Abstract
Thermal pretreatment improves cardiac recovery from subsequent ischemia/reperfusion. Induction of heat shock proteins (hsps) may contribute to this protection. We have demonstrated that augmentation of the constitutive hsp70 (hsc70) in H9c2 heart myoblasts promotes oxidative resistance. We employed a model oxidant to explore potential target(s) of protection by hsc70. Upon exposure to 54 μM of hydrogen peroxide (H2O2), hsc70-overexpressing cells exhibited a lower lipid peroxidation than the sham-transfected control. Constituitive hsc70 overexpression, however, did not protect against H2O2-induced depletion of ATP and glutathione (GSH). Lipid protection also occurred in cells preconditioned at 39°C (selectively induces hsc70) during H2O2 exposure. Interestingly, the protection conferred by hsc70 was comparable in magnitude to that provided by α-tocopherol, and was followed with a reduced release of lactate dehydrogenase and a unaltered calcium uptake during H2O2 challenge. Collectively, our observations suggest that hsc70 may preserve membrane function via attenuation of lipid peroxidation during oxidative insult.
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