THE EFFECT OF COMPOUNDS RELATED TO HYDRAZINE IN PRODUCING ANHYDREMIA AND EXPERIMENTAL ANEMIA

¹ From the Biochemical Laboratory, Department of Physiology and Biochemistry, Cornell University, Ithaca

A preliminary study has been made of the effect of a number of the derivatives of hydrazine in producing experimental anemia.

In hydrazine poisoning, a slight reduction in the red cell count may occur after the disappearance of the anhydremia which is characteristic of the intoxication. Phenylhydrazine, acetylphenylyhydrazine, and p-bromphenylhydrazine produce rapid destruction of red corpuscles. Methylphenylhydrazine and diphenylhydrazine are likewise effective in this regard. In symmetrical diisopropylhydrazine poisoning, the onset of the anemia may be delayed for several days following the administration of the drug. A moderate amount of red cell disintegration occurs in hydrazobenzene and 2-2' azobispropane intoxications.

Mild anemias were produced in rabbits with azobenzene, azoxybenzene, diazoaminobenzene, and aminoazobenzene. Diphenylcarbazide and p-hydrazinobenzoic acid exert little or no destructive action on the blood.

Of the compounds studied, those which are especially destructive of liver tissue appear to be most effective in producing a concentration of the blood (anhydremia) This is true of hydrazine, symmetrical diisopropylhydrazine, and 2-2' azobispropane. That concentration of the blood occurs to some extent in p-bromphenylhydrazine poisoning is indicated by the fact that large amounts of cell debris may be present in the blood at a time when the red count had not decreased appreciably from the normal. Very likely, an increase above the normal red cell count is not observed owing to the rapidity with which the corpuscles are destroyed by the p-bromphenylhydrazine.