An Evaluation of Hepatotoxicity, Nephrotoxicity, and Genotoxicity Induced by Acute Toxicity of Hexavalent Chromium and Comparison of the Possible Protective Role of Selenium and Vitamin E on These Effects

Abstract

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.

Squalene is a potential hypothyroidism modulator: a study of its effect on the Keap1-Nrf2-ARE signaling pathway in potassium dichromate induced hypothyroidism model in rats.

“…Our results explored that treating the groups receiving potassium dichromate with squalene and/ or vitamin E showed elevation in the level of reduced GSH as well as reduction in the elevated level of MDA when compared to the positive control group, which was in harmony to the results of a previous study (20). Meanwhile it was established by previous studies that vitamin E has the ability to safeguard against known induced ROS hepatotoxicity, genotoxicity, nephrotoxicity which estimated MDA levels as an OS marker and ascertained that it was elevated upon intoxication with potassium dichromate (21). Previous studies discovered a potent scavenging effect of squalene in comparison to vitamin E in aged population (22).…”

Features of the influence of S-ethyl-4-aminobenzene thiosulfonate on some biochemical parameters of rat blood under the condition of Cr(VI) intoxication

“…These negative changes can also lead to a decrease in the concentration of total protein in the blood due to its accumulation in the urine (Saidi et al, 2019). The toxic action of Cr(VI) activates the processes of free radicals formation, which in turn stimulates the processes of protein oxidation (Hassan et al, 2019). There were no statistically significant differences in blood plasma total protein level between animals intoxicated with Cr(VI) for 7 (group III) and 14 days (group IV).…”

“…The increase in the activity of ALT and AST is due to the high hepatotoxicity of K 2 Cr 2 O 7 . Cr(VI)-induced oxidative stress is accompanied by damage to hepatocyte cell membranes, after which aminotransferases enter the blood plasma (Hassan et al, 2019). Therefore, changes in blood aminotransferases activity are an important indicator of the structural and functional state of the liver (Ma et al, 2022).…”

Cytogenetic Effect of Heavy Metal Exposure in Alzheimer’s Disease Rat Model

“…The third group was allocated for AD rats receiving the heavy metal, PDC, where AD was induced just as the second group, followed by PDC (10 mg/kg body weight single i.p. injection freshly dissolved in saline 22 ) one hour after the last LPS injection. While the forth group was assigned to investigate the effect of PDC alone, as they were PDC-injected just as the third group, but one hour after the last i.p.…”