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Correspondence to:
Hee-Yong Kim, To whom correspondence should be addressed., hykim{at}nih.gov (E-mail)
In this study, we have examined the effects of n-3 fatty acid deficient diets on the phospholipids (PL) molecular species composition in the hippocampus. Female rats were raised for two generations on diets containing linoleic acid (18:2n-6), with or without supplementation of
The observed decrease of 22:6n-3 species along with PS reduction may represent key biochemical changes underlying losses in brain-hippocampal function associated with n-3 deficiency.Murthy, M., J. Hamilton, R. S. Greiner, T. Moriguchi, N. Salem, Jr., and H-Y. Kim. Differential effects of n-3 fatty acid deficiency on phospholipid molecular species composition in the rat hippocampus. J. Lipid Res. 2002. 43: 611617.
Supplementary key words:
diet, docosahexaenoic acid, essential fatty acids, mass spectrometry
Copyright © 2002 by Lipid Research, Inc.
Differential effects of n-3 fatty acid deficiency on phospholipid molecular species composition in the rat hippocampus
Mahadev Murthya,
Jillonne Hamiltonb,
Rebecca S. Greinera,
Toru Moriguchia,
Norman Salem, Jr.a, and
Hee-Yong Kimb
a Section of Nutritional Neuroscience, Laboratory of Membrane Biochemistry and Biophysics, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, NIH, 12420 Parklawn Drive, Room 114, Rockville, MD 20852
b Section of Mass Spectrometry, Laboratory of Membrane Biochemistry and Biophysics, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, NIH, 12420 Parklawn Drive, Room 114, Rockville, MD 20852
-linolenic acid (18:3n-3) or 18:3n-3 plus docosahexaenoic acid (22:6n-3). At 84 days of age, the hippocampal phospholipids were analyzed by reversed phase HPLC-electrospray ionization mass spectrometry. Depleting n-3 fatty acids from the diet led to a reduction of 22:6n-3 molecular species in phosphatidylcholine (PC), phosphatidylethanolamine (PE), PE-plasmalogens (PLE), and phosphatidylserine (PS) by 7080%. In general, 22:6n-3 was replaced with 22:5n-6 but the replacement at the molecular species level did not always occur in a reciprocal manner, especially in PC and PLE. In PC, the 16:0,22:6n-3 species was replaced by 16:0,22:5n-6 and 18:0,22:5n-6. In PLE, substantial increases of both 22:5n-6 and 22:4n-6 species compensated for the decreases in 22:6n-3 species in n-3 fatty acid deficient groups. While the total PL content was not affected by n-3 deficiency, the relative distribution of PS decreased by 28% with a concomitant increase in PC. ![]()
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