Genomic markers for the biological responses of Triclosan stressed hatchlings of Labeo rohita

Triclosan (TCS) used commonly in pharmaceuticals and personal care products has become the most common pollutant in water. Three-day-old hatchlings of an indigenous fish, Labeo rohita, were given 96h exposure to a nonlethal (60 mu g L-1) and two moderately lethal concentrations (67 and 97 mu g L-1) of TCS and kept for 10 days of recovery for recording transcriptomic alterations in antioxidant/detoxification (SOD, GST, CAT, GPx, GR, CYP1a and CYP3a), metabolic (LDH, ALT and AST) and neurological (AchE) genes and DNA damage. The data were subjected to principal component analysis (PCA) for obtaining biomarkers for the toxicity of TCS. Hatchlings were highly sensitive to TCS (96h LC50 = 126 mu g L-1 and risk quotient = 40.95), 96h exposure caused significant induction of CYP3a, AChE and ALT but suppression of all other genes. However, expression of all the genes increased significantly (except for a significant decline in ALT) after recovery. Concentration-dependent increase was also observed in DNA damage [Tail Length (TL), Tail Moment (TM), Olive Tail Moment (OTM) and Percent Tail DNA (TDNA)] after 96 h. The damage declined significantly over 96h values at 60 and 67 mu g L-1 after recovery, but was still several times more than control. TCS elicited genomic alterations resulted in 5-11% mortality of exposed hatchlings during the recovery period. It is evident that hatchlings of L. rohita are a potential model and PCA shows that OTM, TL, TM, TDNA, SOD and GR (association with PC1 during exposure and recovery) are the biomarkers for the toxicity of TCS.

Automated summary

This study found that Triclosan has significant toxicity to hatchlings of Labeo rohita, inducing alterations in antioxidant/detoxification, metabolic, and neurological genes as well as DNA damage. Principal component analysis identified OTM, TL, TM, TDNA, SOD, and GR as biomarkers for Triclosan toxicity.