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Nutritional Deprivation of α‐Linolenic Acid Decreases but Does Not Abolish Turnover and Availability of Unacylated Docosahexaenoic Acid and Docosahexaenoyl‐CoA in Rat Brain
Author(s) -
Contreras Miguel A.,
Greiner Rebecca Sheaff,
Chang Michael C. J.,
Myers Carol S.,
Salem Norman,
Rapoport Stanley I.
Publication year - 2000
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2000.0752392.x
Subject(s) - docosahexaenoic acid , linolenic acid , biology , polyunsaturated fatty acid , endocrinology , fatty acid , biochemistry , linoleic acid
Abstract: We applied our in vivo fatty acid method to examine concentrations, incorporation, and turnover rates of docosahexaenoic acid (22:6 n‐3) in brains of rats subject to a dietary deficiency of α‐linolenic acid (18:3 n‐3) for three generations. Adult deficient and adequate rats of the F3 generation were infused intravenously with [4,5‐ 3 H]docosahexaenoic acid over 5 min, after which brain uptake and distribution of tracer were measured. Before infusion, the plasma 22:6 n‐3 level was 0.2 nmol ml ‐1 in 18:3 n‐3‐deficient compared with 10.6 nmol ml ‐1 in control rats. Brain unesterified 22:6 n‐3 was not detectable, whereas docosahexaenoyl‐CoA content was reduced by 95%, and 22:6 n‐3 content in different phospholipid classes was reduced by 83‐88% in deficient rats. Neither plasma or brain arachidonic acid (20:4 n‐6) level was significantly changed with diet. Docosapentaenoic acid (22:5 n‐6) reciprocally replaced 22:6 n‐3 in brain phospholipids. Calculations using operational equations from our model indicated that 22:6 n‐3 incorporation from plasma into brain was reduced 40‐fold by 18:3 n‐3 deficiency. Recycling of 22:6 n‐3 due to deacylation‐reacylation within phospholipids was reduced by 30‐70% with the deficient diet, but animals nevertheless continued to produce 22:6 n‐3 and docosahexaenoyl‐CoA for brain function. We propose that functional brain effects of n‐3 deficiency reflect altered ratios of n‐6 to n‐3 fatty acids.