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It was shown in experiments on rats, that dithizone induced zinc deficiency in prostate cells. Three phase type of fluctuations of cytochemically detected zinc concentration was observed in the cells: phase of primary decrease, phase of temporary partial restoration and the phase of secondary decrease. Sodium diethyldithiocarbamate unlike to dithizone didn’t induce damage of cells and secondary decrease zinc content in its.

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It was shown, that dithizone injection to rats induced zinc deficiency in blood granulocytes and Paneth cells. Phase changes of zinc content were observed in the cells. First phase (primary decrease of cytochemically detected zinc content in the cells) was a result of intravital binding of this metal to dithizone. Second one (permanent partial increase of cell zinc content) was a result of decomposition of the product of intravital reaction. Third phase (secondary decrease of cell zinc concentration) was connected with cell necrosis. Dithizone injection to animals also induced cell secretory material deficiency.

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