Ascorbate protects guinea pig tissues against lipid peroxidation

In recent years we and others have shown that ascorbic acid (AH2) is a potential scavenger of superoxide (O2.-) and peroxyl (LOO.) radicals, the species involved in lipid peroxidation (LPO) in animal tissues. In this paper we have demonstrated that AH2 protects guinea pig tissues from LPO both in vivo and in vitro. The extent of LPO has been determined by estimating malonaldehyde using the thiobarbituric acid test and HPLC and also by measuring the accumulation of fluorescent pigment and occurrence of protein changes in the microsomal membranes. In AH2-deficiency, LPO occurs progressively in guinea pig tissues, despite the presence of adequate levels of antioxidants like alpha-tocopherol, GSH, protein thiols, and scavenging enzymes, namely, superoxide dismutase, catalase, and glutathione peroxidase. In a model in vitro system, microsomal LPO initiated by O2.- is completely prevented by AH2 but not by alpha-tocopherol, GSH, uric acid, and catalase. AH2 is also the most effective antioxidant in preventing microsomal LPO mediated by tert-butylhydroperoxide or the chain propagating species LOO., generated from 2,2'-azobis (2-amidinopropane) hydrochloride. The results obtained with guinea pigs may be applicable to humans, because humans are also dependent on dietary AH2. Our data suggest that an adequate vitamin C nutrition may prevent common cellular degenerative diseases associated with LPO.