scholarly journals Oxidation of cis-5-unsaturated fatty acids in intact rat liver mitochondria: the operation of reduction pathways

1995 ◽  
Vol 308 (1) ◽  
pp. 39-44 ◽  
Author(s):  
K Y Tserng ◽  
S J Jin
Keyword(s):  
Fatty Acids ◽  
Rat Liver ◽  
Capillary Column ◽  
Unsaturated Fatty Acids ◽  
Direct Reduction ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Capillary Column Gas Chromatography ◽  
Coa Reductase ◽  
Direct Quantification

The metabolism of cis-5 unsaturated fatty acids was studied in intact rat liver mitochondria to assess the operation of a reduction pathway. By using direct quantification of metabolites with a capillary-column gas chromatography, 3-hydroxydodecanoate was identified among other metabolites when cis-5-dodecenoate was metabolized in intact rat liver mitochondria. The formation of 3-hydroxydodecanoate supports the existence of a reduction pathway in the metabolism of cis-5-unsaturated fatty acids. This metabolite cannot be produced from the conventional isomerase-mediated pathway. However, the data also indicated the possible operation of the conventional isomerase-mediated pathway in intact rat liver mitochondria. The reduction pathway appears to account for at least 61% of the pathway for cis-5-dodecenoate. This reduction pathway was likely to proceed from the dehydrogenation to trans-2,cis-5-dodecadienoyl-CoA, which was isomerized to delta 3, delta 5-dodecadienoyl-CoA, then to trans-2,trans-4-dodecadienoate. The reduction was mediated by 2,4-dienoyl-CoA reductase by the conversion of trans-2,trans-4-dodecadienoyl-CoA into trans-3-dodecenoyl-CoA. However, direct reduction of the cis-5 double bond was also shown to be operating, although to a lesser extent.

scholarly journals A role for 2,4-enoyl-CoA reductase in mitochondrial β-oxidation of polyunsaturated fatty acids. Effects of treatment with clofibrate on oxidation of polyunsaturated acylcarnitines by isolated rat liver mitochondria

1982 ◽  
Vol 208 (3) ◽  
pp. 749-757 ◽  
Author(s):  
H Osmundsen ◽  
J Cervenka ◽  
J Bremer
Keyword(s):  
Fatty Acids ◽  
Rat Liver ◽  
Opposite Effect ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Long Chain Fatty Acids ◽  
Beta Oxidation ◽  
Isolated Rat Liver ◽  
Coa Reductase ◽  
Isolated Rat

1. beta-Oxidation of gamma-linolenoylcarnitine, arachidonoylcarnitine and docosahexaenoylcarnitine by isolated rat liver mitochondria is inhibited by uncoupling conditions. Partial re-activation is obtained with added ATP. With mitochondria from clofibrate-treated rats ATP-stimulated rates of beta-oxidation of docosahexaenoylcarnitine are higher than ADP-stimulated rates. This is not observed with the beta-oxidation of oleoylcarnitine. 2. beta-Oxidation of docosahexaenoylcarnitine, in the presence of rotenone, is inhibited by added oxaloacetate, analogous to previous findings with pent-4-enoylcarnitine [see Osmundsen (1978) FEBS Lett. 88, 219-222]. In the absence of rotenone added oxaloacetate stimulates the beta-oxidation of docosahexaenoylcarnitine, but has the opposite effect on the beta-oxidation of palmitoylcarnitine. 3. beta-Oxidation of polyunsaturated acylcarnitines by isolated rat liver mitochondria is selectively increased after treatment of the animals with a low dietary dose (0.2%, w/w) of clofibrate. Treatment with a higher dose of clofibrate (0.5%, w/w) resulted in a general stimulation of beta-oxidation. 4. The results presented suggest that long-chain fatty acids possessing a delta 4-double bond are not readily beta-oxidized unless the 2,4-enoyl-CoA reductase (EC 1.3.1.-) is operating.

scholarly journals β-oxidation of polyunsaturated fatty acids with conjugated double bonds. Mitochondrial metabolism of octa-2,4,6-trienoic acid

1989 ◽  
Vol 264 (1) ◽  
pp. 47-52 ◽  
Author(s):  
H Y Wang ◽  
H Schulz
Keyword(s):  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Unsaturated Fatty Acids ◽  
Liver Mitochondria ◽  
Trienoic Acid ◽  
Rat Liver Mitochondria ◽  
Double Bonds ◽  
Beta Oxidation ◽  
Rat Heart Mitochondria ◽  
Coa Reductase

The mitochondrial beta-oxidation of octa-2,4,6-trienoic acid was studied with the aim of elucidating the degradation of unsaturated fatty acids with conjugated double bonds. Octa-2,4,6-trienoic acid was found to be a respiratory substrate of coupled rat liver mitochondria, but not of rat heart mitochondria. Octa-2,4,6-trienoyl-CoA, the product of the inner-mitochondrial activation of the acid, was chemically synthesized and its degradation by purified enzymes of beta-oxidation was studied spectrophotometrically and by use of h.p.l.c. This compound is a substrate of NADPH-dependent 2,4-dienoyl-CoA reductase or 4-enoyl-CoA reductase (EC 1.3.1.34), which facilitates its further beta-oxidation. The product obtained after the NADPH-dependent reduction of octa-2,4,6-trienoyl-CoA and one round of beta-oxidation was hex-4-enoyl-CoA, which can be completely degraded via beta-oxidation. It is concluded that polyunsaturated fatty acids with two conjugated double bonds extending from even-numbered carbon atoms can be completely degraded via beta-oxidation because their presumed 2,4,6-trienoyl-CoA intermediates are substrates of 2,4-dienoyl-CoA reductase.

scholarly journals Reduction pathway of cis-5 unsaturated fatty acids in intact rat-liver and rat-heart mitochondria: assessment with stable-isotype-labelled substrates

1996 ◽  
Vol 313 (2) ◽  
pp. 581-588 ◽  
Author(s):  
Kou-Yi TSERNG ◽  
Shiow-Jen JIN ◽  
Lin-Su CHEN
Keyword(s):  
Fatty Acids ◽  
Rat Liver ◽  
Rat Heart ◽  
Unsaturated Fatty Acids ◽  
Direct Reduction ◽  
Saturated Fatty Acids ◽  
Liver Mitochondria ◽  
Hydroxy Fatty Acids ◽  
Heart Mitochondria ◽  
Rat Heart Mitochondria

Besides the conventional isomerase-mediated pathway, unsaturated fatty acids with odd-numbered double bonds are also metabolized by reduction pathways with NADPH as cofactor. The relative contributions of these pathways were measured in intact rat-liver and rat-heart mitochondria with a novel stable isotope tracer technique. A mixture of equal amounts of unlabelled cis-5-enoyl-CoA and 13C4-labelled acyl-CoA of equal chain lengths was incubated with mitochondria. The isotope distribution of 3-hydroxy fatty acids produced from the first cycle of β-oxidation was analysed with selected ion monitoring by gas chromatograph-mass spectrometer. 3-Hydroxy fatty acids produced from the reduction pathway of unsaturated fatty acids were unlabelled (m+0) whereas those produced from saturated fatty acids were labelled (m+4). The m+0 content serves to indicate the extent of reduction pathway. Rotenone treatment was used to switch the pathway completely to reduction. The extent of m+0 enrichment in untreated mitochondria normalized to the m+0 enrichment of rotenone-treated mitochondria was the percentage of reduction pathway. With this technique, cis-4-decenoate was found to be metabolized completely by the reduction pathway in both liver and heart mitochondria. cis-5-Dodecenoate was metabolized essentially by the reduction pathway in liver mitochondria, but only to 75% in heart mitochondria. When the chain length was extended to cis-5-tetradecenoate, the reduction pathway in liver mitochondria decreased to 86% and that in heart mitochondria to 65%. The effects of carnitine, clofibrate and other conditions on the reduction pathway were also studied. Enrichments of the label on saturated fatty acids and 3-hydroxy fatty acids indicated that the major pathway of reduction was not by the direct reduction of the cis-5 double bond. Instead, it is most probably by a pathway that does not involve forming a reduced saturated fatty acid first.

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