| Autor: |
Bornman L; Department of Chemistry and Biochemistry, Rand Afrikaans University, Johannesburg, South Africa., Steinmann CM, Gericke GS, Polla BS |
| Jazyk: |
angličtina |
| Zdroj: |
Biochemical and biophysical research communications [Biochem Biophys Res Commun] 1998 May 29; Vol. 246 (3), pp. 836-40. |
| DOI: |
10.1006/bbrc.1998.8717 |
| Abstrakt: |
Heat shock (HS)/stress proteins (HSP) provide protection from a variety of stresses other than HS, including oxidative stress and mitochondria have been implicated as the target of HS-related protection in stressed cultured cells. Here we investigated whether mitochondria also are targets for the HS-mediated protection in vivo. Sprague Dawley rats were exposed, or not, to HS (41 degrees C, 15 min). After a 21 h recovery period, hearts were excised and perfused with or without H2O2 (0.15 mM). Myocardial mitochondria were then isolated, and their oxygen consumption was analyzed. HS prevented H2O2-induced alterations in state 3 respiration while increasing the expression of Hsp70 and heme oxygenase (HO). Thus, in vivo HS protects rat myocardial mitochondrial respiration against the deleterious effects of oxidative injury, a protection relating to Hsp70 and/or HO and targeting state 3 respiration. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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