50348-20-4Relevant articles and documents
Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes
Hill, Anna B.,Jefferies, Phillip R.,Quistad, Gary B.,Casida, John E.
, p. 159 - 171 (2007/10/03)
Some of the most widely-used herbicides are the chloroacetanilides exemplified by alachlor and butachlor (derived from 2,6-diethylaniline) and metolachlor and acetochlor (synthesized from 2-ethyl-6-methylaniline). This investigation tests the hypothesis that the previously-observed oncogenicity of these herbicides is due to genotoxic intermediates such as diethylbenzoquinoneimine, a purported alachlor metabolite. Syntheses are reported here for the corresponding 2,6-dialkylbenzoquinoneimines, selected chloroacetyldialkylbenzoquinoneimines and several other candidate or known metabolites. The possible mutagenicity of diethylbenzoquinoneimine was tested in Salmonella typhimurium strains TA98 and TA100 with a weakly-positive response in the TA100 strain indicating induction of base-pair substitution mutations. The frequency of sister chromatid exchange (SCE) in Chinese hamster ovary cells was increased by alachlor at 10 μM and diethylaniline but not ethylmethylaniline at 30 and 3 μM. Isolated and cultured peripheral lymphocytes (mostly T cells) were used from two human donors to study the effects of the chloroacetanilides and their metabolites on primary human cells. In tests at 10 μM, the SCE frequency was increased by alachlor and possibly acetochlor but not by butachlor, metolachlor, dimethachlor (a 2,6-dimethyl analog) and dimethenamid (an analog based on 2,4-dimethyl-3-thienylamine). At 0.3 μM in cultured human lymphocytes, alachlor, the corresponding chloroacetanilide (N-dealkyl-alachlor) and aniline metabolites (and their 4-hydroxy derivatives), and diethylbenzoquinone were inactive or active in only one of the two donors whereas at 0.1-0.3 μM the SCE ratio for treated cells divided by the controls was always higher for diethylbenzoquinoneimine than for ethylmethyl- and dimethylbenzoquinoneimines. All the tested compounds were toxic to lymphocytes, but the depression of the mitotic index and increased duration of the cell cycle were not directly linked with SCE induction. Previous investigations have suggested that chloroacetanilide herbicides such as alachlor derived from 2,6-dialkylanilines are metabolized to 2,6-dialkylbenzoquinoneimines and the present study provides the first direct evidence that these metabolites are genotoxic in human lymphocytes.
Oxidative Cross-Coupling of Some 2,6- and N,N-Disubstituted Aniline Derivatives with 4-Aminophenol Mediated by Cerium(IV) Ions in Aqueous Perchloric Acid
Domagala,Dziegiec
, p. 749 - 757 (2007/10/03)
The mechanism of the oxidation of mixtures of 2,6-dimethylaniline (1), N,N-dimethylaniline (2), 2,6-diethylaniline (3), N,N-diethylaniline (4), N-methylaniline (5), 2,6-difluoroaniline (6), and 2,3,5,6-tetrafluoroaniline (7) with 4-aminophenol (8) by cerium(IV) ions in aqueous perchloric acid has been investigated. The indoaniline salts [O=C6H4=N-C6H2(R1) 2NH(R2)2]+ClO- 4 (R1 = H, R2 = CH3, C2H5 or vice versa) are formed as intermediates in the cross-coupling reaction; they undergo oxidation to imino-4-benzoquinone (9) and its corresponding derivatives by cerium(IV) ions in high yields. The mechanism of this process is discussed.
Migrations in Oxidations of Mesidine
Goldstein, Stephen L.,McNelis, Edward
, p. 1613 - 1620 (2007/10/02)
The oxidation of mesidine in methanolic media by ferricyanide, dichromate, and persulfate afforded an anil 4 containing a shifted methoxymethyl group in addition to the principal anil 3 formed by oxidative dealkylation.Possible intermediates 6, 7, and 8 were prepared and oxidized to the product anils.Oxidations of related anilines 9, 10, and 13 did not parallel those of mesidine but afforded analogues of 3.There is significant spectral evidence for anils with alkyl shifts but little for anils analogous to 4.
