Boron (B) deprivation increases plasma homocysteine and decreases liver S‐adenosylmethionine (SAM) and S‐adenosylhomocysteine (SAH) in rats

Abstract

The diverse effects of B deprivation suggest that B affects a biomolecule involved in a variety of biochemical reactions. An experiment was conducted to determine whether dietary B affects the liver concentration of SAM, a frequently used enzyme substrate, especially for methylation reactions that yield SAH. SAH is hydrolyzed to yield homocysteine (Hcy). Weanling male rats (15 per treatment) were fed a ground corn‐casein based diet (0.15 mg B/kg) containing sucrose and fructose to increase oxidative stress. Experimental variables were dietary supplements of 0 and 3 mg B/kg and fat sources (affect the response to B) of 75 g corn oil, 75 g canola oil, or 65 g fish oil plus 10 g linoleic acid/kg. When euthanized at age 18 wk, rats fed the B‐low diet were considered B‐deprived because they had decreased B concentrations in femur, tibia, and kidney. Decreased plasma C‐reactive protein indicated that fish oil decreased oxidative stress; the decrease was more noticeable in B‐deprived rats. Boron deprivation regardless of dietary oil decreased liver SAM and SAH, and increased plasma Hcy. Fish oil decreased liver SAM, which attenuated the SAM response to B. Femur, tibia and liver iron (bound by SAM) was decreased in B‐supplemented and fish oil‐fed rats. The findings suggest that B is bioactive through affecting the formation or utilization of SAM, and this effect is enhanced by oxidative stress. (Supported by USDA)