The effects of toluene in dimethylformamide (DMF)-induced hepatotoxicity were investigated with respect to the induction of cytochrome P-450 (CYP) and the activities of related enzymes. The rats were treated intraperitoneally with the organic solvents in olive oil (Single treatment groups: 450 [D1], 900 [D2], 1,800 [D3] mg DMF, and 346 mg toluene [T] per kg of body weight; Combined treatment groups: D1+T, D2+T, and D3+T) once a day for three days, while the control group received just the olive oil. Each group consisted of 4 rats. The activities of the xenobiotic metabolic enzymes and the hepatic morphology were assessed. The immunoblots indicated that the expression of CYP2E1 was considerably enhanced depending on the dosage of DMF and the CYP2E1 blot densities were significantly increased after treatment with both DMF and toluene, compared to treatment with DMF alone. The activities of glutathione-S-transferase and glutathione peroxidase were either decreased or remained unaltered after treatment with DMF and toluene, whereas the lipid peroxide levels were increased with increasing dosage of DMF and toluene. The liver tissue in the D3 group (1,800 mg/kg of DMF) showed signs of microvacuolation in the central vein region and a large necrotic zone around the central vein, in rats treated with both DMF (1,800 mg/kg) and toluene (D3T). These results suggest that the expression of CYP2E1 is induced by DMF and enhanced by toluene. These changes may have facilitated the accelerated formation of N-methylformamide (NMF) from toluene, and the generated NMF may directly induce liver damage.
Animals ; Body Weight ; Cytochrome P-450 CYP2E1 ; Cytochrome P-450 Enzyme System ; Dimethylformamide* ; Formamides ; Glutathione Peroxidase ; Lipid Peroxides ; Liver ; Olea ; Plant Oils ; Rats* ; Solvents ; Toluene* ; Veins ; Olive Oil

Adult ; Chemical and Drug Induced Liver Injury ; Dimethylformamide ; adverse effects ; Formamides ; analysis ; Humans ; Kidney ; physiopathology ; Kidney Diseases ; chemically induced ; physiopathology ; urine ; Kidney Function Tests ; Liver ; physiopathology ; Liver Diseases ; physiopathology ; urine ; Liver Function Tests ; Male ; Middle Aged ; Occupational Exposure

Arsenic ; urine ; Chromatography, High Pressure Liquid ; methods ; Formamides ; analysis ; Humans ; Urinalysis ; methods

OBJECTIVE: To study the effect of 5-aminoimidazole-4-formamide ribonucleotide (AICAR) combined with interferon (IFN-α-2b) on the proliferation and apoptosis of chronic myeloid leukemia K562 cells, and explore its possible mechanism. METHODS: CCK-8 method was used to detect the inhibition of cell proliferation. Wright Giemsa method was used to stain and cell morphology was observed by light microscopy. FITC Annexin V/PI double staining method was used to analyze the change of apoptosis rate. Immunocytochemistry method was used to detect the expression of wild-type P53 protein. RESULTS: Different concentration of AICAR was inhibitory effect on K562 cells at different time point of action for 24 h, 48 h, and 72 h, and the inhibition was time and dose-dependent (r=0.71, r=0.84). The combination of AICAR and IFN-α-2b could effectively inhibit the proliferation and promote apoptosis of K562 cells. The inhibition rate of K562 cells was (45.26±2.54)%, and the early apoptosis rate was (33.72±0.23)%, which was statistically significantly different from the control group, AICAR or IFN-ɑ-2b alone (P<0.05). The combination of two drugs promoted the expression of wild-type p53 protein. CONCLUSION AICAR and/or IFN-ɑ-2b can inhibit the cell proliferation and promote the apoptosis of K562 cells. The combination of two drugs shows synergistic antitumor effect, and its mechanism may be related to the promotion of high expression of wild-type p53 protein.
Apoptosis ; Cell Proliferation ; Formamides ; Humans ; Imidazoles ; Interferons ; K562 Cells ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; Ribonucleotides/pharmacology*

OBJECTIVES: In this study, we summarized the External Quality Assessment Scheme (EQAS) for the biological monitoring of occupational exposure to toxic chemicals which started in 1995 and continued until a 31st round robin in the spring of 2010. The program was performed twice per year until 2009, and this was changed to once a year since 2010. The objective of the program is to ensure the reliability of the data related to biological monitoring from analytical laboratories. METHODS: One hundred and eighteen laboratories participated in the 31st round robin. The program offers 5 items for inorganic analysis: lead in blood, cadmium in blood, manganese in blood, cadmium in urine, and mercury in urine. It also offers 10 items for organic analysis, including hippuric acid, methylhippuric acid, mandelic acid, phenylglyoxylic acid, N-methylformamide, N-methylacetamide, trichloroacetic acid, total trichloro-compounds, trans,trans-muconic acid, and 2,5-hexanedione in urine. Target values were determined by statistical analysis using consensus values. All the data, such as chromatograms and calibration curves, were reviewed by the committee. RESULTS: The proficiency rate was below 70% prior to the first round robin and improved to over 90% for common items, such as PbB and HA, while those for other items still remained in the range of 60-90% and need to be improved up to 90%. CONCLUSION: The EQAS has taken a primary role in improving the reliability of analytical data. A total quality assurance scheme is suggested, including the validation of technical documentation for the whole analytical procedure.
Acetamides ; Cadmium ; Calibration ; Consensus ; Dietary Sucrose ; Environmental Monitoring ; Formamides ; Glyoxylates ; Hexanones ; Hippurates ; Mandelic Acids ; Manganese ; Occupational Exposure ; Songbirds ; Sorbic Acid ; Trichloroacetic Acid

OBJECTIVETo study the effect of ZGDHu-1 on proliferation, differentiation and apoptosis in SHI-1 human leukemia cell line and explore its possible mechanism. Methods SHI-1 cells were cultured with different concentration of ZGDHu-1 and for different time. The cell proliferation was analysed by cell counting, alive cell count, MTT assay and Brdu-ELISA. Cell apoptosis was analysed by morphology, DNA content, Annexin-V/PI and Hoechst 33258 labeling method. Cell differentiation were assayed by morphology,expression of CD11b,CD14 and CD64 and NBT reduction. The expressions of phosphorylated p38MAPK or STAT3 were analysed by flow cytometry.

RESULTSZGDHu-1 inhibited SHI-1 cell proliferation in a time and dose dependent manner, the IC50- 48 h and IC50- 72 h were 250 ng/ml and 85 ng/ml, respectively. The majority of SHI-1 cells were arrested in G2/M phase. 48h after treated with 200 ng/ml ZGDHu-1, and those in G2/M phase accounted for (48.4 +/- 2.1)%. The SHI-1 cells apoptosis was increased with a time- and does-dependent manner. The morphology of SHI-1 cells cultured with 2-50 ng/ml ZGDHu-1 for three days become more mature with higher NBT positivity and up-regulated expressions of CD11b,CD14 and CD64. The expression of phosphor-p38MAPK was increased and phosphor-STAT3 down-regulated by the treatment of ZGDHu-1.

CONCLUSIONZGDHu-1 can inhibit SHI-1 cell proliferation and induce the cell differentiation and apoptosis. The mechanism may associate with its up-regulation of phosphor-p38MAPK and down-regulation phosphor-STAT3.

Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Cell Differentiation ; drug effects ; Cell Line, Tumor ; Dose-Response Relationship, Drug ; Formamides ; pharmacology ; Heterocyclic Compounds, 1-Ring ; pharmacology ; Humans ; Leukemia ; pathology ; Phosphorylation ; STAT3 Transcription Factor ; biosynthesis ; p38 Mitogen-Activated Protein Kinases ; biosynthesis

No abstract available.
Dimethylformamide* ; Liver Diseases* ; Liver*

This study was conducted to examine the excretion rate of dimethylformamide (DMF) from the workers exposed to DMF. The study was done at two synthetic leather factories located in Kyeonggi-do from the period of May 2 to 30, 1996. N-methyl- formamide (NMF) concentrations in urine were measured and compared by the three exposure level of DMF in air. The mean concentration of the Low (dry and winder part). Moderate (rinsing part) and High (mixing and coating part) exposure group were 3.99+/-3.54. 10.19 +/-5.69 and 32.10+/-7.87 mg/m3 during workshift of 8 hours, respectively. The mean concentration of urinary N-methylforinamide (NMF) were 2.13+/-2.58, 11.16+/-4.98 and 26.24 +/-7.35 mg/g creatinine, respectively. The concentration of NMIF in urine could reach to maximum in 3 hours and was reduced nearly to zero in about 18 hours after exposure to DMF.
Creatinine ; Dimethylformamide ; Environmental Monitoring ; Gyeonggi-do ; Korea*

Biomarkers ; blood ; Dimethylformamide ; pharmacokinetics ; Humans ; Occupational Exposure

Adult ; Dermatitis, Contact ; Dimethylformamide ; poisoning ; Female ; Humans