Maximum contaminant level of arsenic in drinking water potentiates quinalphos-induced renal damage on co-administration of both arsenic and quinalphos in Wistar rats.

Abstract

This study was designed to determine alterations in renal biomarkers, antioxidant profile, and histomorphology of renal tissue following subacute exposure to quinalphos alone or in conjunction with arsenic in rats. A total of 54 adult Wistar rats were randomly divided into nine groups of six rats each and were administered sub-lethal concentrations of quinalphos (1/100th and 1/10th of LD50) orally daily and arsenic (50 and 100ppb) in drinking water for 28days. Significantly (p < 0.05) decreased levels of antioxidant biomarkers in renal tissue, viz., total thiols, catalase, superoxide dismutase, glutathione peroxidase, glutathione-s-transferase, and glutathione reductase along with increased (p < 0.05) thiobarbituric acid reacting substance (TBRAS) levels indicated that significant oxidative damage to renal tissue occurred following repeated administrations of quinalphos at either dose levels or arsenic at the concentration of 100ppb when compared with the control rats. The alterations in the antioxidant parameters were observed to be more pronounced in co-administered groups as compared with either toxicant administered group. Similarly, activity of renal acetylcholinesterase was decreased after repeated exposure to quinalphos or arsenic, but inhibition was higher (up to 48%) in rat renal tissue co-exposed with quinalphos and arsenic at the higher concentration. These findings corroborated with the histopathological alterations in renal tissue of toxicant exposed rats. The altered plasma and tissue antioxidant biomarkers along with histopathological changes in the kidney at higher dose level of either toxicant indicate that renal tissue is significantly impacted by these toxicants, and these effects become more pronounced after their co-administration.