Malecki E A, Huttner D L, Greger J L
Department of Nutritional Sciences, University of Wisconsin, Madison 53706.
Biol Trace Elem Res. 1994 Jul;42(1):17-29. doi: 10.1007/BF02990485.
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.
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。