Structure/activity studies of the nephrotoxic and mutagenic action of cysteine conjugates of chlgro and fluoroalkenes
References (34)
- et al.
A pathological study of the toxicity of S- (dichlorovinyl) -L-cysteine in the rat
Food Cosmet. Toxicol.
(1965) - et al.
The metabolism and disposition of hexachloro-1:3-butadiene in the rat and its relevance to nephrotoxicity
Toxicol. Appl. Pharmacol.
(1984) - et al.
The metabolism and nephrotoxicity of tetrafluoroethylene in the rat
Toxicol. Appl. Pharmacol.
(1984) - et al.
Cleavage of S- (12-dichlorovinyl) -L-cysteine by an enzyme of bovine origin
Arch. Biochem. Biophys.
(1965) - et al.
Cysteine conjugate β-lyase in rat liver. A novel enzyme catalysing the formation of thiol containing metabolites of drugs
J. Biol. Chem.
(1978) - et al.
Conjugation and bioactivation of chlorotrifluoro-ethylene
Life Sci.
(1981) - et al.
Differentiation of the mechanisms of oncogenicity of 14-dioxane and 13-hexachlorobutadiene in the rat
Toxicol. Appl. Pharmacol.
(1981) - et al.
Fluoride ion excretion by male rats after inhalation of one of several fluoroethylenes or hexafluoropropene
Toxicol. Appl. Pharmacol.
(1974) - et al.
Effects of inhaled chloro-trifluoroethylene and hexafluoropropene on the rat kidney
Toxicol. Appl. Pharmacol.
(1981) - et al.
Protein measurement with the folin phenol reagent
J. Biol. Chem.
(1951)
Enzymatic determination of ammonia in blood plasma
Clin. Chim. Acta
Methods for detecting carcinogens and mutagens with the Salmonella/mammalian microsomes mutagenicity test
Mutat. Res.
Synthesis of enantiomers of S- (12-dichlorovinyl) -L-cysteine: their use with E. coli B
Biochim. Biophys. Acta
Interaction of S- (12-dichlorovinyl) -L-cysteine with proteins
Arch. Biochem. Biophys.
Properties of DNA treated with S- (12-dichlorovinyl) -L-cysteine and a lyase
Arch. Biochem. Biophys.
Properties of DNA isolated from tissues of calves treated with S- (12-dichlorovinyl) -L-cysteine.I. Chemical and physical proper-ties
Arch. Biochem. Biophys.
Properties of DNA isolated from tissues of calves treated with S- (12-dichlorovinyl) -L-cysteine.II. Primertemplate activity for bacterial DNA polymerases
Arch. Biochem. Biophys.
Cited by (149)
AGXT2: A promiscuous aminotransferase
2014, Trends in Pharmacological SciencesCitation Excerpt :They have nephrotoxic effects in rodents and are associated with kidney and liver tumors in experimental animals and humans [63]. One mechanism of the toxicity of halogenated alkenes is the formation of corresponding S-conjugates, which are subsequently metabolized by cysteine S-conjugate β-lyases into pyruvate, ammonium, and reactive sulfur-containing fragments (Figure 2) [64]. Some of the resulting sulfur containing fragments are reactive molecular species that can thioacylate macromolecules, especially at ɛ-amino groups of protein lysine residues [65].
Trichloroethylene and trichloroethanol-induced formic aciduria and renal injury in male F-344 rats following 12 weeks exposure
2014, ToxicologyCitation Excerpt :This causes marked toxicity to the proximal renal tubules in rats and mice administered DCVC (Gandolfi et al., 1981; Darnerud et al., 1988; Vaidya et al., 2003; Green et al., 1997). DCVC is also weakly mutagenic in bacteria, induces mitochondrial toxicity and perturbation of intracellular calcium homeostasis (Green and Odum, 1985; Groves et al., 1990; Stonard and Parker, 1971). DCVC can also undergo metabolism by cytochrome P450 to form a sulphoxide, which is also nephrotoxic and mutagenic to bacteria (Lash et al., 1994; Irving et al., 2013; Irving and Elfarra, 2013).
Mutagenicity of the glutathione and cysteine S-conjugates of the haloalkenes 1,1,2-trichloro-3,3,3-trifluoro-1-propene and trichlorofluoroethene in the Ames test in comparison with the tetrachloroethene-analogues
2003, Mutation Research - Genetic Toxicology and Environmental MutagenesisAssessing the health risks following environmental exposure to hexachlorobutadiene
2003, Toxicology LettersHuman mitochondrial and cytosolic branched-chain aminotransferases are cysteine S-conjugate β-lyases, but turnover leads to inactivation
2003, Biochemical PharmacologyCitation Excerpt :Toxicity is due in part to the high reactivity of the sulfur-containing fragment eliminated by the action of cysteine S-conjugate β-lyases. Evidence suggests that the fragments eliminated from DCVC and TFEC (and CTFC) breakdown to a thioketene [47] and a dihalothionoacetyl fluoride [43,48], respectively, both of which act as thioacylating agents particularly of lysine residues in proteins [49–52]. Proteins in the kidney mitochondria are especially vulnerable to thioacylation after rats are administered TFEC.