[Effect of triphenyltin chloride on superoxide (O2-.) production in human neutrophils].
Brief treatment (3 min at 37 degrees C) of human neutrophils with triphenyltin chloride (TPTC1) resulted in a dose-dependent inhibition of superoxide (O2-.) production stimulated by concanavalin A+ cytochalasin D. It was considered from the following findings that the inhibition may be caused by some functional disorders of neutrophils: 1) O2-. generated by xanthine oxidase-acetaldehyde system was not inhibited by TPTC1. 2) There was no change in cell viability after treatment with TPTC1. When the other phenyltin compounds were examined, the relative potencies of inhibitory effect were shown to be in the order of TPTC1 greater than diphenyltin dichloride greater than phenyltin trichloride greater than tetraphenyltin on a molar basis. Lysosomal enzyme release caused by neutrophils stimulated by N-formyl-methionyl-leucyl-phenylalanine (FMLP) was also inhibited by TPTC1. These results suggest that TPTC1 inhibits the common pathway(s) of the two stimulus responses.
D005966:Glucuronidase / Q000037:antagonists & inhibitors; D006801:Humans; D009504:Neutrophils / Q000187:drug effects* / Q000201:enzymology; D009947:Organotin Compounds / Q000494:pharmacology*; D013481:Superoxides / Q000097:blood*
D009947:Organotin Compounds; D013481:Superoxides; D005966:Glucuronidase; C012594:triphenyltin chloride