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喂食不同水平锰和脂肪的大鼠的锰状态、肠道内源性锰损失及抗氧化酶活性

Manganese status, gut endogenous losses of manganese, and antioxidant enzyme activity in rats fed varying levels of manganese and fat.

作者信息

Malecki E A, Huttner D L, Greger J L

机构信息

Department of Nutritional Sciences, University of Wisconsin, Madison 53706.

出版信息

Biol Trace Elem Res. 1994 Jul;42(1):17-29. doi: 10.1007/BF02990485.

Abstract

We hypothesized that manganese deficient animals fed high vs moderate levels of polyunsaturated fat would either manifest evidence of increased oxidative stress or would experience compensatory changes in antioxidant enzymes and/or shifts in manganese utilization that result in decreased endogenous gut manganese losses. Rats (females in Study 1, males in Study 2, n = 8/treatment) were fed diets that contained 5 or 20% corn oil by weight and either 0.01 or 1.5 mumol manganese/g diet. In study 2, 54Mn complexed to albumin was injected into the portal vein to assess gut endogenous losses of manganese. The manganese deficient rats: 1. Had 30-50% lower liver, tibia, kidney, spleen, and pancreas manganese concentrations than manganese adequate rats; 2. Conserved manganese through approximately 70-fold reductions in endogenous fecal losses of manganese; 3. Had lower heart manganese superoxide dismutase (MnSOD) activity; and 4. Experienced only two minor compensatory changes in the activity of copper-zinc superoxide dismutase (CuZnSOD) and catalase. Gut endogenous losses of manganese tended to account for a smaller proportion of absorbed manganese in rats fed high-fat diets; otherwise fat intake had few effects on tissue manganese concentrations.

摘要

我们假设,给缺锰动物饲喂高水平与中等水平的多不饱和脂肪,要么会出现氧化应激增加的迹象,要么会经历抗氧化酶的代偿性变化和/或锰利用的改变,从而导致肠道内源性锰损失减少。大鼠(研究1中为雌性,研究2中为雄性,每组n = 8)被饲喂含5%或20%(重量)玉米油且锰含量分别为0.01或1.5 μmol/g的日粮。在研究2中,将与白蛋白结合的54Mn注入门静脉,以评估肠道内源性锰损失。缺锰大鼠:1. 肝脏、胫骨、肾脏、脾脏和胰腺中的锰浓度比锰充足的大鼠低30 - 50%;2. 通过将内源性粪便锰损失减少约70倍来保存锰;3. 心脏锰超氧化物歧化酶(MnSOD)活性较低;4. 铜锌超氧化物歧化酶(CuZnSOD)和过氧化氢酶的活性仅发生了两个较小的代偿性变化。在高脂日粮喂养的大鼠中,肠道内源性锰损失占吸收锰的比例往往较小;否则,脂肪摄入对组织锰浓度影响不大。

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