Detail of "554-01-8"

Reference

Reaction kinetics and cytosine adducts of chloroethylene oxide and chloroacetaldehyde: direct observation of intermediates by FTNMR and GC-MS

Reaction kinetics and cytosine adducts of chloroethylene oxide and chloroacetaldehyde: direct observation of intermediates by FTNMR and GC-MS.Some chemicals with cas registry numbers like 2140-64-9 and 107807-30-7 are also used. O'Neill, I.; Barbin, A.; Friesen, M.; Bartsch, H. (Unit Environ. Carcinog. Host Factors, Int. Agency Res. Cancer, Lyon, Fr.). IARC Sci. Publ., 70(Role Cyclic Nucleic Acid Adducts Carcinog. Mutagen.), 57-73 (English) 1986. CODEN: IARCCD. ISSN: 0300-5038. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) Section cross-reference(s): 6 As it is not yet known which are the important miscoding adducts formed in the reaction of the relatively unstable compd. chloroethylene oxide (CEO)(I) [7763-77-1] with double-stranded DNA, proton Fourier transform NMR (FTNMR) spectroscopy and gas chromatog. (GC)-mass spectroscopy (MS) were used to directly detect and characterize reaction intermediates. Reaction of CEO with cytidine [65-46-3] gave the (hydrated) 2-oxoethyl deriv. at the N-3 position prior to ring closure to 3,N4-ethenocytidine [39007-52-8]; 5-methylcytosine [554-01-8] gave an analogous reaction. However, reactions of CEO or chloroacetaldehyde (CAA) [107-20-0] with 3-methylcytidine [2140-64-9]-i.e., with the N-3-blocked as in double-stranded DNA (ds DNA)-were shown by GC-MS of the silylated products to give, at a much slower rate, a pattern of at least 17 adducts all of which contained Cl. Based on MS fragmentation and considerations of positional, optical and cis/trans isomerism, the reaction products of the 3-methylcytosine moiety were assigned as cis-trans N4-(2-chlorovinyl)-3-methylcytosine [107807-29-4] which may have arisen from the corresponding N4-(1-hydroxy-2-chloroethyl) adduct. It is postulated that formation of these cytosine-N4 adducts would be more rapid in double-stranded DNA than in the model compd., and that the N4-(2-chlorovinyl) group may be a miscoding adduct. The kinetics for CEO rearrangement, hydroysis, and nucleophilic attack have been studied by proton FTNMR and lead to the hypothesis that concerted nucleophilic attack by cytosine-N4 and CEO rearrangement produce the N4 adducts. .

Studies on DNA methyltransferase and alteration of the enzyme activity by chemical carcinogens

Studies on DNA methyltransferase and alteration of the enzyme activity by chemical carcinogens. Cox, Ray (Veterans Adm. Med. Cent., Memphis, TN 38104, USA). Toxicol. Pathol., 14(4), 477-82 (English) 1986. CODEN: TOPADD. ISSN: 0192-6233. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) Ethionine [13073-35-3], a liver carcinogen, given to rats 17 h after partial hepatectomy inhibited the incorporation of [methyl-3H]methionine into 5-methylcytosine [554-01-8] residues of DNA. DNA isolated from these ethionine-treated rats was able to accept Me groups from S-adenosylmethionine [29908-03-0] 8 times more than control DNA. S-Adenosylethionine competitively inhibited the DNA methylase [9037-42-7] resulting in hypomethylated DNA. MNNG [70-25-7] reacted with the DNA methylase at the sulfhydryl sites inactivating the enzyme. 9037-42-7 and 10102-18-8 are also in the experiment. Methylnitrosourea [684-93-5] did not react directly with the methylase enzyme, but when reacted with DNA, the DNA methylase activity was inhibited by the carcinogen alkylated DNA. Sodium selenite also inhibited the enzyme non-competitively with a Ki of 6.7 mM. 5-Azacytidine [320-67-2] prevented the 2 to 3 fold increase in DNA methylase seen 2 days following partial hepatectomy. All of these data with various carcinogens, altering DNA methylation by different mechanisms, support the hypothesis that DNA methylation plays a role in the initiation of carcinogenesis. .