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Analysis of the putative role of 24‐carbon polyunsaturated fatty acids in the biosynthesis of docosapentaenoic (22:5 n ‐6) and docosahexaenoic (22:6 n ‐3) acids
Author(s) -
Infante Juan P,
Huszagh Virginia A
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)00720-0
Subject(s) - docosapentaenoic acid , peroxisome , docosahexaenoic acid , polyunsaturated fatty acid , biosynthesis , biochemistry , chemistry , biology , enzyme , fatty acid , gene
The recent literature on the putative involvement of a single cycle of peroxisomal β‐oxidation of 24:5 n ‐6 and 24:6 n ‐3 polyunsaturated fatty acids in the biosynthesis of the respective docosapentaenoic (22:5 n ‐6) and docosahexaenoic (22:6 n ‐3) fatty acids is critically reviewed. Present evidence suggests that in vitro data in support of the above proposition is an artifact of a low 2,4‐dienoyl‐CoA reductase activity due to depletion of NADPH resulting from incubation conditions. Kinetic studies with radiolabeled precursors in cell cultures have shown lower initial rates of labeling of 24:6 n ‐3 than that of 22:6 n ‐3, indicating that 24:6 n ‐3 is an elongation product of 22:6 n ‐3 rather than its precursor. Analysis of other literature data supports the proposal that 22:5 n ‐6 and 22:6 n ‐3 are synthesized in mitochondria via channeled carnitine‐dependent pathways involving separate n ‐6‐ and n ‐3‐specific desaturases. It is proposed that impaired peroxisomal function in some peroxisomal disorders is a secondary consequence of defective mitochondrial synthesis of 22:6 n ‐3; moreover, some disorders of peroxisomal β‐oxidation show normal or increased 22:5 n ‐6 concentrations, indicating that 22:5 n ‐6 is synthesized by independent desaturases without peroxisomal involvement.