SUMMARYThis study investigated the role of Na + /H + exchanger (NHE) and signalling molecules, such as cAMP, PKC, PI 3-kinase, and immune defence enzymes, NADPH oxidase and nitric oxide synthase, in the induction of protein glutathionylation and carbonylation in cadmium-treated haemocytes of mussel Mytilus galloprovincialis. Glutathionylation was detected by western blot analysis and showed actin as its main target. A significant increase of both actin glutathionylation and protein carbonylation, were observed in haemocytes exposed to micromolar concentration of cadmium chloride (5moll -1 ). Cadmium seems to cause actin polymerization that may lead to its increased glutathionylation, probably to protect it from cadmium-induced oxidative stress. It is therefore possible that polymerization of actin plays a signalling role in the induction of both glutathionylation and carbonylation processes. NHE seems to play a regulatory role in the induction of oxidative damage and actin glutathionylation, since its inhibition by 2moll -1 cariporide, significantly diminished cadmium effects in each case. Similarly, attenuation of cadmium effects were observed in cells pre-treated with either 11moll -1 GF-109203X, a potent inhibitor of PKC, 50nmoll -1 wortmannin, an inhibitor of PI 3-kinase, 0.01mmoll -1 forskolin, an adenylyl cyclase activator, 10moll -1 DPI, a NADPH oxidase inhibitor, or 10moll -1 L-NAME, a nitric oxide synthase inhibitor, suggesting a possible role of PKC, PI 3-kinase and cAMP, as well as NADPH oxidase and nitric oxide synthase in the enhancement of cadmium effects on both actin glutathionylation and protein carbonylation.
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