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

Author(s):  
Sunil Sharma ◽  
Owias Iqbal Dar ◽  
Kirpal Singh ◽  
Sharad Thakur ◽  
Anup Kumar Kesavan ◽  
...  
2021 ◽  
Author(s):  
Sunil Sharma ◽  
Owias Iqbal Dar ◽  
Kirpal Singh ◽  
Sharad Thakur ◽  
Anup Kumar Kesavan ◽  
...  

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 fish, 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/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 LC 50 = 0.126mg/L 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 96h. The damage declined significantly 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.


2010 ◽  
Author(s):  
Charlotte Leonie Stewart ◽  
Jolanta Opacka-Juffry ◽  
Changiz Mohiyeddini

2018 ◽  
Vol 35 (5) ◽  
pp. 536
Author(s):  
Jiayun LU ◽  
Jianbo SONG ◽  
Xiaoyan WANG ◽  
Xiaowei MO ◽  
Suikang WANG ◽  
...  

2019 ◽  
Author(s):  
Jacob G. Scott ◽  
Geoffrey Sedor ◽  
Michael W. Kattan ◽  
Anthony Waller ◽  
Jeffrey Peacock ◽  
...  

2001 ◽  
Vol 36 (2) ◽  
pp. 319-330 ◽  
Author(s):  
Mark Servos ◽  
Don Bennie ◽  
Kent Burnison ◽  
Philippa Cureton ◽  
Nicol Davidson ◽  
...  

Abstract A number of biological responses and multigenerational effects, mediated through the disruption of endocrine systems, have been observed in biota exposed to relatively low concentrations of environmental contaminants. These types of responses need to be considered within a weight of evidence approach in our risk assessment and risk management frameworks. However, including endocrine responses in an environmental risk assessment introduces a number of uncertainties that must be considered. A risk assessment of nonylphenol and nonylphenol polyethoxylates (NP/NPE) is used as a case study to demonstrate the sources and magnitude of some of the uncertainties associated with using endocrine disruption as an assessment endpoint. Even with this relatively well studied group of substances, there are substantial knowledge gaps which contribute to the overall uncertainties, limiting the interpretation within the risk assessment. The uncertainty of extrapolating from in vitro or biochemical responses to higher levels of organization or across species is not well understood. The endocrine system is very complex and chemicals can interact or interfere with the normal function of endocrine systems in a number of ways (e.g., receptors, hormones) which may or may not result in an adverse responses in the whole organism. Using endocrine responses can lead to different conclusions than traditional endpoints due to a variety of factors, such as differences in relative potencies of chemicals for specific endpoints (e.g., receptor binding versus chronic toxicity). The uncertainties can also be considerably larger and the desirability of using endocrine endpoints should be carefully evaluated. Endocrine disruption is a mode of action and not a functional endpoint and this needs to be considered carefully in the problem formulation stage and the interpretation of the weight of evidence.


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