Lack of oxidative damage on temperate juvenile catsharks after a long-term ocean acidification exposure

Ocean acidification is a consequence of chemical changes driven mainly by a continuous uptake of carbon dioxide, resulting in pH decrease. This phenomenon represents an additional threat to marine life, with expected effects ranging from changes in behavioral responses and calcification rates to the potential promotion of oxidative stress. To unravel the impacts of ocean acidification on the antioxidant system of sharks, we performed a long-term exposure (9 months, since early embryogenesis) to high CO2 conditions (pCO(2) similar to 900 mu atm) on a temperate shark (Scyliorhinus canicula). The following biomarkers were measured: enzymatic antioxidant defense (superoxide dismutase, catalase and glutathione peroxidase), protein repair and removal (heat shock proteins and ubiquitin), and oxidative damage on lipids (malondialdehyde) and DNA (8-hydroxy-2 '-deoxyguanosine). Changes in the antioxidant enzyme defense were restricted to an increase in catalase activity in the muscle, an enzyme that plays a major role in oxidative stress mitigation. On the other hand, no evidence of oxidative damage was found, indicating that the observed increase in catalase activity may be enough to neutralize the effects of potentially higher reactive oxygen species. These results further indicate that these sharks' antioxidant system can successfully cope with the levels of carbon dioxide projected for the end of the century. Nonetheless, the interaction between ocean acidification and the rise in temperature expected to occur in a near future may disturb their antioxidant capacity, requiring further investigation.