Regulatory effect of quercetin on hazardous microcystin-LR-induced apoptosis of Carassius auratus lymphocytes in vitro

Abstract

Microcystins (MCs) are secondary metabolites produced by cyanobacteria. Oxidative stress is considered the major cytotoxic mechanism of microcystin-LR (MCLR). Quercetin (QE) is a flavonoid that can eliminate reactive oxygen species (ROS) and elicit anti-inflammatory and anti-apoptotic effects. This study determined the regulatory effect of QE on the cytotoxicity and oxidative stress of Carassius auratus lymphocytes induced by 1 μg/L MCLR in vitro after 24 h. MCLR-mediated cytotoxicity and ROS formation in fish lymphocytes were suppressed by QE in a concentration-dependent manner. In addition, QE enhanced the endogenous antioxidant defense system and the Bax/Bcl-2 ratio to protect fish lymphocytes against oxidative stress and apoptosis induced by MCLR. Glutathione levels and catalase activities increased by approximately 3.9- and 2-fold, respectively, in the QE treatment group (1000 μg/L) compared with the MCLR treatment group. The percentage of apoptosis in the only MCLR treatment group was 59% whereas that in the control group was 23%. The percentage of apoptosis in the high-dose QE treatment group (1000 μg/L) was 29%, lower by nearly half compared with the only MCLR treatment group. QE (1000 μg/L) effectively inhibited the expression of caspase-3 protein by nearly 43% compared with the only MCLR treatment group. The results obtained clearly indicate that QE can effectively prevent MCLR-induced immunotoxicity by eliminating oxidative stress and blocking the mitochondrial apoptotic pathway in fish lymphocytes.