Environmental ammonia exposure induces oxidative stress in gills and brain of Boleophthalmus boddarti (mudskipper)

Abstract

This study aimed to elucidate whether exposure to a sublethal concentration (8 mmol l-1) of NH4Cl (pH 7.0) for 12 or 48 h would induce oxidative stress in gills and brain of the mudskipper Boleophthalmus boddarti which has high tolerance of environmental and brain ammonia. The gills of B. boddarti experienced a transient oxidative stress after 12 h of ammonia exposure as evidenced by an increase in lipid hydroperoxide content, decreases in contents of reduced glutathione (GSH) and total GSH equivalent, and in activities of total glutathione peroxidase, glutathione reductase and catalase. There were also transient increases in protein abundance of p53 and p38 in gills of fish exposed to ammonia for 12 h, although the protein abundance of phosphorylated p53 remained unchanged and there was a decrease in the protein abundance of phosphorylated p38, at hour 12. Since the majority of these oxidative parameters returned to control levels at hour 48, the ability of the gills of B. boddarti to recover from ammonia-induced oxidative stress might contribute to its high environmental ammonia tolerance. Ammonia also induced oxidative stress in the brain of B. boddarti at hours 12 and 48 as evidenced by the accumulation of carbonyl proteins, elevation in oxidized glutathione (GSSG) content and GSSG/GSH, decreases in activities of glutathione reductase and catalase, and an increase in the activity of superoxide dismutase. The capacity to increase glutathione synthesis and GSH content could alleviate severe ammonia-induced oxidative and nitrosative stress in the brain. Furthermore, the ability to decrease the protein abundance of p38 and phosphorylated p53 might prevent cell swelling, contributing in part to the high ammonia tolerance in the brain of B. boddarti. Overall, our results indicate that there could be multiple routes through which ammonia induced oxidative stress in and outside the brain. © 2009 Elsevier B.V. All rights reserved.