The synergistic effects of waterborne microcystin-LR and nitrite on hepatic pathological damage, lipid peroxidation and antioxidant responses of male zebrafish.

Hazardous materials from decaying cyanobacterial blooms, such as microcystin-LR (MC-LR) and nitrite pose serious challenges to aquatic organisms. To assess combined toxic effects of MC-LR and nitrite on hepatic pathology, lipid peroxidation and antioxidant responses of fish, adult male zebrafish (Danio rerio) were exposed to solutions with different combined concentrations of MC-LR (0, 3, 30 μg/L) and nitrite (0, 2, 20 mg/L) for 30 d. The results showed that hepatic pathological lesions progressed in severity and extent with increasing concentration of single factor MC-LR or nitrite and became more severe in co-exposure groups. Concurrently, significant increases in malondialdehyde (MDA) revealed the occurrence of oxidative stress caused by MC-LR, nitrite and both of them, which was indirectly verified by remarkable decreases in the total antioxidant capacity (T-AOC) as well as the transcription and activity of antioxidant enzymes (CAT and GPx). Hepatic mitochondria were damaged as the common action site of MC-LR and nitrite, suggesting that oxidative stress played a significant role in the mechanisms of the hepatotoxicity of MC-LR and nitrite. The depletion of hepatic glutathione (GSH) indicated the importance of GSH/glutathione-S-transferases (GST) system in these two chemicals detoxification. These results clearly illustrated that MC-LR and nitrite have synergistic effects on the histostructure, antioxidant capacity and detoxification capability in the liver of zebrafish. Therefore, the combined pollution of MC-LR and nitrite in eutrophic lakes can reduce the defense mechanism of the fish and accelerate the consumption of GSH, which compromise the survival of the fish during prolonged cyanobacterial blooms episodes.