Abstract
Schwarz and Cisloghi1 in 1935 reported that the development of anaphylactic shock in actively sensitized guinea pigs could not be prevented by the simultaneous administration of vitamin C with the shocking antigen. Hochwald2 on the contrary, was able to inhibit the anaphylactic syndrome in a high percentage of guinea pigs similarly treated. He reported also that the administration of ascorbic acid prior to the injection of the shocking dose of antigen completely failed to protect sensitized animals. Lemke3 extended this work further and claimed that a single parenteral injection of vitamin C 30 minutes before either the sensitizing or shocking dose of foreign protein suppressed the development of hypersensitivity and shock. The daily administration of ascorbic acid to actively sensitized guinea pigs protected the animals against shocking doses of antigen several times larger than those uniformly fatal to the controls. Solomonica4 has recently reported that the daily parenteral administration of sodium ascorbate (Cebione, Merck) in 1, 5 or 10 mg. doses for three weeks prior to the sensitizing injection and during also the 3 following weeks, completely protects guinea pigs from a certainly fatal shocking dose of antigen. A high incidence of protection was also afforded animals given Cebione during only the 3 week presensitization period. Irregular results followed the daily injection of sodium ascorbate during the sensitization period; the same was true when the vitamin was given as a single injection either shortly before or mixed with the shocking dose. Von Niekirk5 found that absolutely no protection was conferred upon actively sensitized guinea pigs regardless of whether the sodium ascorbate was administered daily prior to and during the sensitizing period, or shortly before, or mixed with the shocking dose of antigen. Hochwald and Schwarz6 reported that contrary to Hochwald' s2 previous finding, the administration of ascorbic acid failed to protect actively sensitized guinea pigs. These workers also studied the effect of vitamin C on specific precipitin formation in the same animals, and failed to find any significant differences between the titers in control and vitamin treated groups of guinea pigs. This is somewhat un-
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