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Mitochondrial metabolism of (D,L)‐threo‐9, 10‐dibromo palmitic acid
Author(s) -
Mohamed H. F.,
Andreone T. L.,
Dryer R. L.
Publication year - 1980
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02535836
Subject(s) - palmitoylcarnitine , palmitoleic acid , fatty acid , palmitic acid , chemistry , carnitine , biochemistry , metabolism , beta oxidation , mitochondrion , incubation , organic chemistry
Bromination of palmitoleic or palmitelaidic acid proceeds by trans addition and yields dibrominated products which cannot undergo β‐oxidation when incubated with mitochondria isolated from hamster brown adipose tissue. These mitochondria were selected because they have a high capacity for oxidation of C 16 fatty acids and because they are readily uncoupled by an excess of free fatty acids of this chain length. The only metabolites which could be recovered from the incubation mixtures were dibromopalmitoylcarnitine and dibromopalmitoyl CoA. Free fatty acid was also recovered. Addition of synthetic carnitine or CoA esters of brominated fatty acids did not interfere with subsequent oxidation of palmitoylcarnitine. Addition of the free brominated fatty acids did significantly increase the rate of oxidation of subsequent additions of palmitoylcarnitine, as did other known synthetic uncouplers. These results are consistent with observations by others that feeding brominated oils leads to brominated fatty acid incorporation into tissue lipids, and indicate why this is so. They also provide a possible explanation for the hepatic damage noted in feeding experiments.