kg body weight) were administered to evaluate protective action against Cr (VI). The sperm were analyzed by computer-assisted semen analysis (CASA) and chromium concentration in testicular tissue was measured via the atomic absorption spectrophotometer. ResultsThe CASA analysis showed that Cr (VI) was directly linked with a decline in sperm concentration, motility, distance, velocity, straightness, and head beat frequency attributes. However, the administration of Nigella sativa seed extract and its green synthesized silver nanoparticles improved sperm concentration, motility, distance, velocity, straightness, and head beat frequency. The chromium content in the testes of Cr-exposed animals significantly increased, which negatively affected sperm parameters. However, Nigella sativa and Nigella sativa conjugated silver nanoparticles appeared to help in the removal of Cr content from testes hence improving the sperm parameters in exposed mice. ConclusionThe decrease in Cr concentration improved sperm quality and quantity, hence, improve male fertility.

Microbial colony sequencing combined with metabolomics revealed the effects of chronic hexavalent chromium and nickel combined exposure on intestinal inflammation in mice

The pollution and toxic effects of hexavalent chromium [Cr(VI)] and divalent nickel [Ni(II)] have become worldwide public health issues. However, the potential detailed effects of chronic combined Cr(VI) and Ni exposure on colonic inflammation in mice have not been reported. In this study, 16S rDNA sequencing, metabolomics data analysis, qPCR and other related experimental techniques were used to comprehensively explore the mechanism of toxic damage and the inflammatory response of the colon in mice under the co-toxicity of chronic hexavalent chromium and nickel. The results showed that long-term exposure to Cr(VI) and/or Ni resulted in an imbalance of trace elements in the colon of mice with significant inflammatory infiltration of tissues. Moreover, Cr(VI) and/or Ni poisoning upregulated the expression levels of IL-6, IL-18, IL-1β, TNF-α, IFN-γ, JAK2 and STAT3 mRNA, and downregulated IL-10 mRNA, which was highly consistent with the trend in protein expression. Combined with multiomics analysis, Cr(VI) and/or Ni could change the α diversity and β diversity of the gut microbiota and induce significant differential changes in metabolites such as Pyroglu-Glu-Lys, Val-Asp-Arg, stearidonic acid, and 20-hydroxyarachidonic acid. They are also associated with disorders of important metabolic pathways such as lipid metabolism and amino acid metabolism. Correlation analysis revealed that there was a significant correlation between gut microbes and metabolites (P < 0.05). In summary, based on the advantages of comprehensive analysis of high-throughput sequencing sets, these results suggest that chronic exposure to Cr(VI) and Ni in combination can cause microbial flora imbalances, induce metabolic disorders, and subsequently cause colonic damage in mice. These data provide new insights into the toxicology and molecular mechanisms of Cr(VI) and Ni.

Tissue Distributions and Toxic Effects of Hexavalent Chromium in Laboratory-Exposed Periwinkle (Littorina littorea Linnaeus).

The increased use of hexavalent chromium (Cr6+) in various industrial applications has contributed to its elevated levels in the environment, especially the aquatic environment. Thus, there is the potential for accumulation of Cr6+ in the tissues of aquatic organisms and consequent toxic effects. The toxic effects of Cr6+ in aquatic organisms have been widely reported; however, little is known about the patterns of tissue accumulation of Cr6+ and its toxicity in aquatic mollusks. Thus, the present study investigated the effects of Cr6+ exposure on the tissue distribution, proximate composition, and histopathology of an aquatic mollusk, periwinkle (Littorina littorea). The animals were exposed to sublethal concentrations of Cr6+ (0.42, 0.84, and 4.2 mg/L) for 30 days, after which the condition index, tissue accumulation, proximate composition, and histopathological effects were determined. The control animals were maintained in a medium that did not contain Cr6+ (0 mg/L). The condition index did not differ significantly among the groups. The levels of Cr6+ in the tissues differed significantly among the different tissue types while there was no significant effect of the exposure concentration, except in the foot tissue. The proximate parameters (protein, carbohydrates, lipid, crude fiber, and moisture contents) differed significantly among the groups. The protein contents of the exposed animals were significantly lower than those of the control animals and the histological architecture of the major organs was altered in the chromium-exposed animals. The findings from this study indicate a low potential of L. littorea to bioaccumulate Cr6+ in its tissues at the low exposure concentrations tested in this study; as such, its consumption may not pose any serious health risks to humans. However, changes in the proximate composition and histological architecture of the exposed L. littorea show that Cr6+ is potentially toxic to periwinkles.

Assessment of the toxic effect of hexavalent chromium on the hematological indices in Nile tilapia, Oreochromis niloticus

The presence of heavy metals, which are typically released into water bodies as a result of fast industrialization, causes the aquatic environment to become extremely contaminated. Chromium is one of the most common heavy metal in the environment and is used in several types of industries. The effect of sublethal toxicity of hexavalent chromium Cr(VI) on hematological indices of the Nile tilapia, Oreochromis niloticus has been analyzed following exposure of concentration 9.349 mg/L and 18.698 mg/L (10% &amp; 20% of LC50 value ) of potassium dichromate (K2Cr2O7) as hexavalent chromium for 7, 15, 30 days. Hematological parameters are the most important indicators of fish health status. The aim of this study was to determine the effect of Cr(VI) toxicity on hematological parameters in O. niloticus. The results show that hemoglobin percentage (Hb%), red blood cell (RBC), mean corpuscular volume (MCV), and platelet count level were significantly (P &gt; 0.05) decreased and the total count of white blood cell (WBC) was significantly (P &gt; 0.05) increased with increasing time of exposure at a concentration of 9.349 mg/L of K2Cr2O7 in the test groups compared to the control group. At the concentration of 18.69 mg/L, Hb%, RBC, MCV, mean corpuscular hemoglobin concentration (MCHC), and platelet count level were significantly (P &gt; 0.05) decreased and the total count of WBC and erythrocyte sedimentation rate (ESR) value were significantly (P &gt; 0.05) increased with the increasing time of exposure in the test groups compared to the control group. To study the R2 value of the linear regression equation, we found that the trend of the chronic toxic effect of hexavalent chromium at 60 and 90 days of both the sublethal concentrations 9.349 mg/L and 18.69 mg/L of K2Cr2O7, where the value of Hb, RBC, packed volume cell (PCV), MCV are found to drastically decreased and the value ESR and WBC are found to drastically increased in the experimental groups compared to the control group. The investigation recommended that the presence of hexavalent chromium in the aquatic medium has a strong impact on the hematological indices in O. niloticus.

Assessment of the Toxic Effect of Hexavalent Chromium on the Hematological Indices in Nile Tilapia, Oreochromis Niloticus

The presence of heavy metals, which are typically released into water bodies as a result of fast industrialization, causes the aquatic environment to become extremely contaminated. Chromium is one of the most common heavy metals in the environment and is used in several types of industries. The effect of sublethal toxicity of hexavalent chromium Cr (VI) on hematological indices of the Nile tilapia, Oreochromis niloticus has been analyzed following exposure of concentration 9.349 mg/L and 18.698 mg/L (10% &amp; 20% of LC50 value) of potassium dichromate (K2Cr2O7) as hexavalent chromium for 7, 15, 30 days. Hematological parameters are the most important indicators of fish health status. The aim of this study was to determine the effect of Cr (VI) toxicity on hematological parameters in O. niloticus. The results show that hemoglobin percentage (Hb%), red blood cell (RBC), mean corpuscular volume (MCV), and platelet count level were significantly (P &gt; 0.05) decreased and the total count of white blood cell (WBC) was significantly (P &gt; 0.05) increased with increasing time of exposure at a concentration of 9.349 mg/L of K2Cr2O7 in the test groups compared to the control group. At the concentration of 18.69 mg/L, Hb%, RBC, MCV, mean corpuscular hemoglobin concentration (MCHC), and platelet count level were significantly (P &gt; 0.05) decreased and the total count of WBC and erythrocyte sedimentation rate (ESR) value were significantly (P &gt; 0.05) increased with the increasing time of exposure in the test groups compared to the control group. To study the R2 value of the linear regression equation, we found that the trend of the chronic toxic effect of hexavalent chromium at 60 and 90 days of both the sublethal concentrations 9.349 mg/L and 18.69 mg/L of K2Cr2O7, where the value of Hb, RBC, packed volume cell (PCV), MCV are found to drastically decreased and the value ESR and WBC are found to drastically increased in the experimental groups compared to the control group. The investigation recommended that the presence of hexavalent chromium in the aquatic medium has a strong impact on the hematological indices in O. niloticus.

Toxic Effects on Oxidative Stress, Neurotoxicity, Stress, and Immune Responses in Juvenile Olive Flounder, Paralichthys olivaceus, Exposed to Waterborne Hexavalent Chromium.

Simple SummaryMetals such as chromium can be exposed at high levels in the marine environment, and exposure to these heavy metals can have a direct effect on marine organisms. High levels of chromium exposure can have a direct impact on organisms in a coastal cage and terrestrial aquaculture. Hexavalent chromium exposure of more than 1.0 and 2.0 mg Cr6+/L induced physiological responses such as antioxidant, neurotransmitter, immune, and stress indicators in Paralichthys olivaceus. Therefore, this study will provide a reference indicator for stable aquaculture production through reference indicators for toxicity due to chromium exposure that may exist in the marine environment.Juvenile Paralichthys olivaceus were exposed to waterborne hexavalent chromium at various concentrations (0, 0.5, 1.0, and 2.0 mg/L) for 10 days. After chromium exposure, the activities of superoxide dismutase and glutathione S-transferase, which are oxidative stress indicators, were significantly increased; however, the glutathione level was significantly reduced. Acetylcholinesterase activity as a neurotoxicity marker was significantly inhibited upon chromium exposure. Other stress indicators, including plasma cortisol and heat shock protein 70, were significantly increased. The immune response markers (lysozyme and immunoglobulin M) were significantly decreased after chromium exposure. These results suggest that exposure to environmental toxicity in the form of waterborne chromium at concentrations higher than 1.0 mg/L causes significant alterations in antioxidant responses, neurotransmitters, stress, and immune responses in juvenile olive flounders. This study will provide a basis for an accurate assessment of the toxic effects of hexavalent chromium on aquatic organisms.

Toxic effects of hexavalent chromium (Cr6+) on bioaccumulation, apoptosis, oxidative damage and inflammatory response in Channa asiatica

The objective of this study was to evaluate the toxic effects of Cr6+ on bioaccumulation, digestion, immunity, oxidative stress, apoptosis and inflammation-related genes in Channa asiatica. The fish was exposed to waterborne Cr6+ concentrations (0, 0.5, 1.0 and 2.0 mg/L) for 28 and 56 days. Our results demonstrated that the accumulation of Cr6+ in tissues increased in a concentration-dependent manner, and the content in tissue was liver > gill > gut > muscle. Meanwhile, Cr6+ exposure led to a remarkable suppression of digestion, immunity and antioxidant capacity in C. asiatica. Inversely, MDA and PC content were positively correlated with Cr6+ exposure concentration. Furthermore, the expression of genes went up with the increase of waterborne Cr6+ concentration. Among them, HSP90, NF-κB and TNF-α have a sharp increase. These results elucidate that waterborne Cr6+ exposure may induce bioaccumulation, inhibit digestion and immunity, promote oxidative stress and up-regulate the expression of apoptosis and inflammation-related genes in C. asiatica.

The potential toxic effects of hexavalent chromium on oxidative stress biomarkers and fatty acids profile in soft tissues of Venus verrucosa.

Hexavalent chromium (chromium (VI)), a highly toxic heavy metal, is a common pollutant of aquatic ecosystems. The present study aimed to elucidate the potential toxic effects of chromium (VI) on oxidative stress biomarkers and fatty acids profile in the gills and digestive gland of Venus verrucosa, an ecologically and economically important bivalve species. Three doses of chromium (VI) (1, 10 and 100μg.L-1) were chosen for V. verrucosa exposure during 7 days under controlled conditions. A significant increase in the levels of malondialdehyde, lipid hydroperoxides and hydrogen peroxide was observed in the gills and digestive gland of chromium (VI)-exposed V. verrucosa as compared to the control group. Furthermore, an induction of enzymatic antioxidant activities (superoxide dismutase, glutathione peroxidase and glutathione S-transferase) and an enhancement of non-enzymatic antioxidant levels (non-protein thiols, glutathione and vitamin C) were marked. An alteration of fatty acids composition was also noted following chromium (VI) exposure. The obtained results highlighted the importance of assessing oxidative damage biomarkers and fatty acids profile in the study of chromium (VI)-induced toxicity in V. verrucosa.

Bone marrow mesenchymal stem cells could reduce the toxic effects of hexavalent chromium on the liver by decreasing endoplasmic reticulum stress-mediated apoptosis via SIRT1/HIF-1α signaling pathway in rats

This study focused on the effect of bone marrow mesenchymal stem cells (BMSCs) on the repair of rat liver injury induced by Cr (VI). Twenty-four Wistar rats were randomly divided into the control, model and cell therapy group, with 8 rats in each group. Potassium dichromate solution containing 0, 0.4 and 0.4 mg/kg·bw Cr (VI) was administered 5 times a week for 30 days. At the end of treatment, rats in the cell therapy group were administered 1 × 107 BMSCs. Two weeks later, serum alanine and aspartate aminotransferase levels in the cell therapy group were significantly improved compared with those in the model group, CM-Dil-labeled BMSCs were localized in rat livers. Compared with the model group, in the cell therapy group the number of apoptotic hepatocytes by TUNEL assay, MDA content, the expression of HIF-1α, endoplasmic reticulum (ER) stress-mediated apoptosis-related proteins including Grp78, CHOP, Cleaved-Caspase-12, ATF6, and Bax was significantly lower, and SOD activity, the expression of SIRT1 and Bcl-2 was significantly higher. It is suggested that BMSCs are localized in livers and reduce the toxic effects of Cr (VI) on the liver, and the possible mechanism may be related to the mechanisms of BMSCs decreasing ER stress-mediated hepatocyte apoptosis via the SIRT1/HIF-1α signaling pathway.

Melatonin protects mouse spermatogonial stem cells against hexavalent chromium-induced apoptosis and epigenetic histone modification

Given the potential biological functions of spermatogonial stem cells (SSCs) in spermatogenesis and in delivering parental genetic information to the next generation, how these cells respond to environmental toxins and carcinogens should be investigated. We examined the toxic effect of hexavalent chromium (Cr(VI)) on global histone modifications and apoptotic signaling pathways in SSCs. We determined the effect of melatonin, one of the most powerful endogenous free radical scavengers and wide-spectrum antioxidants, in protecting SSCs from Cr(VI)-induced apoptosis and global histone modification by Western blot analysis. In addition, we examined the in vivo effect of melatonin on Cr(VI)-induced histological changes of seminiferous tubules in mouse testes. We also evaluated the fertility of male mice by monitoring litter size following intraperitoneal injection of these chemicals. Our study demonstrated the Cr(VI)-induced global increases in H3K9me3 and H3K27me3 and activated the apoptotic signaling pathway. Pretreatment of SSCs with melatonin alleviated Cr(VI)-induced apoptosis and the global increase of H3K9me3. Exposure to melatonin also attenuated the Cr(VI)-induced increase of the abundance of histone methyltransferase ESET. Furthermore, exogenous administration of melatonin protected mice against Cr(VI)-induced changes in testicular histology and germ cell apoptosis, which helped maintain normal spermatogenesis and male fertility. Our study revealed a potential new therapeutic approach for male reproductive injury caused by Cr(VI).

Chromium (VI) Affected Nutritive Value of Forage Clusterbean (Cyamopsis TetragonolobaL.)

Hexavalent chromium is highly reactive and shown to be toxic for plants at higher concentrations. In present study, a pot experiment was conducted with important forage crop ‘clusterbean’ to determine the toxic effect of hexavalent chromium on its nutritive value on advancement of plant growth. The plants were grown in soil containing varying chromium concentration ranging from 0.0–4.0 mg Cr (VI) kg−1 soil. Nutritive parameters viz structural carbohydrates, protein content and in vitro dry matter digestibility were studied in different plant parts and growth stages. Toxic effects of hexavalent chromium were reflected by no survival of plants at 4.0 mg Cr (VI) kg−1 soil, upto 28% reduction in protein content and high variation in structural carbohydrates contents. Irrespective of these changes, the in vitro dry matter digestibility largely remains unaffected with very less change (0–6%). The study concludes that hexavalent chromium adversely affected nutritive value of clusterbean at higher concentrations.

Uptake and Reduction of Hexavalent Chromium by Aspergillus Niger and Aspergillus Parasiticus

The uptake and reduction of Cr(VI) by Aspergillus niger and A. parasiticus was studied. After 96 hours of growth, the culture solutions spiked with an initial dichromate concentration of 20 mg/l, were completely decolorized and had residual Cr(VI) concentrations of only 0.74 ± 0.55 and 1.69 ± 0.29 mg/l in A. niger and A. parasiticus cultures representing Cr(VI) removal of 96.3% and 91.6%, respectively. In the A. niger culture, significantly (P < 0.01) lower Cr(VI) concentrations were observed within 72 hours of growth compared to those of A. parasiticus, but in both cultures complete removal was almost achieved by 144 hours of growth. The rate of Cr(VI) removal was 0.21 ± 0.09 mgl-1hr-1 and 0.20 ± 0.07 mgl-1hr-1 for A. niger and A. parasiticus, respectively. Cellular concentrations of Cr(VI) in the two fungi increased significantly (P < 0.05 – 0.001) with increasing concentrations of the dichromate treatments. Although tannic acid as sole source of carbon and energy gave significantly lower Cr(VI) removal than glucose (P < 0.001) and acetate (P < 0.01), it supported the removal of about 85.0% and 68.8% of the metal ion by A. niger and A. parasiticus, respectively. The active mycelia of both fungi showed significantly (P < 0.001) higher Cr(VI) removal than inactivated mycelia after incubation at 30°C for 72 hours. Incubation of cell – free extracts of both fungi with NADH at 30°C for 2 hours showed Cr(VI) reduction of 68.0% and 55.5% for A. niger and A. parasiticus, respectively. These findings suggest that uptake and metabolic reduction may be the process by which the two fungi are able to tolerate the toxic effects of hexavalent chromium. However, Cr removal via uptake by the two fungal biomass was observed to be in the range of 0.5 – 1.78% only, for all the concentrations applied, which is insignificant when compared with the initial Cr concentration in the culture medium. The results obtained through this investigation indicate the possibility of treating waste effluents containing hexavalent chromium using Aspergillus niger and A. parasiticus.

Comparison of the preventive effect of vitamin C and E on hexavalent chromium induced pulmonary fibrosis in rat

Many studies have shown that hexavalent chromium (Cr(6+)) compounds cause variety of toxicity, such as carcinogenic effects and pulmonary fibrosis. The aim of this study was to investigate the effect of vitamins C and E on hexavalent chromium-induced lung fibrosis in animal model. Rats weighing 180-210 g were used during the study. The negative control group received a single dose of 0.2 ml intratracheal normal saline. Other groups were given single intratracheal instillation of 50 mg/kg sodium dichromate in saline vehicle and then treated with either vitamin C or E orally. Vit C group treated with 75 mg/kg/day vit C. Vit E group treated with 20 mg/kg/day vit E. Vit C+E group treated with 75 mg/kg/day vit C + 20 mg/kg/day vit E. Three weeks after such treatments animals were killed, lungs were removed for histology and biochemical investigation. Collagen and hydroxyproline content of lung tissue were determined using spectrophotometric methods. Hexavalent chromium caused marked alveolar thickening associated with fibroblasts and myofibroblasts proliferation and collagen production in interstitial tissue leading to pulmonary fibrosis. Administration of vitamins C and E reduced the fibrotic damage in lung tissue. The combination of vit E and C had more pronounced effect. From this study it can be concluded that co-administration of vit C & E may significantly diminish the toxic effects of hexavalent chromium on lung.

Microcalorimetric study the toxic effect of hexavalent chromium on microbial activity of Wuhan brown sandy soil: An in vitro approach

A multi-channel thermal activity monitor was applied to study soil microbial activity in Wuhan brown sandy soil in the presence of different concentrations of hexavalent chromium ( K 2 Cr 2 O 7 ) . In order to stimulate the soil microbial activity, 5.0 mg of glucose and 5.0 mg of ammonium sulfate were added to a 1.20-g soil sample under a controlled humidity of 35%. The results show that the poisonous species of K 2 Cr 2 O 7 at an half inhibitory concentration ( IC 50 ) value of 4.27 μ g mL - 1 against soil microbe, and an increase of the amount of hexavalent chromium is associated to a decrease in the microbial activity of the soil, probably due to an increase in the toxicity of hexavalent chromium, affecting strongly the life in this soil microbial environment. Our work also suggests that microcalorimetry is a fast, simple and more sensitive method that can be easily performed to study the toxicity of different species of heavy metals on microorganism compared to other biological methods.

In vivo spermatotoxic effect of chromium as reflected in the epididymal epithelial principal cells, basal cells, and intraepithelial macrophages of a nonhuman primate ( Macaca radiata Geoffroy)

To understand, through a simulation experiment in a nonhuman primate model, the potential in vivo spermatotoxic toxic effect of hexavalent chromium (CrVI) in men who are occupationally or environmentally exposed to it. Controlled laboratory study. Research laboratory in a department of endocrinology in a university in India. Male bonnet monkey, Macaca radiata Geoffroy. Monkeys were exposed ad libitum to 100, 200, and 400 ppm CrVI, dissolved in drinking water, for a chronic period of 180 days. Examination of epididymis with a transmission electron microscope and assessment of the effect of CrVI in terms of accumulation of sperm-derived lipofuscin (LF) material in the principal cells, basal cells, and intraepithelial macrophages of the epithelium. The abundance of basal cells and intraepithelial macrophages and the content of LF material in these cell types increased. The principal cells phagocytosed from the lumen the dead sperm resulting from CrVI exposure and processed them partially into LF material, which was acquired by the basal cells and intraepithelial macrophages and processed further. The LF material-laden basal cells and intraepithelial macrophages appeared to leave the epithelium, accompanied by recruitment of fresh basal cells and intraepithelial macrophages. Occupational or environmental exposure to CrVI, as would occur in the tannery, soap, and other industries in developing and underdeveloped countries, can be toxic in vivo to spermatozoa.

Acute toxicity of hexavalent chromium in isolated teleost hepatocytes

Acute toxic effects of hexavalent chromium [Cr(VI)], a widely recognised carcinogenic, mutagenic and redox active metal, were investigated in isolated hepatocytes of goldfish ( Carassius auratus). Exposure to 250 μM Cr(VI) induced a significant decrease of cell viability from 94% in controls to 88% and 84% after 30 min and 4 h of exposure, respectively. Cr-toxicity was associated with a concentration-dependent stimulation of the formation of reactive oxygen species (ROS). As one potential source of ROS formation we identified the lysosomal Fe 2+ pool, since the ferric ion chelator deferoxamin inhibited ROS formation by approximately 15%. Lysosomal membranes remained nevertheless intact during Cr-exposure, as determined from neutral red retention in this compartment. Another significant source of ROS appear to be the mitochondria, where a presumably uncoupled increase of respiration by 20–30% was triggered by the metal. Inhibition of mitochondrial respiration by cyanide caused an approximately 40% decrease of Cr-induced ROS-formation, whereas the uncoupling agent carbonyl cyanide m-chlorophenyl hydrazine was without effect. Cellular Ca 2+ homeostasis was not disturbed by Cr(VI) and thus played no role in this scenario. Overall, our data show that Cr(VI) is acutely toxic to goldfish hepatocytes, and its toxicity is associated with the induction of radical stress, presumably involving lysosomes and mitochondria as important sources of ROS formation.

In vivo recovery of glycogen metabolism in hemolymph and tissues of a freshwater field crab Barytelphusa guerini on exposure to hexavalent chromium

The in vivo toxic effects of hexavalent chromium (20 mg/liter) on hemolymph glucose, tissue glycogen, total free sugars, and active and total phosphorylases of an edible, freshwater crab Barytelphusa guerini were studied. In a 15-day exposure span followed by a 15-day postexposure recovery, the time-course alterations in these constituent segments of the glycogen metabolism indicate an inconsistent depletion in metabolite levels and elevated enzyme activities during exposure period as well as hyperglycemia. An insignificant recovery was observed in these parameters on the 15th day of the postexposure phase.

Hexavalent chromium and ascorbic acid interaction on proliferation of the human cell line NHIK3025

When cells from the human cell line NHIK3025 were cultured for 4 days, with hexavalent chromium (K 2Cr 2O 7) at a concentration of 8 · 10 −7M, the relative cell number was reduced to 38%. This effect of hexavalent chromium was abolished if ascorbic acid and chromate were added simultaneously to the incubation medium, but not if ascorbic acid was added 24 h prior to chromate addition. Dehydroascorbic acid was not able to reduce the effect of K 2C 2O 7 either when added simultaneously or when added 24 h prior to chromate exposure. Therefore, the cells could only be protected against the toxic effect of hexavalent chromium when ascorbic acid was added at the same time as K 2C 2O 7.