Carnitine prevents cyclic GMP-induced inhibition of peroxisomal enzyme activities
Peroxisomes, also termed as microbodies, are now known to carry out several specialized metabolic activities that are vital to cellular function. A defect in peroxisomal function leads to development of a fatal human disease, and a number of peroxisomal disorders are now linked to inherited peroxiso...
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Published in | Cell biochemistry and function Vol. 22; no. 6; pp. 365 - 371 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Chichester, UK
John Wiley & Sons, Ltd
01.11.2004
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Subjects | |
Online Access | Get full text |
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Summary: | Peroxisomes, also termed as microbodies, are now known to carry out several specialized metabolic activities that are vital to cellular function. A defect in peroxisomal function leads to development of a fatal human disease, and a number of peroxisomal disorders are now linked to inherited peroxisomal enzyme abnormalities. Peroxisomal enzyme activities are also altered during pathophysiological conditions through various endogenously produced bio‐molecules such as nitric oxide (NO). NO produced by cytokines or NO‐donors is known to modulate peroxisomal functions, and these effects of NO are mediated through cGMP. We are reporting for the first time that L‐carnitine (1–5 mm) prevents cGMP‐mediated impairment of peroxisomal enzyme activities. Cyclic GMP (250–1000 μM) significantly inhibited (p < 0.01) the specific activities of catalase, acyl CoA oxidase and dihydroxyacetone‐phosphate acyltransferase (DHAPATase) in human dermal fibroblasts, and treatment of cells with 1–5 mM of carnitine significantly (p < 0.001) reduced the inhibitory effects of cGMP on peroxisomal enzyme activities. These findings suggest that carnitine, previously thought to participate only in fatty acid oxidation, may in fact be regulating other cellular events including oxidative stress, and could possibly be used to correct cytokine‐impaired peroxisomal functions. Copyright © 2004 John Wiley & Sons, Ltd. |
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Bibliography: | istex:2FCAC5A56CCB03D8D660FA51B7F4D1F3E2B0C010 ArticleID:CBF1117 ark:/67375/WNG-178BCCBX-X ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0263-6484 1099-0844 |
DOI: | 10.1002/cbf.1117 |