Ghosh M K, Chattopadhyay D J, Chatterjee I B
Dr. B.C. Guha Centre for Genetic Engineering & Biotechnology, University College of Science, Calcutta, India.
Free Radic Res. 1996 Aug;25(2):173-9. doi: 10.3109/10715769609149922.
Ascorbate-deficiency leads to extensive oxidative damage of proteins and protein loss in the guinea pig tissue microsomes as evidenced by sodium dodecyl sulfate polyacrylamide gel electrophoresis, accumulation of carbonyl, bityrosine as well as by tryptophan loss. Oxidative damage is reversed by ascorbate therapy. Oxidative damage in ascorbate deficiency also leads to lipid peroxidation in guinea pig tissue microsomes as evidenced by accumulation of conjugated dienes, malondialdehyde and fluorescent pigment. Lipid peroxides, disappear after ascorbate therapy but not by vitamin E. The observations substantiate the previous in vitro findings that ascorbate specifically prevents oxidative degradation of microsomal membranes. The results indicate that vitamin C may exert a powerful protection against degenerative diseases associated with oxidative damage and play a critical role in wellness and health maintenance.
抗坏血酸缺乏会导致豚鼠组织微粒体中蛋白质的广泛氧化损伤和蛋白质损失，这通过十二烷基硫酸钠聚丙烯酰胺凝胶电泳、羰基积累、双酪氨酸以及色氨酸损失得以证明。抗坏血酸治疗可逆转氧化损伤。抗坏血酸缺乏引起的氧化损伤还会导致豚鼠组织微粒体中的脂质过氧化，这通过共轭二烯、丙二醛和荧光色素的积累得以证明。脂质过氧化物在抗坏血酸治疗后消失，但维生素E治疗无效。这些观察结果证实了之前的体外研究结果，即抗坏血酸能特异性地防止微粒体膜的氧化降解。结果表明，维生素C可能对与氧化损伤相关的退行性疾病发挥强大的保护作用，并在维持健康方面发挥关键作用。
