141-83-3Relevant articles and documents
Aerobic soil metabolism of metsulfuron-methyl
Li,Zimmerman,Gorman,Reiser,Fogiel,Haney
, p. 434 - 445 (1999)
A laboratory study was conducted to determine the degradation rates and identify major metabolites of the herbicide metsulfuron-methyl in sterile and non-sterile aerobic soils in the dark at 20°C. Both [phenyl-U-14C]- and [triazine-2-14C]metsulfuron-methyl were used. The soil was treated with [14C]metsulfuron-methyl (0.1 mg kg-1) and incubated in flow-through systems for one year. The degradation rate constants, DT50, and DT90 were obtained based on the first-order and biphasic models. The DT50 (time required for 50% of applied chemical to degrade) for met sulfuron-methyl, estimated using a biphasic model, was approximately 10 days (9-11 days, 95% confidence limits) in the non-sterile soil and 20 days (12-32 days, 95% confidence limits) in the sterile soil. One-year cumulative carbon dioxide accounted for approximately 48% and 23% of the applied radioactivity in the [phenyl-U-14C] and [triazine-2-14C]metsulfuron-methyl systems, respectively. Seven metabolites were identified by HPLC or LC/MS with synthetic standards. The degradation pathways included O-demethylation, cleavage of the sulfonylurea bridge, and triazine ring opening. The triazine ring-opened products were methyl 2- [[[[[[[(acetylamino)carbonyl]amino]carbonyl]amino] carbonyl]- amino]sulfonyl]benzoate in the sterile soil and methyl 2- 1[[[[[amino](aminocarbonyl)imino]methyl] amino]carbonyl]amino]sulfonyl]benzoate in the non-sterile soil, indicating that different pathways were operable.
Herth, R.
, (1880)
Retinoidal pyrimidinecarboxylic acids. Unexpected diaza-substituent effects in retinobenzoic acids
Ohta, Kiminori,Kawachi, Emiko,Inoue, Noriko,Fukasawa, Hiroshi,Hashimoto, Yuichi,Itai, Akiko,Kagechika, Hiroyuki
, p. 1504 - 1513 (2007/10/03)
Several pyridine- and pyrimidine-carboxylic acids were synthesized as ligand candidates for retinoid nuclear receptors, retinoic acid receptors (RARs) and retinoic X receptors (RXRs). Although the pyridine derivatives, 6-[(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)carbamoyl]pyridine- 3-carboxylic acid (2b) and 6-[(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)carboxamido]pyridin e-3-carboxylic acid (5b) are more potent than the corresponding benzoic acid-type retinoids, Am80 (2a) and Am580 (5a), the replacement of the benzene ring of Am580 (5a), Am555 (6a), or Am55 (7a) with a pyrimidine ring caused loss of the retinoidal activity both in HL-60 cell differentiation assay and in RAR transactivation assay using COS-1 cells. On the other hand, pyrimidine analogs (PA series, 10 and 11) of potent RXR agonists (retinoid synergists) with a diphenylamine skeleton (DA series, 8 and 9) exhibited potent retinoid synergistic activity in HL-60 cell differentiation assay and activated RXRs. Among the synthesized compounds, 2-[N-n-propyl-N-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)amino] pyrimidine-5-carboxylic acid (PA013, 10e) is most active retinoid synergist in HL-60 assay.
