Sublethal concentrations of triclosan elicited oxidative stress, DNA damage, and histological alterations in the liver and brain of adult zebrafish.

Abstract

Triclosan (TCS), an antimicrobial agent, has been a pollutant of increasing concern owing to its potential health risk on humans and aquatic animals. The present study seeks to test the hypothesis that TCS could alter the oxidative stress-related parameters in the brain and liver, as well as eliciting DNA damage in hepatocytes of adult zebrafish. On the basis of the 96h LC50 (398.9μg/L), adult zebrafish were separately exposed to 50, 100, and 150μg/L TCS for 30days. The brain and liver tissues from adult zebrafish were excised and assayed for a suite of antioxidant parameters and oxidative stress biomarkers including DNA damage in the liver. The induced effect by TCS on the activity of acetylcholinesterase (AChE) was also analyzed in the brain. Results showed a significant decrease in superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in the brain and liver of adult zebrafish. Also, the contents of the glutathione system (GSH and GSSH), as well as the activity of the glutathione reductase (GR), assayed in the liver, were reduced while the contents of malondialdehyde (MDA) were elevated in the liver. A comet assay revealed dose-dependent DNA damage in zebrafish hepatocytes. The 8-hydroxy-2'-deoxyguanosine (8-OHdG), MDA, and carbonyl protein contents in brain tissues significantly increased. Moreover, the AChE in the zebrafish brain was induced. Apparently, no obvious histological changes in brain tissues of zebrafish were observed compared with those of the control whereas atrophy and necrosis of hepatocytes and increased hepatic plate gap were observed in zebrafish hepatocytes after TCS exposure. The obtained results highlight that sublethal concentrations of TCS may be deleterious to the liver and brain of adult zebrafish upon subchronic exposure.