In recent years we and others have shown that ascorbic acid (AH(2)) is
a potential scavenger of superoxide ( O-2(.-)) and peroxyl (LOO(.)) r
adicals, the species involved in lipid peroxidation (LPO)in animal tis
sues. In this paper we have demonstrated that AH(2) protects guinea pi
g tissues from LPO both in vive and in vitro. The extent of LPO has be
en determined by estimating malonaldehyde using the thiobarbituric aci
d test and HPLC and also by measuring the accumulation of fluorescent
pigment and occurrence of protein changes in the microsomal membranes.
In AH(2)-deficiency, LPO occurs progressively in guinea pig tissues,
despite the presence of adequate levels of antioxidants like alpha-toc
opherol, GSH, protein thiols, and scavenging enzymes, namely, superoxi
de dismutase, catalase, and glutathione peroxidase. In a model in vitr
o system, microsomal LPO initiated by O-2(.-) is completely prevented
by AH(2) but not by alpha-tocopherol, GSH, uric acid, and catalase. AH
(2) is also the most effective antioxidant in preventing microsomal LP
O 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, be
cause humans are also dependent on dietary AH(2). Our data suggest tha
t an adequate vitamin C nutrition may prevent common cellular degenera
tive diseases associated with LPO.