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Mechanism of lysophosphatidylcholine accumulation in the ischemic canine heart

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Lipids

Abstract

The metabolism of lysophosphatidylcholine (LPC) in non-ischemic and ischemic canine heart was investigated byin vitro enzyme analysis. Selected subcellular fractions were assayed for the LPC-producing enzyme phospholipase A and the LPC-eliminating enzymes LPC:acyl-CoA acyltransferase, LPC:LPC transacylase and lysophospholipase. The canine heart was found to contain all enzymes differing, however, in subcellular distribution and specific activity. Phospholipase A activity did not change significantly in any of the fractions prepared from the ischemic tissue of hearts rendered ischemic for 1, 3 or 5 hr when compared to non-ischemic tissue. Changes in the activity of the microsomal LPC:acyl-CoA acyltransferase over the course of 5 hr of ischemia were observed. Significant decreases in the activity of the cytosolic and microsomal lysophospholipases were detected especially after 3 and 5 hr of ischemia. Similarly, a decrease in the activity of the microsomal LPC:LPC transacylase was noted after 3 and 5 hr of ischemia. Our results suggest that impaired catabolism of LPC rather than an enhanced production of LPC is the principal mechanism for the increase in LPC levels in the ischemic canine heart.

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Abbreviations

ANOVA:

analysis of variance

FA:

fatty acid

LPC:

lysophosphatidylcholine

PC:

phosphatidylcholine

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Authors and Affiliations

  1. Department of Pharmacology and Therapeutics, University of Manitoba, Faculty of Medicine, 770 Bannatyne Ave., R3E OW3, Winnipeg, Manitoba, Canada

    Thomas Mock & Ricky Y. K. Man

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  1. Thomas Mock
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  2. Ricky Y. K. Man
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Mock, T., Man, R.Y.K. Mechanism of lysophosphatidylcholine accumulation in the ischemic canine heart. Lipids 25, 357–362 (1990). https://doi.org/10.1007/BF02537977

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  • DOI: https://doi.org/10.1007/BF02537977

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