Ovothiol A synthase transcription levels in different tissues of the mussels Mytilus galloprovincialis exposed to copper

Marine organisms are continuously exposed to reactive oxygen species (ROS). Although ROS can act as signaling molecules, thus showing a physiological role, their excess may cause oxidative stress resulting in multiple adverse effects such as protein and lipid oxidation and DNA damage. A part of the antioxidant system of marine organisms consists of low molecular weight scavengers, including thiols. Many studies focused on ovothiol, a thiol isolated from marine invertebrate eggs, because of its high antioxidant power. Ovothiol A synthase (Ovo-A) is an iron (II) dependent sulfoxide synthase which catalyzes ovothiol A biosynthesis, and therefore may be a marker of ovothiol response to environmental stress in marine animals. This study investigates transcriptional response of an Ovo-A gene product to oxidative stress in three different tissues of M. galloprovincialis (gonads, digestive glands and gills) and considering sex bias. Mussels were in vivo exposed to copper (Cu2+=10 µg/l) and tissues were dissected at 3 and 7 days of exposure. Ovo-A expression was assessed by quantitative real time PCR. Gonads were also collected for the histological analyses to determine the development stages. Female gonads showed significant Ovo-A downregulation in stage 5 organisms compared to stage 2 and stage 3. In Cu-treated mussels, down-regulation was observed in male gonads. No significant response occurred in treated digestive glands and gills. Downregulation of Ovo-A in relation to female gonads development may be due the conversion to Ovo-A mRNA into the protein which is then accumulated in oocytes as a part of the ‘‘be prepared’’ adaptive strategy allowing fast induction of embryo stress defenses. The lack of Ovo-A regulation by Cu in extragonadal tissues and the relevant influence of gonadal maturation stage in Ovo-A baseline expression lead to hypothesise that maturation processes may display a major role in Ovo-A regulation than exposure oxidative stress generating chemicals.