The Protective and Antidotal Effects of Taurine on Hexavalent Chromium-Induced Oxidative Stress in Mice Liver Tissue

Acute exposure to hexavalent chromium [Cr(VI)] compounds can cause hepatotoxicity. Reactive intermediates and free radicals generated during reduction process may be responsible for Cr(VI) toxicity. In this study, the effects of pretreatment or posttreatment of taurine on Cr(VI)-induced oxidative stress and chromium accumulation in liver tissue of Swiss Albino mice were investigated. Single intraperitoneal (ip) potassium dichromate treatment (20 mgCr/kg), as Cr(VI) compound, significantly elevated the level of lipid peroxidation as compared with control group (p < 0.05). This was accompanied by significant decreases in nonprotein sulfhydryls (NPSHs) level, superoxide dismutase (SOD), and catalase (CAT) enzyme activities as well as a significant chromium accumulation in the tissue (p < 0.05). Taurine administration (1 g/kg, ip) before or after Cr(VI) exposure resulted in reduction of lipid peroxidation (p < 0.05) showed rebalancing effect on tissue NPSH levels either in pretreatment or in posttreatment (p < 0.05). Enzyme activities of SOD and CAT were restored by taurine pretreatment (p < 0.05), whereas posttreatment had less pronounced effects on these parameters. On the other hand, taurine treatment, before or after exposure, could exert only slight decreases in tissue Cr levels (p > 0.05). In view of the results, taurine seems to exert some beneficial effects against Cr(VI)-induced oxidative stress in liver tissue.     

N-Acetyl-L-Cysteine Protects Liver and Kidney Against Chromium(VI)-Induced Oxidative Stress in Mice

Acute hexavalent chromium [Cr(VI)] compound exposure may lead to hepatotoxic and nephrotoxic effects. Cr(VI) reduction may generate reactive intermediates and radicals which might be associated with damage. We investigated effects of N-acetyl-l-cysteine (NAC) pre- or post-treatment on oxidative stress and accumulation of Cr in liver and kidney of Cr(VI)-exposed mice. Intraperitoneal potassium dichromate injection (20 mg Cr/kg) caused a significant elevation of lipid peroxidation in both tissues as compared to control (p < 0.05). Significant decreases in non-protein sulfhydryl (NPSH) level, as well as enzyme activities of catalase (CAT) and superoxide dismutase (SOD) along with significant accumulation of Cr in the tissues (p < 0.05) were of note. NAC pre-treatment (200 mg/kg, ip) provided a noticeable alleviation of lipid peroxidation (p < 0.05) in both tissues, whereas post-treatment exerted significant effect only in kidney. Similarly, Cr(VI)-induced NPSH decline was restored by NAC pre-treatment in both tissues (p < 0.05); however, NAC post-treatment could only replenish NPSH in liver (p < 0.05). Regarding enzyme activities, in liver tissue NAC pre-treatment provided significant restoration on Cr(VI)-induced CAT inhibition (p < 0.05), while SOD enzyme activity was regulated to some extent. In kidney, SOD activity was efficiently restored by both treatments (p < 0.05), whereas CAT enzyme alteration could not be totally relieved. Additionally, NAC pre-treatment in both tissues and post-treatment in liver exerted significant tissue Cr level decreases (p < 0.05). Overall, especially NAC pre-treatment seems to provide beneficial effects in regulating pro-oxidant/antioxidant balance and Cr accumulation caused by Cr(VI) in liver and kidney. This finding may be due to several mechanisms including extracellular reduction or chelation of Cr(VI) by readily available NAC.     

Antioxidant properties of chromium and zinc

The effects of chromium (chromium picolinate, CrPic) and zinc (ZnSO₄H₂O) supplementation on serum concentrations of malondialdehyde (MDA) (an indicator of lipid peroxidation) and serum status of some antioxidant vitamins and minerals of laying hens (Hy-Line) reared at a low ambient temperature (6.8°C) were evaluated. One hundred twenty laying hens (Hy-Line; 32 wk old) were divided into 4 groups, 30 hens per group. The hens were fed either a basal diet or the basal diet supplemented with either 0.4 mg Cr/kg of diet, 30 mg Zn/kg of diet, or 0.4 mg Cr plus 30 mg Zn/kg of diet. Digestibility of nutrients (dry matter [DM], organic matter [OM], crude protein [CP], and ether extract [EE]) increased by supplementation of chromium and zinc (p<0.05). Supplemental chromium and zinc increased serum vitamins C and E but decreased MDA concentrations (p<0.05). Additionally, supplemental chromium and zinc caused an increase in the serum concentrations of Fe, Zn, Mn, and Cr (p < 0.05). The present study showed that low ambient temperature causes detrimental effects on the digestibility of nutrients and antioxidant status and that such detrimental effects caused by low ambient temperature can be alleviated by chromium and zinc supplementation, particularly when Cr and Zn were simultaneously included into the diet. Data obtained in the present study suggest that such supplementation can be considered as a protective management practice in a diet of laying hens for alleviating negative effects of cold stress.     

Trivalent chromium pretreatment alleviates the toxicity of oxidative damage in wheat plants exposed to hexavalent chromium

Treating plants with abiotic or biotic factors can lead to the establishment of a unique primed state of defense. Primed plants display enhanced defense reactions upon further challenge with environmental stressors. Here, we report that trivalent chromium (Cr(III)) pretreatment can alleviate hexavalent chromium (Cr(VI)) toxicity in 2-week-old wheat plants. The data indicate that Cr(III)-pretreated wheat displayed longer survival times and less heavy metal toxicity symptoms under Cr(VI) exposure than the control. To investigate the possible mechanism from an antioxidant defense perspective, we determined the H₂O₂ and lipid peroxide content (TBARS), the activities of antioxidant enzymes (SOD, CAT, APX and GR) and the antioxidant metabolite content (ascorbate and glutathione content, AsA/DHA and GSH/GSSG ratios) in pretreated wheat roots. The results showed that 0.5 μM Cr(III) pretreatment can alleviate oxidative damage, such as H₂O₂ and TBARS accumulation, in root tissues compared to the control during the first 3 days of Cr(VI) exposure. Furthermore, we determined that this pretreatment can significantly increase the antioxidant enzyme activities and total ascorbate and glutathione contents compared to the control treatment. In addition, redox homeostasis declined slightly in pretreated wheat compared to the control in the presence of Cr(VI). We discuss a possible mechanism for Cr(III)-mediated protection of wheat.     

In vivo nephrotoxicity induced in mice by chromium(VI)

The role of glutathione (GSH) and chromium (V) in chromium (VI)-induced nephrotoxicity in mice was investigated at 24 h after K2Cr(VI)2O7 ip injection. Nephrotoxicity was assessed by measurements of relative kidney weight and serum urea nitrogen. Cr(VI) nephrotoxicity was accompanied by decreased renal GSH and glutathione reductase (GSSG-R) levels. Pretreatment with buthionine sulfoximine, an inhibitor of GSH biosynthesis, enhanced Cr(VI)-induced nephrotoxicity, and remarkably diminished kidney GSH and GSSG-R levels. In contrast, pretreatment with glutathione methyl ester, a GSH-supplying agent, prevented Cr(VI) from exerting a harmful effect on mouse kidney and restored kidney GSH level. Administration of a Cr(V) compound, K3Cr(V)O8, induced much higher toxicity in mouse kidney than Cr(VI), but it failed to diminish renal GSH level. Another Cr(V) compound, Cr(V)-GSH complex, and Cr(III) nitrate did not cause a nephrotoxic effect in mice. The mechanism of Cr(VI)-induced nephrotoxicity was explained using GSH and Cr(V).     

Supplementation with chromium picolinate recovers renal Cr concentration and improves carbohydrate metabolism and renal function in type 2 diabetic mice

To study the preventive effect of supplemented chromium picolinate (CrPic) on the development of diabetic nephropathy in mice, we analyzed the effects of CrPic supplementation on renal function and concentrations of serum glucose and tissue chromium (Cr). In experiment 1, male KK-Ay obese diabetic mice were fed either a control diet (control) or a diet supplemented with 2 mg/kg diet (Cr2) or 10 mg/kg diet (Cr10) of Cr for 12 wk. Cr10 significantly ameliorated hyperglycemia after a glucose load, creatinine clearance rates, and urinary microalbumin levels (p<0.05). In experiment 2, the Cr10 diet was fed to male KK-Ay obese diabetic mice and C57BL nondiabetic mice for 4 wk. The CrPic diet reduced urinary albumin excretion in the diabetic mice (p<0.05). Inductively coupled plasma-mass spectrometry analysis revealed that the renal Cr content and the recovery of renal Cr concentration after Cr supplementation were significantly lower in the diabetic mice than in the nondiabetic mice (p<0.01). These observations suggest that Cr supplementation of type 2 diabetic mice reduces the symptoms of hyperglycemia and improves the renal function by recovering renal Cr concentration.     

Uptake of chromium(III) and chromium(VI) compounds in the yeast cell structure

The study presented in this article investigated the influence of different Cr(III) and Cr(VI) compounds in the cultivation medium on the uptake and localization of chromium in the cell structure of the yeast Candida intermedia. The morphology of the yeast cell surface was observed by the scanning electron microscopy. Results demonstrated that the growth inhibitory concentration of Cr(III) in the cultivation medium induced changes in the yeast cell shape and affected the budding pattern, while inhibitory concentration of Cr(VI) did not cause any visible effects on morphological properties of the yeast cells. The amount of total accumulated chromium in yeast cells and the distribution of chromium between the yeast cell walls and spheroplasts were determined by atomic absorption spectroscopy. No significant differences were found neither in total chromium accumulation nor in the distribution of chromium in yeast cell walls and spheroplasts between the two of Cr(VI) compounds. Conversely, substantial differences between Cr(III) compounds were demonstrated in the total uptake as well as the localization of chromium in yeast cells.     

Effect of rosmarinic acid on inhibition of gentamicin induced nephrotoxicity in rats

The present investigation reports the effect of rosmarinic acid (RA), an antioxidant on gentamicin sulphate (GS)-induced renal oxidative damage in rats. Rosmarinic acid (RA) has been demonstrated to have antioxidant, free radical scavenger and anti-inflamatory effects. Twenty-eight Sprague-Dawley rats were divided in to four equal groups as follows: group 1 (control), group 2 (GS 100 mg/kg/d ip), group 3 (GS 100 mg/kg/d ip + RA 50 mg/kg/d) and group 4 (GS 100 mg/kg/d ip + RA 100 mg/kg/d). Treatments were administrated once daily for 12 days. After 12 days 24 h urine was collected, blood was sampled and kidneys were removed. Serum and kidney tissue MDA assessed by thiobarbituric acid. Kidney paraffin sections (5 μm thickness) from the left kidney stained with periodic acid Schiff. Tubular necrosis was studied semiquantitatively and glomerular volume and volume density of proximal convoluted tubule (PCT) estimated stereologically. Kidney homogenize were prepared from right kidney. Serum creatinine, urea and kidney antioxidant enzymes activity were assessed by special kits. Data were compared by SPSS 13 software and Mann–Whitney test at p < 0.05. Co treatment of GS and RA (High dose) significantly decreased serum creatinine, MDA, urea, tubular necrosis (p < 0.05) and increase renal GSH, GPX, CAT, SOD, volume density of PCT and creatinine clearance significantly in comparison with GS group (p < 0.05). Treatment with RA (high dose) maintained serum creatinine, volume density of PCT, renal GSH, GPX, SOD and MDA as the same level as control group significantly (p < 0.05). In conclusion, RA alleviates GS nephrotoxicity via antioxidant activity, increase of renal GSH content and increase of renal antioxidant enzymes activity.     

Involvement of Asada-Halliwell Pathway During Phytoremediation of Chromium (VI) in Brassica juncea L. Plants

Brassica juncea (Indian mustard) L. plants were exposed to different concentrations (0.0, 0.1, 0.3 and 0.5 mM) of Chromium (Cr) and harvested after 30 and 60 days of sowing for the analysis of growth parameters, metal uptake and oxidative stress markers. Significant accumulation of Cr (VI) by B. juncea L. plants resulted in the reduced growth and modulations in the pool of various biochemical stress markers. The toxic effects of Cr (VI) on growth and other stress markers (protein content, lipid peroxidation and antioxidative enzymes viz.SOD, CAT, POD, APOX, GR, DHAR and MDHAR) in B. juncea L. were observed to be concentration and time dependent. Effect of Cr (VI) on biochemical parameters was differential and their maximum activities of SOD, POD, APX, GR, DHAR and lipid peroxidation were recorded at 0.5 mM concentration in 30 days old plants. Whereas, trend in the activities of most of the stress markers was reversed in 60 days old plants. The results obtained from the study suggested that Cr (VI) stress inhibited growth of B. juncea L. plants is directly interrelated with its accumulation and resulted in the modulation in activities of various stress markers.     

Antioxidant enzyme activities and lipid peroxidation induced by eicosapentaenoic acid (EPA) in PC12 cells

Eicosapentaenoic acid (EPA) is one of the major dietary polyunsaturated fatty acids and induces apoptosis in several cancer cells. In this study, the EPA induced lipid peroxidation and response of antioxidative enzymes have been investigated in rat pheochromocytoma PC12 cells to elucidate the mechanisms of apoptosis induced by the polyunsaturated fatty acid EPA. We have analyzed superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities and glutathione (GSH) contents in PC12 cells after exposure to different concentrations of EPA. Lipid peroxidation was shown to increase in the presence of EPA as an indication of the oxidative damage. Lipid peroxidation was enhanced by EPA in a dose-dependent manner, and the loss of cell viability was partially reversed by vitamin E. In the case of antioxidant enzyme activities, SOD and GPX activities and GSH contents increased significantly at 50 μmol/L EPA and were respectively 2.41-fold (p < 0.01), 3.49-fold (p < 0.05), and 1.43-fold (p < 0.05) higher than controls. The CAT activity at 10 μmol/L had the highest value and was increased by 25.83% (p < 0.05) compared to control. The results suggest that in PC12 cells the mechanism of apoptosis induced by EPA may be partly due to lipid peroxidation.     

Evaluation of the effects of cadmium on rat liver

Abstact Cadmium is one of the most toxic pollutants in environment. Cadmium accumulation in blood affects the renal cortex and causes renal failure. In this study, we aimed to evaluate the effects of cadmium on rat liver tissue. Eighteen male albino rats aged ten weeks old were used in the study. 15 ppm of cadmium was administered to rats via consumption water daily. At the end of the 30th study day, the animals were killed under ether anesthesia. After the liver tissue samples were taken, histopathological and biochemical examinations were performed. Histopathologic changes have included vacuolar and granular degenerations in hepatocytes, heterochromatic nucleuses and sinusoidal and portal widenings. Central vein diameters were normal in cadmium exposed group. Whereas, there was statistically significant difference between two groups by means of sinusoidal (p< 0.001) and portal triad diameters (p< 0.01). Malondialdehyde (MDA) is an indicator of lipid peroxidation. In this study, MDA was used as a marker of oxidative stress-induced liver impairment in cadmium exposed rats. Superoxide dismutase (SOD) and catalase (CAT) activities were also measured to evaluate the changes in antioxidative system in liver tissues. Current findings showed that MDA levels were increased and SOD and CAT activities were decreased in cadmium exposed group compared to control group. The difference between two groups was statistically significant (pvalues: MDA,p< 0.01; CAT,p< 0.01 and SOD,p< 0.05). In conclusion, these findings suggest the role of oxidative mechanisms in cadmium-induced liver tissue damage     

Spectroscopic studies on the interaction of chromium (VI) and chromium (III) with keyhole limpet hemocyanin

The interactions of keyhole limpet hemocyanin (KLH) with chromium nitrate, potassium dichromate, and chromate were investigated using fluorescence, UV–vis absorption and circular dichroism (CD) spectroscopy under simulated physiological conditions. The experimental results showed that the different forms of chromium could quench the intrinsic fluorescence of KLH following a static quenching mechanism rather than by dynamic collision, which indicated that a Cr–KLH complex was formed. The Stern–Volmer quenching constants for the interaction indicated that the binding reaction of KLH with Cr(VI) was stronger the binding of KLH with Cr(III). The thermodynamic values for binding of Cr(VI) to KLH are ΔH > 0 and ΔS > 0. By contrast, the values for the interaction of Cr(III) with KLH are ΔH < 0 and ΔS < 0. The results of synchronous fluorescence, UV–vis absorption and CD spectroscopy showed that the α‐helical secondary structure and conformation of KLH were altered by different forms of chromium. Copyright © 2016 John Wiley & Sons, Ltd.     

Speciation dependant antioxidative response in roots and leaves of sorghum (Sorghum bicolor (L.) Moench cv CO 27) under Cr(III) and Cr(VI) stress

Growth, lipid peroxidation, H₂O₂ produciton and the response of the antioxidant enzymes and metabolites of the ascorbate glutathione pathway to oxidative stress caused by two concentrations (50 and 100 µM) of Cr(III) and Cr(VI) was studied in 15 day old seedlings of sorghum (Sorghum bicolor (L.) Moench cv CO 27) after 10 days of treatment. Cr accumulation in sorghum plants was concentration and organ dependant. There was no significant growth retardation of plants under 50 µM Cr(III) stress. 100 µM Cr(VI) was most toxic of all the treatments in terms of root and leaf growth and oxidative stress. 50 µM Cr(VI) treated roots exhibited high significant increase in superoxide dismutase (SOD), dehydroascorbate reductase (DHAR) and glutathione reductase (GR) (p < 0.01) and significant increases in catalse (CAT), ascorbate peroxidase (APX) and monodehydroascorbate reductase (MDHAR) (p < 0.05). A high increase in ascorbic acid (AA) level was seen in roots of 50 µM Cr(VI) treated plants in comparison with control. Levels of reduced glutathione (GSH) showed a varied and complex response in all the treatments in both plant parts. GSH/GSSG ratio was not affected by Cr(III) treatment in leaves, in contrast, roots exhibited significant reduction in the ratio. Results indicate that GSH depletion increased sensitivity to oxidative stress (Cr(VI) roots and leaves and Cr(III) 100 µM roots) and AA in tandem with APX compensated for GSH depletion by acting directly on H₂O₂ and the mechanism of defensive response in roots as well as leaves varied in its degree and effectiveness due to the concentration dependant differences observed in translocation of the element itself, reactive oxygen species (ROS) generation and enzyme inhibition based on the oxidation state supplied to the plants.     

Selection and properties of mutant yeast <Emphasis Type="Italic">Pichia guilliermondii</Emphasis> strains resistant to chromium (VI)

Yeast Pichia guilliermondii strains L3 and L2, exposed to UV mutagenesis, produced over 80 mutants capable of growing on media containing 1.5 mM bichromate (Cr(VI)). The mutations making the strains resistant to Cr(VI) were dominant or semidominant. The mutants varied in Cr(VI) resistance, the degree of chromium accumulation in the cells (from 0.1 to 11.6 mg/g dry cells), and the degree of Cr(VI) reduction (from 50% to complete disappearance of bichromate from the culture liquid). Chromium accumulation in mutant cells depended on medium composition, Cr(VI) concentration, and the time of exposure to Cr(VI). The resistance to bichromate can be caused by various reasons: decrease in chromium absorption, altered ability to reduce Cr(VI), or damage of sulfate transport mechanisms.Translated from Prikladnaya Biokhimiya i Mikrobiologiya, Vol. 41, No. 2, 2005, pp. 204–209.Original Russian Text Copyright © 2005 by Babyak, Ksheminskaya, Gonchar, Yanovich, Fedorovich.     

Moderate selenium dosing inhibited chromium (VI) toxicity in chicken liver

This study aimed to clarify the effect of selenium (Se) on chromium (VI) [Cr(VI)]‐induced damage in chicken liver. A total of 105 chickens were randomly divided into seven groups of 15. Group I received deionized water; group II received Cr(VI) (7.83 mg/kg/d) alone; and other groups orally received both Cr(VI) (7.83 mg/kg/d) and Se of different doses (0.14, 0.29, 0.57, 1.14, and 2.28 mg/kg/d). The levels of superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA), Ca²⁺‐ATPase, and mitochondrial membrane potential (MMP) were measured. Results showed that Cr(VI) increased MDA content and decreased GSH content, T‐SOD activity, Ca²⁺‐ATPase activity, and MMP level. Meanwhile, Se co‐treatment (0.14, 0.29, and 0.57 mg/kg/d) increased the viability of the above indicators compared with Cr(VI)‐treatment alone. In addition, histopathologic examination revealed that Cr(VI) can cause liver damage, whereas Se supplementation of moderate dose inhibited this damage. This study confirmed that Se exerted protective effect against Cr(VI)‐induced liver damage.     

Comparison of the uptake and distribution of chromate in rats and mice

The purpose of this study was to evaluate species differences in tissue accumulation of chromium. Rats and mice were orally exposed to Cr(VI) (potassium chromate) via drinking water (8 mg/d/kg body wt for 4 or 8 wk) or by ip injection (0.3 and 0.8 mg/d/kg, for 4 or 14 d). Chromium concentrations were measured by atomic absorption spectrophotometry, and tissues were compared for exposure route and species differences. After oral exposure, irrespective of treatment duration, liver concentrations of chromium were three to four times higher in mice than rats, whereas kidney concentrations were about 50% lower. However, after ip injection, kidney and blood concentrations in rats were two- and four-fold, higher, respectively. Both rats and mice showed high values of Cr concentration in the bone. After single ip injection of Na₂ ⁵¹CrO₄; Cr concentrations were higher in the blood of rats than mice both after 24 and 72 h. Red blood cell concentrations of Cr were also greater in rats than mice by approximately threefold, whereas white blood cell Cr concentrations were higher in mice than rats. There was also a twofold greater binding of Cr/μmol of hemoglobin in rats compared to mice. These data indicate that species differences exist for Cr metabolism and that they differ with respect to the route of exposure. These results may be owing to species differences in the reduction of Cr and different binding of Cr to hemoglobin.     

Efficient removal of hexavalent chromium by a tolerant Streptomyces sp. affected by the toxic effect of metal exposure

AIMS: To isolate and analyse chromium-resistant micro-organisms suitable for bioremediation. METHODS AND RESULTS: Strain CG252, with a minimal inhibitory concentration of 500 microg ml(-1), was isolated from contaminated soils and identified as a Streptomyces sp. by 16S rDNA sequence analysis. Assays carried out at various Cr(VI) concentrations indicated that chromium removal was more efficient at lower concentrations and that this activity resulted in accumulation of Cr(III). Atomic adsorption analysis indicated that the chromium removed was not associated with cell mass and activity assays showed that the capacity to reduce Cr(VI) was most probably due to a soluble cytosolic enzyme. Cells grown as biofilms showed enhanced removal of Cr(VI) with respect to planktonic cells, while analysis of growth and colony morphology indicated that Cr(VI) had a toxic effect on this strain. CONCLUSIONS: Streptomyces sp. CG252 tolerated heavy metals and elevated levels of chromium, despite its negative effect on growth and development, and was efficient at removing Cr(VI) by promoting reduction to Cr(III). SIGNIFICANCE AND IMPACT OF THE STUDY: Strain CG252's capacity to tolerate heavy metals and to reduce Cr(VI) to the less toxic Cr(III), especially when forming biofilms, makes it a promising candidate for detoxification of sites containing this heavy metal.     

Investigating DNA damage in tannery workers occupationally exposed to trivalent chromium using comet assay

DNA damage of peripheral lymphocytes in 60 workers occupationally exposed to trivalent chromium [Cr(III)] in a tannery was studied using comet assay. The urinary and blood chromium levels were detected as a biomarker of internal exposure. The 90 subjects were divided into three groups: (i) exposure group I included 30 tannery workers highly exposed to chromium from tanning department; (ii) exposure group II included 30 tannery workers with moderate chromium exposure from finishing department; (iii) control group included 30 individuals without exposure to physical or chemical genotoxic agents. No significant difference was found among the three groups for age and smoking. The results showed that the medians of blood and urinary Cr of two exposure groups were significantly higher than those of control group (P < 0.01). And the medians of blood and urinary Cr of exposure group I were significantly higher than those of exposure group II (P < 0.05 or P < 0.01). The medians of mean tail length (MTL) of the three groups were 5.33 (2.90–8.50), 3.43 (2.31–8.29) and 2.04 (0.09–3.83) μm, respectively; The medians of mean tail moment (MTM) of the three groups were 6.28 (2.14–11.81), 3.41 (1.25–11.07) and 0.53 (0.13–3.29), respectively. The MTL and MTM of two exposure groups were significantly higher than those of control group (P < 0.01). The MTL and MTM of exposure group I were significantly higher than those of exposure group II (P < 0.01). The results of the present investigation suggest that occupational exposure to trivalent chromium can lead to a detectable DNA damage of human peripheral lymphocytes. Moreover, DNA damage was associated with chromium levels in blood. DNA damage may serve as a valuable effective biomarker and total chromium in blood may serve as a useful internal exposure biomarker in the population occupationally exposed to trivalent chromium.     

Single and Combined Effects of Exposure Concentration and Duration on Biological Responses of Ceratophyllum demersum L. Exposed to Cr Species

This study aimed to demonstrate the ways in which two chromium species, Cr (III) and Cr (VI), can affect various physiological and biochemical parameters in the plant Ceratophyllum demersum L., and to evaluate the single and combined impact of exposure concentration and duration. C. demersum was exposed to Cr (III) and Cr (VI) at a variety of concentrations (1, 2, 5, and 10 mM) and for differing durations (1, 2, 4, and 7 days), after which Cr accumulation, relative growth rate (RGR), malondialdehyde (MDA) content, electrical conductivity (EC), photosynthetic pigmentation, proline content and antioxidant enzyme activities were examined. The single and combined effects of exposure duration and Cr concentration on each parameter were determined using a two-way analysis of variance. For both the Cr (III) and Cr (VI) applications, it was observed that concentration had a significant effect on all parameters assessed. However, duration had no statistically significant effect on proline content in the Cr (III) application, or on MDA and protein content in the Cr (VI) application. It was determined that concentration exerted greater effects than duration for both Cr species studied. In addition, the results indicated that duration and concentration had a synergistic effect on variations of RGR, EC, protein content, and antioxidant enzyme activities in both the Cr (III) and Cr (VI) applications. These results may be useful when planning further phytoremediation and plant biotechnology studies.     

Rats retain chromium in tissues following chronic ingestion of drinking water containing hexavalent chromium

Humans have sometimes been exposed to as much as 10 ppm Cr(VI) in drinking water from contaminated wells. The risks to these individuals are not well understood because the digestive tract reduces some of the Cr(VI) to the less bioavailable Cr(III) prior to absorption, and the disposition of the remaining Cr(VI) has not been well studied. We determined tissue Cr concentrations in rats after chronic ingestion of Cr(VI) in drinking water at concentrations relevant to human exposure levels. Adult male and female Fischer 344 rats consumed ad libitum 0, 0.5, 3, or 10 ppm Cr(VI) as K₂CrO₄ in drinking water for 44 wk. Rats then were given deionized water 4–6 d prior to sample collection. Females given 3 or 10 ppm Cr(VI) consumed more Cr(VI) per unit of body weight than did males. Bone Cr concentrations were significantly elevated in rats that drink 10 ppm Cr(VI). Renal Cr concentrations were significantly elevated in male rats that drink 3 or 10 ppm Cr(VI) and in female rats dosed with 10 ppm Cr(VI). Female rats had elevated liver Cr concentrations after drinking 3 or 10 ppm Cr(VI). Testicular Cr concentrations were slightly elevated in rats that drank 10 ppm Cr(VI). Brain, ovarian, and whole-blood Cr concentrations were below detection limits in all exposure groups. Although tissue Cr accumulation may have resulted from absorption of Cr(III), it is poorly absorbed. Therefore, the increased tissue retention may also have resulted, in part, from increased absorption of Cr(VI) and its subsequent uptake from the systemic circulation.