Abstract：
:We have investigated how [1-14C]propionyl-CoA, which is the first product of the peroxisomal beta-oxidation of [1-14C] pristanic acid, is transported to mitochondria for further oxidation in human skin fibroblasts from patients with a defect in the mitochondrial carnitine/acylcarnitine translocase and carnitine-palmitoyltransferase II (CPT II) (EC 2.3.1.21), respectively. Oxidation of pristanic acid was found to be partially deficient in both types of mutant cells. More important, 14CO2 production was completely deficient in the carnitine/acylcarnitine translocase deficient cells but not in the carnitine-palmitoyltransferase II deficient cells. These results strongly suggest that formation of 14CO2 in the Krebs cycle from [1-14C]propionyl-CoA as generated in peroxisomes requires the active participation of the mitochondrial carnitine/acylcarnitine translocase. The results described in this paper provide the first evidence suggesting that propionyl-CoA leaves the peroxisome as a carnitine ester and strongly suggest that the commonly accepted concept that peroxisomal beta-oxidation is not dependent on carnitine is incorrect.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Jakobs BS,Wanders RJdoi
10.1006/bbrc.1995.2232subject
Has Abstractpub_date
1995-08-24 00:00:00pages
1035-41issue
3eissn
0006-291Xissn
1090-2104pii
S0006-291X(85)72232-2journal_volume
213pub_type
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journal_title：Biochemical and biophysical research communications
pub_type： 杂志文章
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更新日期：2019-01-08 00:00:00
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journal_title：Biochemical and biophysical research communications
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journal_title：Biochemical and biophysical research communications
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journal_title：Biochemical and biophysical research communications
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更新日期：2008-01-25 00:00:00
