Butler J A, Whanger P D, Patton N M
Department of Agricultural Chemistry, Oregon State University, Corvallis 97331.
J Am Coll Nutr. 1988 Feb;7(1):43-56. doi: 10.1080/07315724.1988.10720219.
Pregnant rhesus monkeys (Macaca mulatta) were fed either selenium (Se) deficient or Se supplemented diets with adequate vitamin E. Except for some cardiac irregularities in the first babies born to these females, no physiological disorders due to Se deficiency were seen in a subsequent offspring. Plasma and erythrocyte glutathione peroxidase activities and blood Se levels increased in the Se supplemented monkeys but decreased in the deficient ones. The data indicated that hair Se levels reflect long term exposure to this element. In a very preliminary experiment, evidence was obtained to indicate that dietary protein deficiency along with Se deficiency will generate cardiomyopathic lesions characteristic of Se deficiency. It is hypothesized that, in addition to Se deficiency, another dietary deficiency (or abnormality) is necessary to produce Se deficiency lesions in higher primates. Higher glutathione transferase (or non-Se glutathione peroxidase) activity in tissues of rhesus monkeys may account for this resistance.
给怀孕的恒河猴(猕猴)喂食缺硒或补硒且维生素E充足的日粮。除了这些雌性所生的头胎幼崽出现一些心脏节律异常外,后续后代未出现因缺硒导致的生理紊乱。补硒猴子的血浆和红细胞谷胱甘肽过氧化物酶活性以及血硒水平升高,而缺硒猴子的则降低。数据表明毛发硒水平反映了长期对该元素的暴露。在一项非常初步的实验中,获得的证据表明,膳食蛋白质缺乏与缺硒共同作用会产生缺硒特有的心肌病病变。据推测,除了缺硒外,另一种膳食缺乏(或异常)对于在高等灵长类动物中产生缺硒病变是必要的。恒河猴组织中较高的谷胱甘肽转移酶(或非硒谷胱甘肽过氧化物酶)活性可能解释了这种抗性。