Kang S A, Jang Y J, Park H
Department of Physiology, University of Ulsan College of Medicine, Seoul, South Korea.
Free Radic Res. 1998 Jan;28(1):93-107. doi: 10.3109/10715769809097880.
Vitamin C, a potent antioxidant, can act as a pro-oxidant in the presence of free transition metal ions by accelerating the Fenton reaction. An in vivo pro-oxidant role of vitamin C has been suggested, but direct evidence for it is scant. Here, we report the dual role of vitamin C on paraquat-induced lung injury, which appears to depend on the metal ions released from damaged cells. Vitamin C (10 mg/kg) given at the time when the extensive tissue damage was in progress aggravated the oxidative damage, while it protected against the damage when given before the initiation of the damage. The extent of oxidative tissue damage was monitored by measuring the expiratory ethane, one of the hydrocarbons produced during lipid peroxidation. Deferoxamine, given intraperitoneally as a bolus dose of 50 mg/kg, completely blocked the aggravation of oxidative damage by vitamin C. Moreover, deferoxamine unmasked the antioxidant effect of vitamin C. The results show that vitamin C can either aggravate or alleviate the oxidative tissue damage depending on the presence of metal ions released from damaged cells.
维生素C是一种强效抗氧化剂，在游离过渡金属离子存在的情况下，通过加速芬顿反应可充当促氧化剂。有人提出维生素C在体内具有促氧化剂作用，但直接证据很少。在此，我们报告了维生素C对百草枯诱导的肺损伤的双重作用，这似乎取决于受损细胞释放的金属离子。在广泛组织损伤正在进行时给予维生素C（10毫克/千克）会加重氧化损伤，而在损伤开始前给予则可防止损伤。通过测量呼气乙烷（脂质过氧化过程中产生的碳氢化合物之一）来监测氧化组织损伤的程度。以50毫克/千克的大剂量腹腔注射去铁胺，可完全阻断维生素C对氧化损伤的加重作用。此外，去铁胺还揭示了维生素C的抗氧化作用。结果表明，维生素C根据受损细胞释放的金属离子的存在情况，既可以加重也可以减轻氧化组织损伤。
