Biomarkers responses in the amphipod Tiburonella viscana exposed to the biocide DCOIT and CO2-induced ocean acidification.

Anthropogenic carbon dioxide emissions (CO2) have led to climate change and marine acidification, with an estimated decrease in ocean surface pH of 0.3-0.4 units by the end of the current century. Chemical pollution also contributes to biodiversity loss in marine environments. This issue is particularly critical in areas under pressure from shipping activities, where the introduction of new antifouling system formulations poses a major threat to non-target species. The biocide DCOIT is the most widely used alternative to organotin compounds due to its rapid degradation in seawater. The toxicity of waterborne DCOIT to marine organisms has been documented, but sediment-bound effects are limited to apical responses and pH scenarios corresponding to current levels. In this study, we determine in a combined way, the toxicity of DCOIT under marine acidification scenarios assessing biomarker responses in the burrowing amphipod Tiburonella viscana as a parameter of sublethal effects in solid phase exposures. Environmental relevant concentrations of DCOIT caused inhibition of the enzyme glutathione S-transferases (GST), changed acetylcholinesterase-like activity (AChE), and increased DNA damage at pHs of 7.7 and 7.4. For lipid peroxidation (LPO), increased levels caused by DCOIT were found for both control (8.1) and intermediate (7.7) conditions of pH. Our data provides evidence of oxidative and genotoxic effects induced by DCOIT, with activation of detoxification and defense mechanisms in T. viscana. These results are important for ecological risk assessment and managing of antifouling paint biocides in multiple stressors scenarios.