|Stoecker, Barbara - OKLAHOMA STATE UNIV|
Submitted to: Symposium Proceedings
Publication Type: Proceedings
Publication Acceptance Date: October 1, 2005
Publication Date: August 1, 2006
Repository URL: http://handle.nal.usda.gov/10113/45968
Citation: Nielsen, F.H., Stoecker, B.J., Penland, J.G. 2006. Boron as a dietary factor for bone microarchitecture and central nervous system function. In: Fangsen Xu, Heiner E. Goldback, Patrick H. Brown, Richard W. Bell, Toru Fujiwars, Curtiss D. Hunt, Sabine Goldberg, Lei Shi, editors. Advances in Plant and Animal Boron Nutrition. Boron 2005, September 10-13, 2005, Wuhan, China. p. 255-268. Technical Abstract: Since 1981, considerable evidence has been presented that indicates nutritional amounts of boron beneficially affect bone formation, composition and physical characteristics; brain composition, electrical activity, and function; and eye development and photoreceptor function. The long chain omega-3 polyunsaturated fatty acids (n-3 PUFA) docosahexaeonic acid and eicosapentaenoic acid also have been found to be beneficial for normal visual and brain function, and bone formation, turnover, composition and strength. Both boron and n-3 PUFA may affect brain and bone through modulating oxidative stress because both low boron and low n-3 PUFA in the diet increase the concentration of plasma 8-iso-prostaglandin F2' (an indicator of lipid oxidation). Increased 8-iso-prostaglandin F2' has been associated with decreased bone density and neurological disorders. The similarity of boron and n-3 PUFA beneficial effects on bone and brain, and the possibility that this occurs through oxidant stress modulation, suggested that the response to boron deprivation would be modified by n-3 PUFA supplementation, or that n-3 PUFA supplementation would have a greater effect when boron is low than when present in beneficial amounts in the diet. Thus, a study was initiated to determine whether dietary fatty acid composition would modify the effect of boron deprivation on bone characteristics, behavior, and vision. Female rats were fed diets containing 0.1 mg boron/kg in a factorial arrangement with variables of supplemental boron at 0 (B-def) or 3 (B-adq) mg/kg and fat sources of 75 g safflower oil/kg or 65 g fish oil plus 10 g linoleic acid rich oil/kg (added to assure adequacy of omega-6 fatty acids). After 6 weeks, 6 females per treatment were bred. Dams and pups continued on their respective diets through gestation, lactation and after weaning. Fifteen males from each treatment were used for behavioral testing. Twelve weeks after weaning the response of the males to light (brightness discrimination) was determined. Three and 15 weeks after weaning the rats were tested on a plus maze. Vertebrae for bone architecture and femurs for bone strength and mineral composition determinations were collected 16 weeks after weaning. Rats fed the B-def diet were boron deficient because their mean body weight and femur boron concentration were lower than for those fed B-adq diet. Plasma 8-iso-prostaglandin F2' was decreased and the maximum force needed to break the femur was increased by the B-adq and fish oil diets. Femur copper concentration was significantly decreased by boron deprivation in rats fed fish oil, but not in rats fed safflower oil. Boron deprivation decreased vertebra trabecular thickness. Vertebra trabecular connection density was higher in B-def than B-adq rats fed safflower oil; dietary boron did significantly affect connection density in rats fed fish oil. Plus maze and brightness testing showed several significant interactions between dietary oil and boron that was characterized by dietary oil having an effect in B-def rats but not in B-adq rats, or dietary boron having the most marked effect in rats fed fish oil. As a result, the B-def rats fed fish oil often showed behavior different than the other 3 groups (e.g., more active). The findings indicate that boron deprivation can affect bone microarchitecture, strength and composition and central nervous system function, but that the effects can be modified by the fatty acid composition of the diet.