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High Content Screening Analysis to Evaluate the Toxicological Effects of Harmful and Potentially Harmful Constituents HPHC
Published on: May 10, 2016
Alkylphenols cause cytotoxicity and genotoxicity induced by oxidative stress in RTG-2 cell line
William de Almeida1, Jéssica Crecencio Matei2, Rafael Shinji Akiyama Kitamura3
1Ecology and Conservation Program, Federal University of Paraná, Brazil; Genetics Department, Federal University of Paraná, Brazil.
Abstract:
Alkylphenols ethoxylates are industrial surfactants, and the release in the environmental matrices produces degraded products, of which nonylphenol (NP) and octylphenol (OP) were the most common. They can be classified as endocrine disruptors since the estrogenic potential is widely recognized, but some others toxic aspects are in discussion. This study aimed to evaluate the toxicity of NP, OP, and mixtures of both through cellular, biochemical and genetic biomarkers in fish gonadal cell line RTG-2 exposed to nominal concentrations of 0.05; 0.5; 5; 50, and 100 μg mL-1 of each chemical and their mixtures of 0.05, 0.5; 5 μg mL-1 concentrations. After 24 h, the cells were collected for cytotoxic (neutral red - NR; crystal violet - CV, resazurin assay - RA and lactate-dehydrogenase - LDH), antioxidant system (glutathione-s-transferase - GST; superoxide-dismutase - SOD; glutathione-peroxidase - GPx and malondialdehyde - MDA) and genotoxic assays (alkaline comet assay and Fpg-modified alkaline comet assay). The chemicals and their mixtures were cytotoxic at 50 and 100 μg mL-1, in general aspect, but LDH showed cytotoxicity since 0.05 μg mL-1. The GST and SOD showed an activity increase trend in most tested groups, while GPx decreased at 5 μg mL-1 of the mixture. The MDA increase in all groups resulted in lipid peroxidation. The reactive oxygen species caused DNA damage for all groups. The tested chemicals and concentrations have been found in the freshwater systems. They can induce cell toxicity in several parameters that could impair the gonadal tissues considering the RTG-2 responses.
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