Charles W. Mushett

Antidotal efficacy of vitamin B12a (hydroxo-cobalamin) in experimental cyanide poisoning.

Summary and Conclusion 1. Vit. B12a (hydroxo-cobalamin), but not vitamin B12a (cyano-cobalamin), has been found to be capable of preventing in mice the toxic symptoms and death due to cyanide administration. 2. When injected into mice exhibiting complete respiratory arrest and coma due to cyanide poisoning, vit. B12a effected rapid recovery of most animals. 3. In mice injected with potassium cyanide followed by vit. B12a some of the cyanide appears in the urine as thiocyanate, but a greater percentage of the cyanide appears as vit. B12 having formed this compound by reacting with the vit. B12a.

Studies on the chronic toxicity of pyranisamine maleate (neo-antergan maleate) in animals.

Abstract 1.1. Neo-Antergan maleate (brand of pyranisamine maleate) has been administered to rats, dogs, and monkeys for varying lengths of time up to six months. The following doses appeared to be entirely safe: (a) In rats, 10 mg. per kilogram five times weekly for six months and up to 200 mg. per kilogram daily for thirty-two days; (b) in dogs, 20 mg. per kilogram five times weekly for six months; (c) in monkeys, 50 mg. per kilogram daily for thirty-five days. No toxic signs, nor any hematologic, biochemical, or pathologic abnormalities were found in the animals on these doses. 2.2. One monkey tolerated 100 mg. per kilogram daily for thirty-five days, but this proved to be a toxic level for another monkey which succumbed after five such doses. In rats, daily doses of 500 mg. per kilogram for sixty-one days and 1,000 mg. per kilogram for forty-two days proved to be toxic for some animals because many died on these dose levels. Those which survived, however, grew at a nearly normal rate. 3.3. There is no evidence that Neo-Antergan has a cumulative effect at small or moderate doses, since the drug may be administered over a long period of time with no apparent ill effects.

Influence of Protein and Thiamine Intake on Pathologic and Weight Changes produced by Atabrine.

Summary The hepatic damage resulting from continued atabrine administration was more severe in rats maintained on a low protein diet than in those on a high protein diet. On the other hand, the incidence and degree of myocardial damage were slightly greater in the rats fed the high protein diet. Thiamine deficiency had no effect upon the hepatic and myocardial damage produced by atabrine. The daily administration of atabrine to rats maintained on high and low protein rations resulted in a retardation of growth beyond that observed in their isocaloric controls which did not receive atabrine.