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One-pot alpha-glycosylation method using Appel agents in N,N-dimethylformamide.

[reaction: see text] A concept for the development of practical glycosylation is presented and demonstrated by one-pot alpha-glycosylation applying Appel agents for 2-O-benzyl-1-OH hexoses in DMF. The reaction, in situ giving the equilibrium of glycosyl bromides and more reactive O-glycoside intermediates, accomplishes a near-quantitative alpha-glycosylation removing the water molecules.

Dimethylformamide↗

Abnormal liver function associated with occupational exposure to dimethylformamide and glutathione S-transferase polymorphisms.

Dimethylformaide (DMF) is a major solvent predominately used in synthetic leather and resin production. Many human and animal studies have linked the cause of hepatoxicity to DMF. Previously, the authors demonstrated the significant dose-response relationship between abnormal liver function tests and DMF exposure and the interaction with hepatitis B virus (HBV) infection in Taiwanese workers. Because the toxic effect of various chemicals can be modified by metabolic traits, the study also investigated the influence of the glutathione S-transferases (GSTM1 and GSTT1) on the toxic effect of DMF. The average DMF exposure concentration was 23.87 ppm (range 5.2-86.6 ppm) in the high-exposure (>/=5 ppm) group and 2.41 ppm (range 0.9-4.3 ppm) in the low-exposure (<5 ppm) group. There were 13 of 44 (29.6%) abnormal liver function tests (elevations of either glutamate oxaloacetate transaminase (GOT) or glutamate pyruvate transaminase (GPT)) among the high DMF exposure workers, two of 22 (9.1%) abnormal liver function tests among the low DMF exposure workers. Chronic liver disease as determined by ultrasonography was present in seven of 44 (15.9%) high DMF exposure workers, and 0 of 22 (0%) low DMF exposure workers. There were 11 of 34 (32.4%) abnormal liver function tests among the GSTT1 null genotype workers, and four of 32 (12.5%) abnormal liver function tests among the GSTT1-positive genotype workers. Compared with the low DMF exposure workers, the adjusted odds ratio and 95% confidence intervals for abnormal liver function tests was 6.78 (0.94-48.7) for the high DMF exposure workers. Compared with the GSTT1-positive genotype workers, the adjusted odds ratio and 95% confidence intervals for abnormal liver function tests was 4.41 (1.15-16.9) for the GSTT1 null genotype workers. Compared with the low DMF group with GSTT1-positive genotype workers, the odds ratio (adjusted for HBV status) of abnormal liver function test was 12.38, 95% CI=(1.04-146.9) for the high DMF group with GSTT1 null genotype workers. This study indicates that abnormal liver function and chronic liver disease are associated with DMF exposure, and there are more than multiplicative interaction effects on abnormal liver function tests between the DMF exposure and the GSTT1 genotype.

Adult↗

Monomethylformamide levels in human urine after repetitive exposure to dimethylformamide vapor.

Eight healthy male subjects were exposed to DMF vapor at a concentration of 8.79 +/- 0.33 ppm for six hours daily for five consecutive days. All urine voided by the subjects was collected from the beginning of the first exposure to 24 hours past the end of the last exposure and each sample was analyzed for monomethylformamide (MMF). MMF was rapidly eliminated from the body with urine values peaking within a few hours following the end of each exposure period. Very little was found in the 24-hour postexposure sample and none was found in a 48-hour postexposure sample. There was no increased excretion of MMF in the urine following repetitive exposure. The mean for the seven-hour (end of exposure) sample was 4.74 microgram/ml or 736.8 microgram. Lower and upper one-sided 95% tolerance limits for 95% of the population were 1.2 microgram/ml (367 microgram) and 13.9 microgram/ml (1625 microgram). The coefficient of variation (CV) for microgram MMF/ml was approximately 25 times more variable than the CV for total microgram.

Adult↗

A Schiff base formed from sulfanilic acid and dimethylformamide.

The crystal structure the Schiff base contains one 4-dimethylaminomethyleneaminobenzenesulfonic acid molecule in zwitterionic form [4-(dimethylaminomethyleneammonio)benzenesulfonate], and one water molecule in the asymmetric unit (C9H12N2O3S.H2O). Protonation occurs at nitrogen atom N1, but the charge is delocalized.

Crystallography, X-Ray↗