Oxidative stress and histopathological alterations in liver of Cyprinus carpio L. induced by intraperitoneal injection of microcystin-LR.

Abstract

Microcystins (MCs) are a group of cyclic heptapeptide hepatotoxic peptides produced by cyanobacteria. Microcystins-LR (MC-LR) can inhibit the activities of protein phosphatase type 1 and type 2A (PP1 and PP2A) and induce excessive production of reactive oxygen species (ROS). However, the detailed toxicological mechanism involving oxidative stress in carp (Cyprinus carpio L.) remains largely unclear. In our present study, the effects of sublethal intraperitoneal doses of MC-LR on the oxidative stress and pathological changes in carp liver were investigated. No significant changes of xanthine oxidase were observed, suggesting it might not contribute to over-production of ROS in the liver of fish during 48 h exposure to sublethal intraperitoneal doses of MC-LR. Superoxide dismutase activity in the 50 μg kg(-1) group was significantly induced at 1-24 h. The strongest inhibition of the catalase activity was shown at 48 h after 120 μg kg(-1) MC-LR exposure, with an inhibition rate of 33.7% compared to the control group. In general, a significant depletion of intracellular reduced glutathione was found at 5-12 h after 50 and 120 μg kg(-1) MC-LR exposure, which was mainly due to the conjugation reaction to MC-LR catalyzed by glutathione-S-transferase and its subsequent excretion. Oxidative damages induced by MC-LR were evidenced by the significant elevation in malondialdehyde levels. In addition, a series of histopathological alterations in fish livers were observed, and the most severe hepatic injuries were found at 5-12 h, which could contribute to the efflux of intracellular GSH. Our study further supports the important role of oxidative stress involved in MC-LR induced liver injury in aquatic organisms.