| Literature DB >> 10558857 |
C Y Su1, K Y Chong, K Edelstein, S Lille, R Khardori, C C Lai.
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 microM of hydrogen peroxide (H(2)O(2)), hsc70-overexpressing cells exhibited a lower lipid peroxidation than the sham-transfected control. Constitutive hsc70 overexpression, however, did not protect against H(2)O(2)-induced depletion of ATP and glutathione (GSH). Lipid protection also occurred in cells preconditioned at 39 degrees C (selectively induces hsc70) during H(2)O(2) exposure. Interestingly, the protection conferred by hsc70 was comparable in magnitude to that provided by alpha-tocopherol, and was followed with a reduced release of lactate dehydrogenase and a unaltered calcium uptake during H(2)O(2) challenge. Collectively, our observations suggest that hsc70 may preserve membrane function via attenuation of lipid peroxidation during oxidative insult. Copyright 1999 Academic Press.Entities:
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Year: 1999 PMID: 10558857 DOI: 10.1006/bbrc.1999.1649
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575