Role of phospholipase A2 in hypoxia-induced renal cell injury.
- Author:
Won Rak CHOI
1
;
Sun Hee KO
;
Su In CHO
;
Jae Suk WOO
;
Jin Sup JUNG
;
Sang Ho LEE
;
Yong Keun KIM
Author Information
1. Department of Physiology, College of Medicine, Pusan National University, Pusan, 602-739 South Korea.
- Publication Type:Original Article
- Keywords:
Oxidant;
PLA2;
LDH release;
Hypoxia;
Rabbit kidney
- MeSH:
Acidosis;
Alanine;
Amino Acids;
Anoxia;
Arachidonic Acid;
Dibucaine;
Fatty Acids, Nonesterified;
Glycine;
Phospholipases A2*;
Phospholipases*;
Quinacrine
- From:The Korean Journal of Physiology and Pharmacology
1999;3(1):93-100
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
