ARS | Publication request: DIETARY BORON MODIFIES THE EFFECT OF CHANGING DIETARY FATTY ACID COMPOSITION ON RAT BEHAVIOR AND EYE MITOCHONDRIAL MORPHOLOGY

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: December 1, 2003
Publication Date: March 24, 2004
Citation: Nielsen, F.H., Penland, J.G., Newman Jr, S.M. 2004. Dietary boron modifies the effect of changing dietary fatty acid composition on rat behavior and eye mitochondrial morphology [abstract]. The Federation of American Societies for Experimental Biology Journal. 18(4):A491.

Technical Abstract: Female and male Sprague-Dawley rats were fed diets containing about 70 ug boron (B)/kg in a factorial arrangement with variables being supplemental B at 0 (deficient) and 3 (adequate) mg/kg and canola oil (CO) or palm oil (PO) at 75 g/kg. After 5 wks, 6 females per treatment were bred. Pup diets were the same as their mothers. At age 5 wks, the ultrastructure of eyes of 6 pups in each treatment was examined by transmission electron microscopy. At age 12 wks, 12 males and 12 females in each treatment underwent behavioral testing; after which the fragilities of their erythrocytes were determined. Compared to the other 3 groups, the rats fed the B-adequate diet with CO had less rod inner segment mitochondria with a high abundance of cristal folds. Rats fed the B-adequate diet with PO had the lowest number of hydropic (swollen) mitochondria. CO compared to PO decreased exploratory behavior and increased behavioral anxiety in B-adequate rats. In B-deficient rats, CO compared to PO decreased erythrocyte fragility; in B-adequate rats, CO increased fragility. Because the mitochondrion is the major site of fatty acid metabolism, hydropsis indicates the influx of water through the mitochondrion membrane, and erythrocyte fragility is a proxy for brain membrane phospholipid composition, the findings support the hypothesis that changes in mitochondrial membrane lipid metabolism may be the basis for neurological effects of B deprivation.