Halocarbons, cellular toxicity

Basak, S. C., Balasubramanian, K., Gute, B. D., Mills, D., Gorczynska, A., Roszak, S. Prediction of cellular toxicity of halocarbons from computed chemodescriptors A hierarchical QSAR approach. J. Chem. Inf. Comput. Sci. 2003, 43, 1103-1109. 

A study is being conducted by R.G. Schnellmann (University of Georgia) for the National Institute of Environmental Health Sciences to evaluate the mechanism of nephrotoxicity of halocarbons, including hexachlorobutadiene. The mechanism of how metabolites alter proximal tubular cellular physiology to produce toxicity is being investigated, with particular emphasis on the effects of metabolites on mitochondria (CRISP 1993). 

The hepatotoxicity of 1,1,1-trichloroethane is quite low compared to other chlorinated hydrocarbons, including 1,1,2-trichloroethane. The relatively low toxicity of 1,1,1-trichloroethane may be due to its relatively low metabolism rate, since the more hepatotoxic halocarbons are extensively metabolized. Whether the mild effects of repeated 1,1,1 -trichloroethane exposure are evoked by the parent compound or the limited quantities of metabolites produced is not known, however. The available data indicate that the acute effects on the central nervous and the cardiovascular systems are caused by 1,1,1-trichloroethane and not its metabolites. The interference of 1,1,1-trichloroethane with membrane-mediated processes, due to lipophilicity, may be responsible for the acute effects on these systems several cellular and biochemical processes appear to be affected by... 

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