Effects of Acute Ammonia Exposure on the Antioxidant System and Anti-Inflammatory Factors in Opsariichthys bidens

Abstract

The present experiment was performed to reveal the mechanisms of toxic effects of ammonia nitrogen on Chinese hook snout carp (Opsariichthys bidens) based on the levels of antioxidant enzyme activities and the expression of 70-kDa heat shock protein gene (HSP70) and tumor necrosis factor-α (TNF-α) after 96 h of acute toxic ammonia exposure to investigate its adaptability. The result showed that activities of antioxidant enzymes and lipid peroxidation in the intestine, liver, brain, and gills showed a general trend of increasing and then decreasing when exposed to ammonia nitrogen. The intestinal tissue structure was damaged to varying degrees, the expression of the HSP70 in the brain and gills increased at 0–12 h, and the expression of the TNF-α in brain tissues decreased at 0–12 h. The expression of TNF-α in the liver was continuously upregulated in the late stages of stress, and it did not decrease until the stress was released. The above results indicate that high concentrations of ammonia nitrogen caused varying degrees of damage to the neurological, respiratory, and metabolic-related organs of the O. bidens.