Abstract
The mechanism of arsenate inhibition of the glucose active transport system in wild-type cells of Neurospora crassa has been examined. Arsenate treatment results in approximately 65% inhibition of the glucose active transport system with only a small depression of cellular ATP levels. The transport system is not inhibited in cells treated with sodium arsenate in the presence of sodium azide. The transport inhibition is suppressed when orthophosphate is present during arsenate treatment, but is not reversed by orthophosphate when added after the arsenate treatment. The transport inhibition is completely reversed by treatment of the cells with mercaptoethanol. Gel chromatography of sonicates of intact cells which had been treated with [ 74As]arsenate reveals three radioactive peaks, one with the elution volume of arsenate, one with the elution volume of arsenite, and a high molecular-weight radioactive fraction. Treatment of the high molecular-weight radioactive fraction with mercaptoethanol results in the production of radioactive arsenite. In view of these findings, it is proposed that arsenate inhibition of the glucose active transport system in Neurospora involves transport of arsenate into the cells, probably via the orthophosphate transport system, reduction of the transported arsenate to arsenite, and interaction of arsenite with some component of the glucose active transport system, presumably via covalent binding with vicinal thiol groups.
Published Version
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