Oxidative Damage in Erythrocytes of Rats after 1 and 2 Weeks of Exposure to Chromium (VI): Protective Effect of Selenium (original) (raw)
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Oxidative damage induced by chromium (VI) in rat erythrocytes: protective effect of selenium
Journal of Physiology and Biochemistry, 2011
Excess chromium (Cr) exposure is associated with various pathological conditions including hematological dysfunction. The generation of oxidative stress is one of the plausible mechanisms behind Cr-induced cellular deteriorations. The efficacy of selenium (Se) to combat Cr-induced oxidative damage in the erythrocytes of adult rats was investigated in the current study. Female Wistar rats were randomly divided into four groups of six each: group I served as controls which received standard diet, group II received in drinking water K 2 Cr 2 O 7 alone (700 ppm), group III received both K 2 Cr 2 O 7 and Se (0.5 Na 2 SeO 3 mg/kg of diet), and group IV received Se (0.5 mg/kg of diet) for 3 weeks. Rats exposed to K 2 Cr 2 O 7 showed an increase of malondialdehyde and protein carbonyl levels and a decrease of sulfhydryl content, glutathione, non-protein thiol, and vitamin C levels. A decrease of enzyme activities like catalase, glutathione peroxidase, and superoxide dismutase activities was also noted. Co-administration of Se with K 2 Cr 2 O 7 restored the parameters cited above to near-normal values. Therefore, our investigation revealed that Se was a useful element preventing K 2 Cr 2 O 7 -induced erythrocyte damages.
Asian Journal of Pharmaceutical and Clinical Research, 2020
Objective: The present study assessed the hepatotoxicity and nephrotoxicity associated with oxidative stress induced by chronic exposure to a very low environmentally relevant dose of hexavalent chromium along with the ameliorative potential of selenium and Vitamin E in male rats. Methods: Twenty-four male albino rats were divided into four groups. Animals of control group received only distilled water. The treated group received solution of potassium dichromate (K 2 Cr 2 O 7) at a dose of 1 mg/kg b.w./day. The third group received sodium selenate (0.25 mg/kg bw) plus Vitamin E (100 mg/kg bw). The supplemented group received sodium selenate plus Vitamin E along with K 2 Cr 2 O 7 solution. The animals were treated for 90 consecutive days. Results: There was a significant decrease in body weight gain and an increase in liver and kidney weight along with an increase in serum glucose, cholesterol, urea, and creatinine; a decrease in protein and albumin levels in the rats treated with K 2 Cr 2 O 7. The activities of serum enzymes, serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase, acid phosphatase, and alkaline phosphatase, were also increased in treated animals. The activities of enzymes catalase, superoxide dismutase, GPx and the levels of GSH reduced significantly and level of malondialdehyde increased in K 2 Cr 2 O 7 treated rats. Liver and kidney tissues exhibited features of toxicity in chromium treated animals. All the effects were reversed in supplemented group. Conclusion: Chronic exposure to K 2 Cr 2 O 7 at a very low environmentally relevant dose caused hepatotoxicity and nephrotoxicity induced by oxidative stress in male albino rats; the effects were ameliorated by supplementation with selenium and Vitamin E in combination.
Ameliorating effect of selenium on chromium (VI)-induced oxidative damage in the brain of adult rats
Journal of Physiology and Biochemistry, 2012
Chromium is known for its wide toxic manifestations. This experiment aims to evaluate the effect of selenium against oxidative stress induced by chromium in the cerebrum and cerebellum. Female Wistar rats were randomly divided into four groups of six each: group I served as controls which received the standard diet; group II received drinking water K 2 Cr 2 O 7 alone (700 ppm); group III received both K 2 Cr 2 O 7 and Se (0.5 mg Na 2 SeO 3 /kg of diet); and group IV received Se (0.5 mg/kg of diet) for 3 weeks. The exposure of rats to K 2 Cr 2 O 7 promoted oxidative stress in the cerebrum and cerebellum with an increase in malondialdehyde and a decrease of nonenzymatic antioxidant levels such as glutathione, nonprotein thiol, and vitamin C. An increase of enzyme activities like catalase, glutathione peroxidase, and superoxide dismutase activities was also observed. Acetylcholinesterase activity was inhibited after treatment with K 2 Cr 2 O 7. Co-administration of Se restored the parameters cited above. The histopathological findings confirmed the biochemical results.
International Journal of Anatomy and Research
Background: Potassium dichromate (K2Cr2O7) is a major environmental pollutant and is known for its wide toxic manifestations. The present study shows the protective role of selenium (Na2SeO3) against chromium induced hepatorenal toxicity. Materials and Methods: Sixty adult albino rats were divided into four groups of fifteen each. Group I is control group which received standard diet; group II received K2Cr2O7 (67mg/kg B.W) in drinking water; group III received selenium only (0.5 ìg/kg B.W) and group IV received both K2Cr2O7 (67mg/kg B.W) and selenium (0.5 ìg/ kg B.W) for 6 weeks. Results: Selenium supplementation to the group IV improved all the kidney and liver chemical function parameters. In addition, it down-regulates endoplasmic reticulum stress genes. Conclusion: The biochemical results confirmed the improvement of histopathological findings. Therefore, our study revealed that selenium was effective in preventing K2Cr2O7-induced hepatorenal toxicity.
Ain Shams Journal of Forensic Medicine and Clinical Toxicology, 2019
Introduction Hexavalent chromium Cr (VI) is a strong oxidizing toxic agent. It penetrates cell membrane and quickly reduced with production of reactive intermediates and reactive oxygen species that react with the DNA causing anomalies in the cell structure. Vitamin E (vit. E) is a lipid soluble antioxidant preventing damage to membranes also selenium (Se) is an essential micronutrient with an antioxidant activity. Aim of the present study was to evaluate the hepatotoxicity, nephrotoxicity, and genotoxicity induced by acute Cr (VI) toxicity. Also, to evaluate and compare the possible protective role of vit. E and Se against that toxicity. Methodology: This study was carried out on 60 adult male albino rats divided into 10 rats of six groups, negative control group, selenium control group (0.5 mg/kg IP for 5 consecutive days), vitamin E control group (125 mg/kg orally for 14 days), Cr (VI) group (10 mg/kg single dose IP), Cr (VI) + Selenium group and hexavalent chromium + Vitamin E group. Liver and kidney function tests, total protein, oxidative stress, antioxidant markers and genotoxic analysis were done to all groups. Result: Acute Cr(VI) toxicity resulted in increased levels of the studied liver, kidney , oxidative stress markers, all forms of chromosomal aberrations and elevation of DNA damage. It decreased levels of total protein and antioxidant markers. Treatment with Se or vit. E resulted in improvement in all these effects. Conclusion& recommendation: Cr (VI) is a hepatotoxic, nephrotoxic, and genotoxic. Se or vit. E has the ability for reduction of these deleterious effects. So it is recommended to do regular medical examination of workers exposed to hexavalent chromium for early detection of any health problem and afford dietary supplementation with vitamin E and selenium.
Effects of selenium on chromium (VI)-induced hepatotoxicity in adult rats
Experimental and Toxicologic Pathology, 2011
Chromium, a major environmental pollutant, is known for its wide toxic manifestations. The present experiment pertains to the protective role of selenium (Se) against K 2 Cr 2 O 7-induced hepatotoxicity. Female Wistar rats were divided into four groups of six each: group I served as controls which received standard diet; group II received in drinking water K 2 Cr 2 O 7 alone (700 ppm); group III received both K 2 Cr 2 O 7 and Se (0.5 Na 2 SeO 3 mg/kg of diet); group IV received Se (0.5 mg/kg of diet) for 3 weeks. Exposure of rats to chromium promoted oxidative stress with an increase in malondialdehyde (MDA) and a decrease in glutathione (GSH) levels. A decrease in glutathione peroxidase (GPx) and an increase in superoxide dismutase (SOD) and catalase (CAT) activities were observed. Se supplementation to the diet of group III improved all the parameters cited above. Yet, plasma transaminases (AST and ALT), lactate dehydrogenase (LDH) activities, cholesterol, triglycerides (TG) and low density lipoprotein-cholesterol (LDL-C) levels increased, while high density lipoprotein-cholesterol (HDL-C) decreased. Co-administration of Se to the diet of group III restored hepatic markers to near-normal values. The biochemical results confirmed the histopathological findings. Therefore, our investigation revealed that Se was effective in preventing K 2 Cr 2 O 7-induced hepatotoxicity.
Study on Effects of Chromium on Antioxidant Enzymes in Mice
International Research Journal of Pharmacy, 2019
Chromium, naturally occurring, largest environmental toxicant that affects human health and most common pollutant; over the last few decades, it has been a concern that the fresh water consisting of massive metals can be agitated because of their campaigns primarily through the fraudulent programs of humans, industrial and domestic programs, chromium, heavy metal, primarily in oxidation states of hexavalent. Chromium obstructs the metabolic pathways and despite of all the above Chromium is an essential nutrient. Chromium adverse effects at low level is not well established. Hence, the study intended to examine the alterations of chronic exposure to chromium at low dose on antioxidant defense enzymes in mice. Exposure to chromium depleted significantly in catalyses, superoxide dismutase, and GST activity (p < 0.0001) in brain, liver and kidney when compared with their respective control group. The catalyses are considered one of the most important free radical scavenging enzymes, and the body's secondary protection against oxygen metabolites produced by the transformational massive metals increased activity levels of CAT, GST and SOD formation was observed experimental animals. The increase in antioxidant enzymes in Cr-treated animals indicated that one of the Cr-induced toxic effects as generated free radicals and in turn damages cell membrane.
Environmental Toxicology, 2009
Chromium is a widespread industrial compound. The soluble hexavalent chromium Cr (VI) is an environmental contaminant widely recognized as carcinogen, mutagen, and teratogen toward humans and animals. The fate of chromium in the environment is dependent on its oxidation state. The reduction of Cr (VI) to Cr (III) results in the formation of reactive intermediates leading to oxidative tissue damage and cellular injury. In the present investigation, Potassium dichromate was given intraperitoneally to Sprague-Dawley rats for 5 days with the doses of 2.5, 5.0, 7.5, and 10 mg/kg body weight per day. Oxidative stress including the level of reactive oxygen species (ROS), the extent of lipid peroxidation and the activity of antioxidant enzymes in both liver and kidney was determined. DNA damage in peripheral blood lymphocytes was determined by single-cell gel electrophoresis (comet assay). The results indicated that administration of Cr (VI) had caused a significant increase of ROS level in both liver and kidney after 5 days of exposure, accompanied with a dose-dependent increase in superoxide dismutase and catalase activities. The malondialdehyde content in liver and kidney was elevated as compared with the control animals. Dose-and time-dependent effects were observed on DNA damage after 24, 48, 72, and 96 h posttreatment. The results obtained from the present study showed that Cr (VI) could induce dose-and time-dependent effects on DNA damage, both liver and kidney show defense against chromium-induced oxidative stress by enhancing their antioxidant enzyme activity. However, liver was found to exhibit more antioxidant defense than the kidney.
Cell Biology and Toxicology, 2010
Selected biochemical parameters were studied in the blood of outbred, male Wistar rats which daily received to drink deionized water (Group I, control) or solutions of: sodium metavanadate (SMV; 0.100 mg V/mL)-Group II; chromium chloride (CC; 0.004 mg Cr/mL)-Group III; and SMV-CC (0.100 mg V and 0.004 mg Cr/mL)-Group IV for a 12-week period. The diet and fluid intake, body weight gain, and food efficiency ratio (FER) diminished significantly in the rats of Groups II and IV, compared with Groups I and III. The plasma total antioxidant status (TAS) as well as the MDA and the L-ascorbic acid level in the erythrocytes (RBCs) remained unchanged in all the groups, whereas the plasma L-ascorbic acid concentration decreased markedly in Group II, compared with Group III. The activities of Cu,Zn-superoxide dismutase (Cu,Zn-SOD), catalase (CAT), cellular glutathione peroxidase (cGSH-Px), and glutathione reductase (GR) in RBCs remained unaltered in all the treated rats. However, the activity of glutathione S-transferase (GST) and the content of reduced glutathione (GSH) in RBCs decreased and increased, respectively, in Groups II, III, and IV, compared with Group I. A vanadiumchromium interaction which affected the GST activity was also found. To summarize, SMV and CC administered separately or in combination in drinking water for 12 weeks did not alter either lipid peroxidation (LPO) or the activities of Cu,Zn-SOD, CAT, cGSH-Px, and GR, which allows a conclusion that both metals in the doses ingested did not reveal their pro-oxidant potential on RBCs.
Comparative Biochemistry and Physiology Part C: Pharmacology, Toxicology and Endocrinology, 1995
Chromium and its salts induce cytotoxicity and mutagenesis, and vitamin E has been reported to attenuate chromate-induced cytotoxicity. These observations suggest that chromium produces reactive oxygen species which may mediate many of the untoward effects of chromium. We have therefore examined and compared the effects of Cr(III) (chromium chloride hexahydrate) and Cr(VI) (sodium dichromate) following single oral doses (0.50 ld50) on the production of reactive oxygen species by peritoneal macrophages, and hepatic mitochondria and microsomes in rats. The effects of Cr(III) and Cr(VI) on hepatic mitochondrial and microsomal lipid peroxidation and enhanced excretion of urinary lipid metabolites as well as the incidence of hepatic nuclear DNA damage and nitric oxide (NO) production were also examined. Increases in lipid peroxidation of 1.8- and 2.2-fold occurred in hepatic mitochondria and microsomes, respectively, 48 hr after the oral administration of 25 mg Cr(VI)/kg, while increases of 1.2- and 1.4-fold, respectively, were observed after 895 mg Cr(III)/kg. The urinary excretion of malondialdehyde (MDA), formaldehyde (FA), acetaldehyde (ACT) and acetone (ACON) were determined at 0–96 hr after Cr administration. Between 48 and 72 hr post-treatment, maximal excretion of the four urinary lipid metabolites was observed with increases of 1.5- to 5.4-fold in Cr(VI) treated rats. Peritoneal macrophages from Cr(VI) treated animals 48 hr after treatment resulted in 1.4- and 3.6-fold increases in chemiluminescence and iodonitrotetrazolium reduction, indicating enhanced production of Superoxide anion, while macrophages from Cr(III) treated animals showed negligible increases. Increases in DNA single strand breaks of 1.7-fold and 1.5-fold were observed following administration of Cr(VI) and Cr(III), respectively, at 48 hr post-treatment. Enhanced production of NO by peritoneal exudate cells (primarily macrophages) was monitored following Cr(VI) administration at both 24 and 48 hr post-treatment with enhanced production of NO being observed at both timepoints. The results indicate that both Cr(VI) and Cr(III) induce an oxidative stress at equitoxic doses, while Cr(VI) induces greater oxidative stress in rats as compared with Cr(III) treated animals.