Melatonin protects against chromium (VI) induced hepatic oxidative stress and toxicity: Duration dependent study with realistic dosage

Abstract

The present study was undertaken to assess the degree of oxidative stress and toxic effects induced by chromium on hepatic tissue in male Wistar rats exposed to a realistic dosage of Cr(VI) (20 mg/kg/b.w./day) through drinking water, based on the levels of these metals found in the environment, for a duration of 15, 30 and 60 days. The protective effect of melatonin (10 mg/kg) was also studied by simultaneous administration with the metal. Levels of enzymatic and non-enzymatic antioxidants as well as lipid peroxidation were assessed. There was a significant decrease in enzymatic as well as non-enzymatic antioxidants and an increase in the lipid peroxidation level, which were prevented and maintained at near-normal levels by the administration of melatonin in all treatment periods. Metal accumulation was maximal at 15 days, with gradual decreases till 60 days. Histopathological observations also demonstrated the fact that Cr (VI) exposure leads to cytological lesions in the hepatic tissue promoting cellular necrotic/apoptotic changes, while melatonin was able to counteract insults induced by Cr (VI) at all treatment periods. It also prevented alterations in insulin and glucose levels. Overall, the present study suggests a duration-dependent effect of Cr on hepatic oxidative stress and cytotoxicity and shows the potent activity of melatonin in preventing the negative effects of Cr (VI).

Effects of ethylthiosulfanylate and chromium (VI) on the state of pro/antioxidant system in rat liver

“…After potassium dichromate exposure content of GSH in the rat liver of III and IV experimental groups was significantly decreased by 41 and 33%, respectively ( Table 3). Our results are consistent with studies by other authors that the action of Cr(VI) leads to depletion of GSH content in liver tissue [3].…”

“…Histopathological observations indicate that Cr(VI) exposure lead to cytological liver damages, which cause necrotic and apoptotic changes in rat hepatocytes [3]. Acute action of Cr(VI) by potassium dichromate administration at a dose 20 mg/ kg body weight causes increase in malondialdehyde (MDA) content, depletion of pool of GSH, decrease in superoxide dismutase (SOD) and catalase (CAT) doi: https://doi.org/10.15407/ubj92.05.078 activity in liver of male Swiss Albino mice [4].…”

“…Also, potassium dichromate action causes increase of urea concentration and creatinine level, decrease of total protein content in rat serum [5] and induces increase of alanine aminotransferase and total cholesterol in serum of Rabbit Doe [6]. Nowadays is carried out an active search for biologically active substances with antioxidants, detoxifying and cytoprotective properties, which are capable to attenuate the toxic effect of heavy metals, including Cr(VI) [3,4,7].…”

Modulatory Role of Selenium and Vitamin E Against Oxidative Stress Induced Hepatotoxicity and Nephrotoxicity in Rats Exposed Sub-Chronically to Hexavalent Chromium

“…However, chronic exposure to a lower level of heavy metals through food, water and air is still common in industrial areas and continued to remain as a pertinent global problem [1]. For example, people residing near tanneries are subjected to chronic exposure to a very low level of chromium through ground water [20]. Information on health hazards of such low level chronic exposure to chromium is still scarce.…”

Hexavalent Chromium Exposure Induces Intestinal Barrier Damage via Activation of the NF-κB Signaling Pathway and NLRP3 Inflammasome in Ducks

“…Cr(VI) has wellknown solubility, mobility, and responsiveness that can easily enter animal and human bodies through the skin, gastrointestinal tract, or respiratory tract, thus leading to Cr(VI) poisoning (11). Previous studies have indicated that Cr(VI) exposure could induce immunotoxicity, dermatotoxicity, genotoxicity, neurotoxicity, and carcinogenicity in different tissues of animals and humans (12,13).…”