Atmospheric carbon dioxide (CO2) levels are increasing at the fastest rate ever recorded, causing higher CO2 dissolution in the ocean, leading to a process known as ocean acidification (OA). Unless anthropogenic CO2 emissions are reduced, they are expected to reach ~900 ppm by the century's end, resulting in a 0.13-0.42 drop in the seawater pH levels. Since the transgenerational effects of high CO2 in marine organisms are still poorly understood at lower levels of biological organization (namely at the biochemical level), here we reared a key ecological relevant marine amphipod, Gammarus locusta, under control and high CO2 conditions for two generations. We measured several stress-related biochemical endpoints: i) oxidative damage [lipid peroxidation (LPO) and DNA damage]; ii) protein repair and removal mechanisms [heat shock proteins (HSPs) and ubiquitin (Ub)]; as well as iii) antioxidant responses [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione s-transferase (GST)] and total antioxidant capacity (TAC). The present results support the premise that exposure to high CO2 is expected to decrease survival rates in this species and cause within- and transgenerational oxidative damage. More specifically, the predicted upsurge of reactive oxygen and nitrogen species seemed to overwhelm the stimulated amphipod antioxidant machinery, which proved insufficient in circumventing protein damage within the parents. Additionally, negative effects of OA are potentially being inherited by the offspring, since the oxidative stress imposed in the parent's proteome appears to be restricting DNA repair mechanisms efficiency within the offspring's. Thus, we argue that a transgenerational exposure of G. locusta could further increase vulnerability to OA and may endanger the fitness and sustainability of natural populations.
Keywords: Gammarus locusta; Ocean acidification; Oxidative damage; Oxidative stress; Transgenerational.
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