Golub M S, Han B, Keen C L, Gershwin M E
Department of Internal Medicine, University of California, Davis 95616.
Toxicol Appl Pharmacol. 1992 Jan;112(1):154-60. doi: 10.1016/0041-008x(92)90291-y.
Studies in mice have suggested that both dietary Al excess and dietary Mn deficiency promote oxidative tissue damage. To determine if these factors can interact to produce functional nervous system damage, female mice (N = 10-12 per group) were fed diets with control or low Mn (35 or 3 micrograms Mn/g diet) and/or control or high Al (25 or 1000 micrograms Al/g diet, Al as Al lactate) content for a 90-day period. No overt signs of neurotoxicity were observed in any group. Excess Al produced a threefold Al accumulation in both liver and brain, a slight acceleration of growth, decreased motor activity, decreased grip strength, and decreased startle responsiveness. Manganese deprivation led to liver, brain, and femur Mn depletion and reduced liver MnSOD activity but no neurobehavioral changes. No interactive effects between Al excess and Mn deficiency were observed. Neither Al excess nor Mn deficiency altered brain or liver lipid peroxidation measures. This study suggests that (1) subchronic dietary Al at doses of 1000 micrograms Al/g diet produces elevated brain Al and altered neurobehavioral indices in adult mice; (2) brain lipid peroxidation is not altered by this treatment; (3) dietary Mn deficiency does not influence Al neurotoxicity in adult mice.
对小鼠的研究表明，饮食中铝过量和锰缺乏均会促进组织氧化损伤。为了确定这些因素是否会相互作用导致功能性神经系统损伤，将雌性小鼠（每组10 - 12只）喂食含对照或低锰（35或3微克锰/克饮食）和/或对照或高铝（25或1000微克铝/克饮食，铝以乳酸铝形式存在）的饮食，持续90天。在任何组中均未观察到明显的神经毒性迹象。铝过量导致肝脏和大脑中铝的积累增加了三倍，生长略有加速，运动活动减少，握力下降，惊吓反应性降低。锰缺乏导致肝脏、大脑和股骨中的锰耗竭，并降低肝脏锰超氧化物歧化酶活性，但未出现神经行为变化。未观察到铝过量和锰缺乏之间的交互作用。铝过量和锰缺乏均未改变大脑或肝脏脂质过氧化指标。本研究表明：（1）以1000微克铝/克饮食的剂量摄入亚慢性饮食铝会使成年小鼠大脑铝含量升高并改变神经行为指标；（2）这种处理不会改变大脑脂质过氧化；（3）饮食锰缺乏不会影响成年小鼠的铝神经毒性。
