Organophosphorus flame retardant induced hepatotoxicity and brain AChE inhibition on zebrafish (Danio rerio).

Organophosphorus flame retardants (OPFRs) are high production volume (HPV) chemicals. Recent reports reveal that OPFRs are ubiquitous in the environment. Unfortunately, the toxicity profiles for OPFRs on organisms remain limited. Hence, to illustrate the potential toxic effects of OPFRs at environmental relevant concentrations on aquatic biota, in the present study, we investigated biochemical, enzymological, antioxidants, and histological (at long-term study) changes of zebrafish tissues under short- (96 h) and long- (21 days) -term triphenyl phosphate (TPhP) exposure. The hepatic glucose production (except short-term TPhP treatment up to 48 h), aspartate transaminase, alanine transaminase, lactate dehydrogenase, reactive oxygen species generation, lipid peroxide, and catalase activities were found to be increased in TPhP exposed groups when compared to control groups (normal and solvent control groups). The hepatic protein content and sodium dismutase activity were declined in TPhP exposed groups. Likewise, brain tissue acetylcholinesterase activity was declined in TPhP exposed groups. The hepatic glutathione S-transferase activity increased after 24 h under short-term TPhP exposure (96 h), while under long-term exposure period (21 days) the enzyme activity was accelerated when compared to control groups. Long-term TPhP exposure resulted in a series of morphological anomalies in the hepatic tissues of zebrafish. Our study reveals that TPhP can potentially cause antioxidants imbalance, alterations in enzymological and biochemical profiles, and morphological anomalies in hepatic tissues of zebrafish. Moreover, TPhP could cause neurotoxic effects on zebrafish at studied concentrations. Our findings expand the available toxicity profiles for TPhP on aquatic biota and propose that zebrafish are a good indicator, and studied parameters are valid biomarkers in assessing the eco-toxicological effects of OPFRs.