Cyclosporin A inhibits oxidant and calcium stimulated phospholipase D activity in the rat intestinal mitochondria

Madesh Muniswamy, Kunissery A. Balasubramanian

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Mitochondrial swelling and calcium cycling occurs during oxidative stress and can be prevented by cyclosporin A (CysA). Our earlier work has shown that enterocyte mitochondria contains a phospholipase D (PLD) which can be activated by superoxide or calcium. In this study, we have shown that enterocyte mitochondrial PLD activated by these agents can be inhibited by cyclosporin A. This was clearly shown by the absence of phosphatidic acid (PA) formation and phosphatidylethanolamine (PE) degradation. Since this PLD specifically utilizes PE as substrate, PLD activity was also assessed by ethanolamine formation which was inhibited by CysA. CysA also inhibited the cabbage PLD activity as judged by phosphatidylethanol formation. These results suggest that cyclosporin A is an inhibitor of PLD and this may be one of the mechanism by which CysA protects enterocyte mitochondria from oxidative stress.

Original languageEnglish (US)
Pages (from-to)206-212
Number of pages7
JournalBiochimica et Biophysica Acta - Lipids and Lipid Metabolism
Volume1389
Issue number3
DOIs
StatePublished - Jan 23 1998
Externally publishedYes

Fingerprint

Phospholipase D
Mitochondria
Oxidants
Cyclosporine
Rats
Calcium
Enterocytes
Oxidative stress
Oxidative Stress
Mitochondrial Swelling
Phosphatidic Acids
Ethanolamine
Brassica
Superoxides
Swelling
Degradation
Substrates

Keywords

  • Calcium
  • Cyclosporin A
  • Enterocyte mitochondrion
  • Oxidant
  • Phospholipase D

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Endocrinology

Cite this

Cyclosporin A inhibits oxidant and calcium stimulated phospholipase D activity in the rat intestinal mitochondria. / Muniswamy, Madesh; Balasubramanian, Kunissery A.

In: Biochimica et Biophysica Acta - Lipids and Lipid Metabolism, Vol. 1389, No. 3, 23.01.1998, p. 206-212.

Research output: Contribution to journalArticle

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