Nielsen Forrest Harold
US Department of Agriculture, Agricultural Research Service, Grand Forks Human Nutrition Research Center, Grand Forks, ND 58202-9034, USA.
J Trace Elem Med Biol. 2009;23(3):204-13. doi: 10.1016/j.jtemb.2009.03.001. Epub 2009 May 8.
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 an average of 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-deprived) 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-deprived because they had decreased boron concentrations in femur and kidney. Boron deprivation regardless of dietary oil increased plasma cysteine and homocysteine and decreased liver S-adenosylmethionine, S-adenosylhomocysteine, and spermidine. Plasma concentration of 8-iso-prostaglandin F2alpha (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.
进行了两项实验，以确定断奶的斯普拉格-道利大鼠体内S-腺苷甲硫氨酸利用或代谢的变化是否会导致对硼缺乏的不同反应。在两项实验中，将15只雄性大鼠分为四个处理组，分别喂食以玉米-酪蛋白为基础的研磨饲料，这些饲料平均每千克含有0.05毫克（实验1）或0.15毫克（实验2）硼。在实验2中，用蔗糖和果糖替代了部分玉米粉，以增加氧化应激。饮食变量包括每千克补充0（缺硼）或3（硼充足）毫克硼以及不同的脂肪来源（会影响对硼的反应），即每千克75克玉米油或65克鱼油（鲱鱼油）加10克亚油酸。在20周龄（实验1）和18周龄（实验2）对大鼠实施安乐死时，喂食低硼饮食的大鼠被视为硼缺乏，因为它们股骨和肾脏中的硼浓度降低。无论饮食中的油类如何，硼缺乏都会增加血浆半胱氨酸和同型半胱氨酸水平，并降低肝脏中的S-腺苷甲硫氨酸、S-腺苷同型半胱氨酸和亚精胺水平。血浆8-异前列腺素F2α（氧化应激指标）浓度不受硼影响，但喂食鱼油而非玉米油会使其降低。用鱼油替代玉米油会降低肝脏中的S-腺苷甲硫氨酸水平，增加亚精胺水平，且不影响S-腺苷同型半胱氨酸浓度。此外，在实验1中，鱼油与玉米油相比对血浆同型半胱氨酸没有影响，而在实验2中则使其略有升高。研究结果表明，硼通过影响S-腺苷甲硫氨酸的形成或利用而具有生物活性。饮食脂肪酸组成也会影响S-腺苷甲硫氨酸的形成或利用，但显然是通过与硼不同的机制。
