Boron Deprivation Decreases Liver S-Adenosylmethionine and Spermidine and Increases Plasma Homocysteine and Cysteine in Rats

Authors: Nielsen, Forrest - Frosty

Submitted to: Journal of Trace Elements in Medicine and Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/5/2009
Publication Date: 7/1/2009
Citation: Nielsen, F.H. 2009. Boron Deprivation Decreases Liver S-Adenosylmethionine and Spermidine and Increases Plasma Homocysteine and Cysteine in Rats. Journal of Trace Elements in Medicine and Biology. 23:204-213.

Interpretive Summary: Boron is a bioactive mineral in food that has beneficial effects on bone health, brain function, and the immune or inflammatory response. The reported diverse responses to low boron intakes (boron deprivation) have made it difficult to determine the basis for boron bioactivity. It was hypothesized that the wide range of responses to boron deprivation is the result of boron affecting the formation or activity of an entity that is involved in many biochemical processes. S-adenosylmethionine, which has a very high affinity for binding boron, is an entity used in many biochemical processes in the body. In addition, the use of S-adenosylmethionine in many biochemical processes results in the formation of homocysteine. Increased homocysteine in the blood has been associated with heart disease, osteoporosis, and mental disorders. The body reduces homocysteine by converting it to methionine, which is used to form S-adenosylmethionine, or by converting it to cysteine, which is used in other biochemical processes or broken down to products excreted in the urine. Two experiments were performed with rats to determine whether boron deprivation has a variety of undesirable effects through unfavorably affecting the amount of S-adenosylmethionine (decreases) in liver and homocysteine (increases) in plasma of blood. Boron deprivation increased plasma cysteine and homocysteine and decreased liver S-adenosylmethionine, S-adenosylhomocysteine, and spermidine (formed from S-adenosylmethionine). These findings suggest that boron is bioactive through affecting the formation or utilization of S-adenosylmethionine. Consuming a diet rich in boron provided by foods such as fruits, vegetables, nuts, and pulses may promote bone, brain and heart health through preventing abnormal formation or utilization of S-adenosylmethionine and increased circulating homocysteine in the body.

Technical Abstract: Two experiments were conducted with weanling Sprague-Dawley rats to determine whether changes in S-adenosylmethionine utilization or metabolism contribute to the diverse responses to boron deprivation. In both experiments, four treatment groups of 15 male rats were fed ground corn-casein based diets that contained about 0.05 mg (experiment 1) or 0.15 mg (experiment 2) boron/kg. In experiment 2, some ground corn was replaced by sucrose and fructose to increase oxidative stress. The dietary variables were supplemental 0 (boron-deficient) or 3 (boron-adequate) mg boron/kg and different fat sources (can affect the response to boron) of 75 g corn oil/kg or 65 g fish (menhaden) oil/kg plus 10 linoleic acid/kg. When euthanized at age 20 (experiment 1) and 18 (experiment 2) weeks, rats fed the low-boron diet were considered boron-deficient because they had decreased boron concentrations in femur and kidney. Boron deficiency regardless of dietary oil increased plasma cysteine and homocysteine and decreased liver S-adenosylmethionine, S-adenosylhomocysteine, and spermidine. Plasma concentration of 8-iso-prostaglandin F2a (indicator of oxidative stress) was not affected by boron, but was decreased by feeding fish oil instead of corn oil. Fish oil instead of corn oil decreased S-adenosylmethionine, increased spermidine, and did not affect S-adenosylhomocysteine concentrations in liver. Additionally, fish oil versus corn oil did not affect plasma homocysteine in experiment 1, and slightly increased it in experiment 2. The findings suggest that boron is bioactive through affecting the formation or utilization of S-adenosylmethionine. Dietary fatty acid composition also affects S-adenosylmethionine formation or utilization, but apparently through a mechanism different from that of boron.