Three levels of L-ascorbic acid(AsA) were orally given to 20 male Hartley guinea pigs weighing average 428 g for five weeks. AsA level was 0, 2.5, and 100 mg per 100g body weight per day in the deficient, the adequate, and the excess group, respectively. Plasma lipid peroxide value(TBA value) of deficient was increased to the highest among the three groups and both the adequate and the excess groups exhibited the lower TBA values, suggesting the antioxidant action of AsA. In the excess of AsA, plasma TBA value was greatly lowered one day after the feeding, but TBA value after 5 weeks was elevated comparable to that of the adequate. Aspirin administrating experiment suggested that this elevation was due to increased. production of prostaglandin(PG) endoperoxides induced by excess AsA. Thus it could be concluded that excess AsA actually inhibited the tissue lipid peroxidation in vivo. The activities of both superoxide dismutase(SOD) and catalase in erythrocytes demonstrated the elevations in the deficient comparing with the auequate, but not any significant variations in the excess. SOD activities were correlated with TBA value in liver (r = .324) and with percent hemolysis in erythrocytes (r = .323). Photohemolysis of erythrocyte was increased not only in the AsA deficient but also in the excess comparing with the adequate. A new finding that the large excess administration of AsA in guinea pig demonstrated a significant stimulation of PG endoperoxide biosynthesis, would suggest an important biochemical implication on vitamin C as an activator of phospholipase $A_2$ and/or PG endoperoxide synthetase. The stimulation of PG biosynthesis might be associated with the enhanced photohemolysis, and this problem needs to be further investigated.