H. H. Chen1, S.R. Sirianni1,2, C. C. Huang1
1Department of Experimental Biology, Roswell Park Memorial Institute, Buffalo, New York
2S.R. Sirianni is a medical student at the State University of New York at Buffalo, Buffalo, NY 14214.
Tóm tắt
AbstractThe mutagenicity of several organophosphorus pesticides (OPP) has been demonstrated by Wild [1975] in microorganisms. However, the results as reported in the literature of cytogenic, mutagenic, and carcinogenic tests using mammalian cells or experimental animals were scanty and inconclusive [Huang, 1973; Wild, 1975]. This may be partly due to the high toxicity and rapid degradation of these compounds by mammalian cells both in vitro and in vivo [Wild, 1975]. Since sister chromatid exchange (SCE) has proved to be a highly sensitive indicator of genetic damage [Latt, 1975] and for certain chemicals there was a good correlation between the induction of SCE and point mutations in mammalian cells [Carrano et al, 1978; Sirianni and Huang, 1980], we have studied and reported the effect of a total of 17 OPP on induction of sister chromatid exchange and cell cycle delay in an in vitro system using V79 cells without metabolic activation [Chen et al, 1981, 1982]. Among the 17 OPP tested, 8 were able to induce increased SCE frequencies and the other 9 caused no increase in SCE as compared to the control values. The OPP that proved to be positive SCE inducers were methyl‐parathion, demeton, trichlorfon, dimethoate, malathion, methidathion, oxydemeton methyl, and fenthion. The other nine that caused no SCE increase were diazinion, disyston, amaze, azinphosmethyl, bolstar, DEF, fensulfothion, monitor, and nemacur. In addition, cell cycle delay in various degrees was observed after treatment of V79 cells with all the OPP except for fensulfothion and oxydemeton methyl. However, for all experiments there was no clear correlation between the degree of cell cycle delay and induction of SCE.
