Caffeic acid and ferulic acid, which are naturally occurring phenols present in a wide variety of plants, were examined for their ability to react with nitrite in vitro and to inhibit nitrosamine formation in vivo. Their activities were compared with other phenols (butylated hydroxyanisole and Trolox) and with a non-phenolic polyhydroxylated compound, glycerol guaiacolate. In simulated gastric fluid, caffeic acid and ferulic acid reacted rapidly and completely with an equimolar quantity of sodium nitrite. In rats receiving aminopyrine and nitrite, caffeic acid and ferulic acid blocked the elevation of serum N-nitrosodimethylamine (NDMA) levels and the serum glutamic pyruvic transaminase levels associated with hepatotoxicity. Neither phenol had any effect on serum levels of NDMA in rats treated with NDMA. In both the in vitro (reaction with nitrite) and in vivo (inhibition of hepatotoxicity) systems, caffeic acid was more effective than ferulic acid. Butylated hydroxyanisole and Trolox were partially effective, and glycerol guaiacolate was inactive. The results of this study suggest that dietary caffeic acid and ferulic acid may play a role in the body's defense against carcinogenesis by inhibiting the formation of N-nitroso compounds.
Oral administration of 10 mg per kilogram of body weight of ascorbic acid (AA) completely prevented development of scurvy in juvenile rhesus monkey (Mucaca mulata) fed an AA-free liquid diet. The same dose cured scurvy when injected intramuscularly. An equimolar dose of ascorbic acid 2-sulfate (AA-2-S) did not prevent or cure scurvy. Neither AA nor AA-2-S altered serum cholesterol. AA but not AA-2-S reduced serum triglyceride. A case of scurvy in an AA-2-S treated monkey is described in detail.
Rhesus monkeys fed an ascorbic acid-free, purified liquid diet, developed scurvy in 70 to 105 days as evidenced by loss of weight, anemia, bleeding gums, inflamed palate, diarrhea, and inability to stand. Oral administration of either 10 mg/kg body weight of ascorbic acid or an equimolar amount of the magnesium salt of 1-ascorbic acid phosphate cured all symptoms of scurvy. Similarly, oral administration of 1-ascorbic acid phosphate cured all symptoms of scurvy in the guinea pig and resulted in liver ascorbate levels equal to those of animals feed ascorbic acid. It is concluded that ascorbic acid phosphate is a readily available source of ascorbic acid activity in vivo.
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