 the fundamental reactivity or stability of the chloroethylene molecules affects their hepatotoxic potential . 
 extent and symmetry of the chlorine substitution , which alters electron delocalization , charge polarization , and solubility , affect biologic response . 
 the most nonsymmetrically depolarized chloroethylene , 1,1-dichloroethylene ( 1,1-dce ) is the most hepatotoxic and causes a unique pattern of hepatocellular injury involving mitochondria , plasma membranes , and chromatin . 
 the injury caused by the other chloroethylenes examined appears to profoundly affect the structural integrity of the endoplasmic reticulum with toxic potential in the order : trichloroethylene ( tri ) greater than vinyl chloride ( vcm ) greater than perchloroethylene ( per ) . 
 pretreatments which increased cytochrome p-450 contents , thus presumably augmenting metabolic activation to a reactive intermediate such as an epoxide , enhanced or were synergistic to the hepatotoxic potential of tri , vcm and per but were protective or antagonistic to 1,1-dce hepatotoxicity . 
 biologic response to 1,1-dce may be expressed by a different metabolic pathway . 
 glutathione appears to be involved in the biologic response to all nonsymmetric chloroethylenes and toact as an antagonist against injury . 
 marked differences in the patterns of injury and the biologic responses suggest that more than one mechanism is involved in the production of injury by chloroethylenes.imagesfigure 3.figure 4 . 
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