627-72-5 Usage
Uses
Different sources of media describe the Uses of 627-72-5 differently. You can refer to the following data:
1. A mutagenic and nephrotoxic metabolite of trichloroethylene.
2. 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.
3. Hydrochloride salt of 3-[(1,2-Dichlorovinyl)thio]-L-alanine, a mutagenic and nephrotoxic metabolite of trichloroethylene.
Definition
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.
Environmental Fate
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.
Toxicity evaluation
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.
Check Digit Verification of cas no
The CAS Registry Mumber 627-72-5 includes 6 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 3 digits, 6,2 and 7 respectively; the second part has 2 digits, 7 and 2 respectively.
Calculate Digit Verification of CAS Registry Number 627-72:
(5*6)+(4*2)+(3*7)+(2*7)+(1*2)=75
75 % 10 = 5
So 627-72-5 is a valid CAS Registry Number.
InChI:InChI=1/C5H7Cl2NO2S/c6-1-4(7)11-2-3(8)5(9)10/h1,3H,2,8H2,(H,9,10)/b4-1+/t3-/m0/s1
627-72-5Relevant articles and documents
Renal and hepatic toxicity of trichloroethylene and its glutathione-derived metabolites in rats and mice: Sex-, species-, and tissue-dependent differences
Lash,Qian,Putt,Hueni,Elfarra,Krause,Parker
, p. 155 - 164 (2007/10/03)
Acute cytotoxicity (lactate dehydrogenase release) of trichloroethylene (TRI), S-(1,2-dichlorovinyl)glutathione (DCVG), and S-(1,2-dichlorovinyl)-L-cysteine (DCVC) in freshly isolated renal cortical cells and hepatocytes from male and female rats was evaluated to test the hypothesis that the assay provides a valid indicator of sex- and tissue-dependent differences in sensitivity to TRI and its metabolites. We then determined mitochondrial toxicity (inhibition of state-3 and/or stimulation of state-4 respiration) in renal cortical and hepatic mitochondria from male and female rats and mice to assess sex-, tissue-, and species-dependent susceptibility. TRI was moderately cytotoxic in renal cells from male rats but was nontoxic in renal cells from female rats or hepatocytes from male or female rats. Acute cytotoxicity of both DCVG and DCVC was greater in renal cells from male rats than in renal cells from female rats. Although DCVC does not target the liver in vivo, it was a very potent hepatotoxicant in vitro. Mitochondrial toxicity in kidney and liver showed similar patterns, with mitochondria from male rats being more sensitive than mitochondria from female rats; order of potency was DCVC > DCVG ? TRI. State-3 respiration in mitochondria from mice was also inhibited, but the patterns and relative sensitivities differed from those in mitochondria from rats. Renal and hepatic mitochondria from mice were less sensitive than corresponding mitochondria from rats and renal mitochondria from female mice were significantly more sensitive than renal mitochondria from male mice. Thus, many of the species-, sex-, and tissue-dependent differences in toxicity observed in vivo are also observed in vitro.
