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

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.

Keyword

Oxidant; PLA2; LDH release; Hypoxia; Rabbit kidney

MeSH Terms

Acidosis
Alanine
Amino Acids
Anoxia
Arachidonic Acid
Dibucaine
Fatty Acids, Nonesterified
Glycine
Phospholipases A2*
Phospholipases*
Quinacrine
Alanine
Amino Acids
Arachidonic Acid
Dibucaine
Fatty Acids, Nonesterified
Glycine
Phospholipases
Phospholipases A2
Quinacrine
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