L. Bornman et al., IN-VIVO HEAT-SHOCK PROTECTS RAT MYOCARDIAL MITOCHONDRIA, Biochemical and biophysical research communications, 246(3), 1998, pp. 836-840
Heat shock (HS)/stress proteins (MSP) provide protection from a variet
y of stresses other than HS, including oxidative stress and mitochondr
ia have been implicated as the target of MS-related protection in stre
ssed cultured cells. Here we investigated whether mitochondria also ar
e 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 recov
ery period, hearts were excised and perfused with or without H2O2 (0.1
5 mM). Myocardial mitochondria were then isolated, and their oxygen co
nsumption was analyzed. MS prevented H2O2-induced alterations in state
3 respiration while increasing the expression of Hsp70 and heme oxyge
nase (HO). Thus, in vivo HS protects rat myocardial mitochondrial resp
iration against the deleterious effects of oxidative injury, a protect
ion relating to Hsp70 and/or HO and targeting state 3 respiration. (C)
1998 Academic Press.