Lipid peroxidation and oxidative stress responses in juvenile salmon exposed to waterborne levels of the organophosphate compounds tris(2-butoxyethyl)- and tris(2-chloroethyl) phosphates.

There is limited knowledge on the toxicological, physiological, and molecular effects attributed to organophosphate (OP) compounds currently used as flame retardants or additives in consumer products. This study investigated the effects on oxidative stress and lipid peroxidation in juvenile Atlantic salmon liver and brain samples after exposure to two OP compounds, tris(2-butoxyethyl) phosphate (TBOEP) and tris(2-chloroethyl) phosphate (TCEP). In this study, groups of juvenile Atlantic salmon were exposed using a semistatic experimental protocol over a 7-d period to 3 different concentrations (0.04, 0.2, or 1 mg/L) of TBOEP and TCEP. When toxicological factors such as bioaccumulation and bioconcentration, and chemical structural characteristics and behavior, including absorption to solid materials, are considered, these concentrations represent environmentally relevant concentrations. The concentrations of the contaminants were derived from levels of their environmental occurrence. The expression of genes related to oxidative stress-glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST)-and to lipid peroxidation-peroxisome proliferator-activated receptors (PPAR)-were determined using quantitative (real-time) polymerase chain reaction (PCR). The presence of PPAR proteins was also investigated using immunochemical methods. Levels of thiobarbituric acid-reactive substances (TBARS) in liver were used as a measure of lipid peroxidation. Overall, our data show an increase in lipid peroxidation, and this was associated with an augmented expression of genes from the glutathione family of responses. Interestingly, PPAR expression in liver after exposure to TBOEP and TCEP was consistently decreased compared to controls, while expression in brain did not show a similar trend. The results suggest that OP contaminants may induce oxidative stress and thus production of reactive oxygen substances (ROS), and modulate lipid peroxidation processes in organisms.