Lippincott Williams & Wilkins, Inc., Philadelphia
Nutritional Deprivation of α-Linolenic Acid Decreases but Does Not Abolish Turnover and Availability of Unacylated Docosahexaenoic Acid and Docosahexaenoyl-CoA in Rat Brain
Article first published online: 29 JUL 2008
Journal of Neurochemistry
Volume 75, Issue 6, pages 2392–2400, December 2000
How to Cite
Contreras, M. A., Greiner, R. S., Chang, M. C. J., Myers, C. S., Salem, N. and Rapoport, S. I. (2000), Nutritional Deprivation of α-Linolenic Acid Decreases but Does Not Abolish Turnover and Availability of Unacylated Docosahexaenoic Acid and Docosahexaenoyl-CoA in Rat Brain. Journal of Neurochemistry, 75: 2392–2400. doi: 10.1046/j.1471-4159.2000.0752392.x
Abbreviations used: DHA, docosahexaenoic acid; FA, fatty acid; α-LNA, α-linolenic acid; PUFA, polyunsaturated fatty acid.
- Issue published online: 29 JUL 2008
- Article first published online: 29 JUL 2008
- Docosahexaenoic acid;
- α-Linolenic acid;
- Polyunsaturated fatty acids;
- Brain recycling;
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 [4,5-3H]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.