Korean J Physiol Pharmacol.
1999 Feb;3(1):93-100.
Role of phospholipase A2 in hypoxia-induced renal cell injury
- Affiliations
-
- 1Department of Physiology, College of Medicine, Pusan National University, Pusan, 602-739 South Korea.
Abstract
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The present study was designed to assess the roles of PLA2 activation
and arachidonic acid (AA) metabolites in hypoxia-induced renal cell
injury. Hypoxia increased LDH release in a dose-dependent manner in
rabbit renal cortical slices, and this increase was significant after
20-min hypoxia. The hypoxia-induced LDH release was prevented by amino
acids, glycine and alanine, and extracellular acidosis (pH 6.0).
Buffering intracellular Ca2+ by a chelator, but not omission of Ca2+ in
the medium produced a significant reduction in hypoxia-induced LDH
release. The effect of hypoxia was blocked by PLA2 inhibitors,
mepacrine, butacaine, and dibucaine. A similar effect was observed by a
85-kD cPLA2 inhibitor AACOCF3. AA increased hypoxia-induced LDH
release, and albumin, a fatty acid absorbent, prevented the LDH
release, suggesting that free fatty acids are involved in
hypoxia-induced cell injury. These results suggest that PLA2 activation
and its metabolic products play important roles in pathogenesis of
hypoxia-induced cell injury in rabbit renal cortical slices.