Mode of action

Trichloroethylene is a CNS depressant and most deaths from acute trichloroethylene exposure are due to anaesthesia (Lemen, 2001). Toxic metabolites of trichloroethylene may affect dopaminergic transmission in the brain resulting in CNS dysfunction (Mutti and Franchini, 1987).

Trichloroethylene, like other halogenated hydrocarbons, is thought to sensitise the myocardium to catecholamines, thus causing cardiac arrhythmias (Brüning et al., 1998). This action has been demonstrated in experimental animals where trichloroethylene was shown to be cardiotoxic following sensitisation of the heart with epinephrine (adrenaline) (Johnson and Shanor 1968). It is likely that sensitisation of the heart is due to the action of trichloroethylene itself, since compounds which block the metabolism of trichloroethylene increase the sensitisation of the heart (Lemen, 2001).

Glutathione conjugation of trichloroethylene by glutathione-S-transferases results in the formation of S-(dichlorovinyl)glutathione (DCVG). This is cleaved by the enzymes of the mercapturic acid pathway to form S-(-1,2-dichlorovinyl)-L-cysteine (DCVC). DCVC is a substrate for renal cysteine conjugate ß-lyases leading to the formation of chlorothioketene. The formation of S-conjugates of trichloroethylene and the action of ß-lyases may be responsible for the nephrotoxic effects of trichloroethylene (Brüning et al., 1998) and have been linked with the development of renal cell cancer (Henschler et al., 1995).

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