Acute ecotoxicological effects of salicylic acid on the Polychaeta species Hediste diversicolor: evidences of low to moderate pro-oxidative effects

Contamination of the aquatic environment by pharmaceutical drugs is an emerging issue in ecotoxicology. Aquatic organisms, in the presence of xenobiotics, tend to activate defensive mechanisms against toxic effects in order to mitigate and/or compensate for the toxic damages that frequently result from these interactions. Salicylic acid (SA) is a common drug, widely used in human medicine due to its analgesic, anti-inflammatory, and antipyretic properties, as well as its activity in terms of preventing platelet aggregation, among other clinical and cosmetic uses. It is commonly found in levels of the nanograms per liter to the micrograms per liter range in receiving waters, and its presence has been related to toxic effects in aquatic organisms, including oxidative stress. However, the number of studies that characterize the ecotoxicological profile of salicylates is still scarce and no studies have been published about the putative toxic effects of SA, especially in marine polychaetes. In order to determine the potential ecotoxicological effects caused by SA, individuals of the marine Polychaeta species Hediste diversicolor were exposed for 96 h to ecologically relevant concentrations of this compound, and several biochemical endpoints were evaluated, namely the activity of the antioxidant enzymes glutathione peroxidase (GPx) and catalase (CAT), the phase II biotransformation isoenzymes glutathione S-transferases (GSTs), the cholinergic enzyme acetylcholinesterase (AChE), and the determination of lipoperoxidative damage (thiobarbituric acid-reactive substances (TBARS) assay). The obtained results demonstrated that despite the pro-oxidative effects elicited by SA, exposure to realistic levels of this compound was not able to generate a state of oxidative stress, and the adaptive protective responses elicited by exposed individuals were effective enough to minimize and/or inhibit the damage potentially caused by overproduced reactive oxygen species.