Acute thermal stress and various heavy metals induce tissue-specific pro-or anti-apoptotic events via the p38-MAPK signal transduction pathway in Mytilus galloprovincialis (Lam.)

Abstract

SUMMARY We investigated the effects of various heavy metals such as copper, zinc and cadmium, as well as acute thermal stress, on the signalling mechanisms involved in the protection and/or apoptosis of Mytilus galloprovincialis mantle and gill tissues. The results of our studies revealed that mantle and gill tissues differentially respond to the stressful stimuli examined. In the mantle tissue, 1 μmol l–1Cu2+ and 50 μmol l–1 Zn2+ induced a transient p38-MAPK activation, whereas 1 μmol l–1Cd2+ induced a biphasic profile of the kinase phosphorylation with maximal values at 15 and 120 min of treatment, respectively. Furthermore, 1μmol l–1 SB203580 abolished the Cu2+-induced kinase phosphorylation. In gills, both Cu2+ and Zn2+induced a considerably higher p38-MAPK activation, which remained elevated for at least 60 min, whereas Cd2+ induced a maximal kinase activation within 60 min of treatment. Hypothermia (4°C) induced a moderate kinase phosphorylation (maximised at 30 min), whereas hyperthermia (30°C) induced a rapid (within 15 min) p38-MAPK phosphorylation that remained considerably above basal levels for at least 2 h. Our studies on the synergistic effect of hyperthermia and Cu2+ revealed that these two stressful stimuli are additive in the mantle tissue, inducing an almost double p38-MAPK activation. Further studies on the involvement of the p38-MAPK signalling pathway in tissue-specific pro- or anti-apoptotic events revealed that identical stressful stimuli possibly lead to apoptotic death via the caspase-3 activation in the mantle tissue and to anti-apoptotic events possibly via the induction of Hsp70 overexpression in the gill tissue.