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

Abstract

Triclosan (TCS) used commonly in pharmaceuticals and personal care products has become the most common pollutant in water. Three days old hatchlings of an indegenous sh, Labeo rohita were given 96h exposure to an environmentally relevant (0.06mg/L) and two moderately lethal concentrations (0.067 and 0.097 mg/L) of TCS and kept for 10 days of recovery for recording transcriptomic alterations in antioxidant/detoxi cation (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 LC 50 = 0.126mg/L and risk quotient = 40.95), 96h exposure caused signi cant induction of CYP3a, AChE and ALT but suppression of all other genes. However, expression of all the genes increased signi cantly (except for a signi cant 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 96h. The damage declined signi cantly over 96h values at 0.06 and 0.067 mg/L 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.

Molecular Toxicity Mechanism Induced by the Antibacterial Agent Triclosan in Freshwater Euglena gracilis Based on the Transcriptome

“…This technique is being used to comprehensively analyze transcriptomic changes and reveal the molecular mechanism caused by TCS toxicity in organisms. Transcriptomics and biochemical research in Labeo rohita indicated that TCS caused liver and kidney damage, abnormal metabolic processes, and digestive system disorders [ 34 , 35 ]. Transcriptome analysis of zebrafish revealed the role of the liver as a target organ for TCS toxicity, with liver steatosis mainly resulting from increased fatty acid synthetase activity, and the uptake and suppression of β-oxidation [ 8 ].…”