Dexter D T, Nanayakkara I, Goss-Sampson M A, Muller D P, Harding A E, Marsden C D, Jenner P
Neurodegenerative Disease Research Centre, Biomedical Sciences Division, King's College, London, UK.
Neuroreport. 1994 Sep 8;5(14):1773-6. doi: 10.1097/00001756-199409080-00022.
alpha-Tocopherol concentrations in brain were reduced to 3% of control levels in rats fed a vitamin E deficient diet for 52 weeks. Vitamin E deficiency resulted in a 19-33% loss of tyrosine hydroxylase (TH) immunopositive neurones in the substantia nigra, but not in the adjacent ventral tegmental area, compared with controls. Vitamin E deficiency, however, did not reduce striatal dopamine concentrations or turnover. When antioxidant defence mechanisms are defective, as in chronic vitamin E deficiency, the nigrostriatal pathway may be affected by oxidative damage and this may have implications for Parkinson's disease.
给大鼠喂食维生素E缺乏饮食52周后,其大脑中的α-生育酚浓度降至对照水平的3%。与对照组相比,维生素E缺乏导致黑质中酪氨酸羟化酶(TH)免疫阳性神经元减少19%-33%,但相邻的腹侧被盖区未受影响。然而,维生素E缺乏并未降低纹状体多巴胺浓度或周转率。当抗氧化防御机制存在缺陷时,如在慢性维生素E缺乏的情况下,黑质纹状体通路可能会受到氧化损伤的影响,这可能与帕金森病有关。