Relationship between Plasma Ascorbate and Blood Histamine

Relationship between Plasma Ascorbate and Blood Histamine 

If histamine degradation is a physiological function of vitamin C, it is necessary to delineate the tissue level of ascorbic acid required for this effect. In the rat, which is capable of synthesizing ascorbic acid, serum ascorbic acid rose from 1.10 mg/100 ml to 1.63 mg/100 ml within 30 min of immobilization stress, nearly a 50% increase (Nakano and Suzuki, 1984). Liver ascorbate in these animals fell significantly after 15 min of stress, then rose dramatically to over 60% of the initial value within the next 15 min, indicating elevated hepatic biosynthesis of the vitamin. Adrenal ascorbic acid stores fell to 50% of the initial value following immobilization stress, and these levels remained depressed at 4 hr post-stress. Blood histamine levels rose 80%, from 38 to 68 ng/ml, peaking at about 30 min post-stress (Nakano and Suzuki, 1984). Hence, in the rat, stress induced a rapid rise in serum ascorbate which was fueled by ascorbic acid mobilized from tissue stores and by hepatic synthesis of ascorbate. 

Clemetson (1980) conducted the first study examining the relationship between 

Dickinson et al. (1994) recently analyzed vitamin C status in nearly 13,500 people from the second National Health and Nutrition Examination Survey NHANES II database. Twenty-seven percent of these people were classified as supplement users. The mean serum vitamin C for nonsupplement users ages 20-59 years, 0.85 mg/100 ml, was about 40% below that noted for supplement users (1.36 

Mean Blood Histamine SEM (ng/ml) in 52 Healthy Men and Women with High or Low Vitamin C Status as Determined Using Different Plasma Ascorbate Cutoff Points 

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