627-72-5

A mutagenic and nephrotoxic metabolite of trichloroethylene.

Hydrochloride salt of 3-[(1,2-Dichlorovinyl)thio]-L-alanine, a mutagenic and nephrotoxic metabolite of trichloroethylene.

S-(1,2-Dichlorovinyl)-L-cysteine (DCVC) is a model nephrotoxicant and cataractogen used to induce acute renal failure and cataracts in experimental animals to study the biochemical, physiological, and molecular mechanisms underlying the disease.

ChEBI: An L-alpha-amino acid that is L-cysteine in which the hydrogen attached to the sulfur is replaced by a 1,2-dichlorovinyl group.

Human exposure to DCVC occurs only via potential formation of DCVC in vivo following trichloroethylene (TCE) exposure; therefore, no data are available in this regard.

Cell death is initiated by the metabolism of DCVC via renal cysteine conjugate b-lyase to a sulfur-containing reactive thiol radical that covalently binds to macromolecules. The findings that the nephrotoxicity and cataractogenesis of DCVC can be blocked by aminooxyacetic acid (a selective inhibitor of b-lyase) and probenecid (organic anion transport Encyclopedia of inhibitor) provide evidence for the roles of cysteine conjugate b-lyase and the organic anion transport system, respectively, in DCVC-induced nephrotoxicity. Although the b-lyase enzyme is considered to be the major bioactivating enzyme for DCVC, other bioactivating enzyme activities have been described, and some of these may have relevance to risk assessment. Studies have shown that renal FMO3 can also metabolize DCVC to form DCVC sulfoxide thereby causing nephrotoxicity. Reports from several laboratories indicate that the cytotoxicity of DCVC is mediated at the mitochondrial level. Depletion of GSH, mitochondrial lipid peroxidation and GSSG formation, inhibition of mitochondrial lipoyl dehydrogenase activity, release of Ca²⁺ from mitochondria, and inhibition of mitochondrial membrane potential have been observed prior to renal cell death and correlated well with cytotoxicity.