Abstract

Background. The main pathway of Cr(VI) cytotoxicity is activation of oxidative stress in cells of living organisms, resulting in an imbalance of blood biochemical para­me­ters. Our recent studies indicate that S-ethyl-4-aminobenzenethiosulfonate (ETS), which belongs to thiosulfonate compounds, is able to reduce intensity of Cr(VI)-induced oxidative stress in liver tissue of rats. It is known that oxidative stress induced by Cr(VI) causes liver and kidney tissue damage with a subsequent imbalance of blood biochemical parameters. Therefore, the aim of this study was to evaluate the potential ability of ETS to prevent Cr(VI)-induced disorders of some biochemical blood parameters, which are important biomarkers of Cr(VI) intoxication. Materials and Methods. The object of the research was the separate biochemical parameters of the blood of rats with Cr(VI)-induced oxidative stress after prior exposure to ETS. Two experimental groups of male Wistar rats were intoxicated once per day intraperitoneally with K2Cr2O7 dissolved in physiological saline solution for 7 or 14 days. Two other experimental groups were pretreated once per day intragastrically with ETS dissolved in oil before the period of 7 or 14-day K2Cr2O7 intoxication. We measured total protein, creatinine and urea level, as well as determined the activity of aminotransferases in the blood plasma of rats. Results. Intraperitoneal injection of K2Cr2O7 (dissolved in physiological saline solution at a dose of 2.5 mg Cr(VI)/kg body weight) for 7 and 14 days causes a decrease in total protein level and leads to elevation of plasma creatinine level and urea concentration. The activity of blood aminotransferases increases due to Cr(VI) toxicity. The 14-day exposure to ETS (dissolved in oil at a dose 100 mg/kg body weight) prior to the period of Cr(VI) intoxication is characterized by a smaller percentage increase in the level of crea­tinine, urea and activity of alanine aminotransferase (ALT) in the blood plasma of rats. Conclusion. Cr(VI)-induced toxicity causes an imbalance in biochemical blood parameters. Cr(VI) induces a total protein decrease and leads to an increase in the level of the studied biochemical parameters of blood plasma, which are markers of damage to the liver (aminotransferases) and kidneys (creatinine, urea). In contrast, exposure to ETS for 14 days prior to the period of Cr(VI) intoxication causes percentage decrease in creatinine, urea accumulation and percentage reduction of ALT hyper-activation in the blood of rats. However, the levels of creatinine, urea and ALT activity in this case remained significantly higher than those in the control group. In conclusion, pretreatment with ETS (100 mg/kg) for 2 weeks helps to reduce the level of Cr(VI)-induced disturbances of some blood biochemical parameters, but does not normalize them.

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