Effects of ziram on tumor cell binding capacity, cell‐surface marker expression, and ATP levels of human natural killer cells

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Human natural killer (NK) cells lyse tumor cells, virally infected cells, and antibody coated cells. Increased tumor formation and viral infection may occur if NK lytic function is disrupted. Ziram is used in the production of latex rubber and as an antifungal agent in agriculture. Previous studies have shown that ziram exposure decreased ability of NK cells to lyse tumor cells. To examine the mechanism by which ziram exposure decreases NK lytic function, we have assessed the effects of ziram exposure on the tumor‐cell‐binding function, cell‐surface marker expression, and ATP levels of NK cells. Exposure of NK cells to 1 μM ziram for 24 h decreased NK‐binding to tumor cells by 36%. Levels of expression of CD2, CD11a, CD16, CD18, and CD56 were examined and there were no significant decreases in any of these markers after a 24 h exposure to 1 μM ziram. However, a 24 h exposure to 1 μM ziram caused a 46 % decrease in ATP. These studies indicate that a decrease in the ability of NK cells to bind to tumor cells is, in part, responsible for the loss of NK lytic function and that this binding does not appear to be dependent upon any of the cell surface markers that were examined. Further, the depletion of ATP levels in NK cells after ziram exposure may account, in part, for the decrease in the ability of NK cells to bind target cells. Supported by grant S06 GM008092‐32.