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

Abstract

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.

Transcriptional and cellular effects of benzotriazole UV stabilizers UV‐234 and UV‐328 in the freshwater invertebrates Chlamydomonas reinhardtii and Daphnia magna

“…The balance between production of ROS and scavenging of those radicals by antioxidants reflects the presence of oxidative stress and can be measured by the severity of cellular damage such as lipid peroxidation . The ROS levels produced by C. reinhardtii were measured in terms of a relative increase (percentage) compared to the control (Figure A), and the presence of MDA was measured as an indicator of lipid peroxidation (Figure B) in response to BZT‐UVs.…”

“…•to O 2 and H 2 O 2 that is further scavenged by catalases and peroxidases [60]. Changes in antioxidant responses are generally difficult to predict, and induction, inhibition, or temporary changes may be observed depending on experimental conditions, intensity and duration of exposure, species, tissues, metabolic status, or presence of other confounding factors [31,59]. Because of the lack of data on BZT-UVs, the present study represents the first report of the effects of these compounds on oxidative stress-related genes and shows a potential synergistic effect of both compounds on gpx induction and apx down-regulation.…”

“…Defects in these antioxidant defenses may lead to oxidative damage such as protein oxidation and lipid peroxidation [29]. A wide array of environmental contaminants and chemical compounds can induce oxidative stress through ROS production and the modulation of antioxidant enzyme activities [30,31]. For example, trace metal ions (e.g., silver, mercury, copper), pesticides, hydrocarbons, perfluorooctanoic acids, drugs, and nanoparticles have all been linked to oxidative stress in aquatic organisms such as fish, freshwater crustaceans, and algae, which are particularly exposed to these environmental contaminants [28,[32][33][34][35][36].…”

Associations between urinary organophosphate ester metabolites and measures of adiposity among U.S. children and adults: NHANES 2013–2014

“…Several biological mechanisms by which OPEs could alter metabolism have been proposed. Emerging laboratory and human evidence indicates that OPEs may interfere with sex steroid and thyroid hormones ( Farhat et al 2013 ; Kim et al 2015 ; Krivoshiev et al 2016 ; Liu et al 2012b ; Meeker and Stapleton 2010 ; Preston et al 2017 ; Schang et al 2016 ; Wang et al 2015 ; Zhang et al, 2016a ), peroxisome proliferator-activated receptors (PPARs) ( Belcher et al 2014 ; Fang et al 2015 ; Hu et al 2017 ; Kojima et al 2013 ; Pillai et al 2014 ), and induce oxidative stress ( Arukwe et al 2016 ; Chen et al 2015 ; Jin et al 2016 ; Lu et al 2017 ; Yan et al 2017 ). These biologic pathways serve well-known roles in adipose tissue development and obesity risk.…”

Systemic analysis of gene expression profiles in porcine granulosa cells during aging

“…Various studies have demonstrated that peroxisome proliferator pctivated peceptor-γ (PPARγ) is a key regulator of GLUT1 expression [ 70 - 73 ]. The relationship between ROS and PPARγ has been determined previously; for example, when treated with organophosphate compounds, salmon liver cells showed decreased PPARγ expression and increased ROS production [ 74 ], which were restored to normal levels following antioxidant treatment [ 75 ]. Moreover, aging was found to suppress PPARγ in aged mouse model [ 76 ].…”