In this paper, the clinical data of a case of accidental poisoning of dimethylformamide in a traffic accident was analyzed. The patient was trapped in the driving room, his limbs were soaked in dimethylformamide for a long time, and dimethylformamide was inhaled at the same time. After 4 days of treatment in a local hospital, he was transferred to the Department of Poisoning & Occupational Diseases, Emergency Medicine of Qilu Hospital of Shandong University for treatment. The main clinical manifestation of the patient was liver damage and intractable abdominal pain, which was cured by active treatment.
Male ; Humans ; Dimethylformamide ; Abdominal Pain ; Occupational Diseases/complications* ; Poisoning

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*

Chemical and Drug Induced Liver Injury ; Dimethylformamide ; Humans ; Occupational Exposure

Differentiated HL-60 is an effector cell widely used for the opsonophagocytic-killing assay (OPKA) to measure efficacy of pneumococcal vaccines. We investigated the correlation between phenotypic expression of immunoreceptors and phagocytic ability of HL-60 cells differentiated with N,N-dimethylformamide (DMF), all-trans retinoic acid (ATRA), or 1alpha, 25-dihydroxyvitamin D3 (VitD3) for 5 days. Phenotypic change was examined by flow cytometry with specific antibodies to CD11c, CD14, CD18, CD32, and CD64. Apoptosis was determined by flow cytometry using 7-aminoactinomycin D. Function was evaluated by a standard OPKA against serotype 19F and chemiluminescence-based respiratory burst assay. The expression of CD11c and CD14 gradually increased upon exposure to all three agents, while CD14 expression increased abruptly after VitD3. The expression of CD18, CD32, and CD64 increased during differentiation with all three agents. Apoptosis remained less than 10% until day 3 but increased after differentiation by DMF or ATRA. Differentiation with ATRA or VitD3 increased the respiratory burst after day 4. DMF differentiation showed a high OPKA titer at day 1 which sustained thereafter while ATRA or VitD3-differentiated cells gradually increased. Pearson analysis between the phenotypic changes and OPKA titers suggests that CD11c might be a useful differentiation marker for HL-60 cells for use in pneumococcal OPKA.
Antibodies, Bacterial/immunology ; Antigens, CD11c/metabolism ; Antigens, CD14/metabolism ; Antigens, CD18/metabolism ; Apoptosis/*immunology ; Biological Assay ; Cell Differentiation ; Cell Line, Tumor ; Cholecalciferol/pharmacology ; Dimethylformamide/pharmacology ; Flow Cytometry ; HL-60 Cells ; Humans ; Phagocytosis/*immunology ; Pneumococcal Vaccines/*immunology ; Receptors, IgG/metabolism ; Receptors, Immunologic/*biosynthesis ; Respiratory Burst/immunology ; Streptococcus pneumoniae/*immunology ; Tretinoin/pharmacology

Differentiated HL-60 is an effector cell widely used for the opsonophagocytic-killing assay (OPKA) to measure efficacy of pneumococcal vaccines. We investigated the correlation between phenotypic expression of immunoreceptors and phagocytic ability of HL-60 cells differentiated with N,N-dimethylformamide (DMF), all-trans retinoic acid (ATRA), or 1alpha, 25-dihydroxyvitamin D3 (VitD3) for 5 days. Phenotypic change was examined by flow cytometry with specific antibodies to CD11c, CD14, CD18, CD32, and CD64. Apoptosis was determined by flow cytometry using 7-aminoactinomycin D. Function was evaluated by a standard OPKA against serotype 19F and chemiluminescence-based respiratory burst assay. The expression of CD11c and CD14 gradually increased upon exposure to all three agents, while CD14 expression increased abruptly after VitD3. The expression of CD18, CD32, and CD64 increased during differentiation with all three agents. Apoptosis remained less than 10% until day 3 but increased after differentiation by DMF or ATRA. Differentiation with ATRA or VitD3 increased the respiratory burst after day 4. DMF differentiation showed a high OPKA titer at day 1 which sustained thereafter while ATRA or VitD3-differentiated cells gradually increased. Pearson analysis between the phenotypic changes and OPKA titers suggests that CD11c might be a useful differentiation marker for HL-60 cells for use in pneumococcal OPKA.
Antibodies, Bacterial/immunology ; Antigens, CD11c/metabolism ; Antigens, CD14/metabolism ; Antigens, CD18/metabolism ; Apoptosis/*immunology ; Biological Assay ; Cell Differentiation ; Cell Line, Tumor ; Cholecalciferol/pharmacology ; Dimethylformamide/pharmacology ; Flow Cytometry ; HL-60 Cells ; Humans ; Phagocytosis/*immunology ; Pneumococcal Vaccines/*immunology ; Receptors, IgG/metabolism ; Receptors, Immunologic/*biosynthesis ; Respiratory Burst/immunology ; Streptococcus pneumoniae/*immunology ; Tretinoin/pharmacology

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

OBJECTIVETo investigate the toxicity of intragastrically administered N, N-dimethylformamide (DMF) in female Wistar rats, and to provide experimental data for the overall evaluation of DMF toxicity under different ways of exposure.

METHODSForty female Wistar rats weighing 150∼180 g were randomly divided into four groups: control group (treated with water) and three DMF exposure groups with doses of 50 mg/kg, 100 mg/kg, and 200 mg/kg. After oral administration of DMF once a day for 14 consecutive days, the rats were weighed and sacrificed. The liver, kidney, brain, and uterus were weighed to calculate organ indices. The pathological changes in the liver were examined by HE staining. The protein expression of HSP70 in the liver, kidney, and brain was determined. Finally, peripheral lymphocytes were collected from the arteria cruralis to determine DNA damage by comet assay.

RESULTSFourteen days after DMF exposure, the body weight and organ indices of the kidney, brain, and uterus showed no significant changes. However, the liver index showed concentration-dependent increase in all DMF exposed groups (3.52±0.21, 3.55±0.13, and 3.88±0.22 in the low-, medium-, and high-dose groups, respectively), as compared with the control group (3.24±0.28) (P < 0.05 or P < 0.01). The pathological damage in the liver also showed a concentration-dependent manner. Inflammatory cell infiltration and granular degeneration in centrilobular hepatocytes were observed in the high-dose group. No significant change in protein expression of HSP70 was observed in the liver, kidney, or brain of DMF-exposed rats (P > 0.05). DNA damage was induced by DMF, and the DNA percentage of lymphocyte comet tail, average tail length, and tail moment in exposed groups were all significantly increased as compared with the control group (P < 0.05 or P < 0.01).

CONCLUSIONGavaged DMF can induce liver injury and DNA damage in lymphocytes in rats 14 days after administration. There is no significant change in protein expression of HSP70 in the liver, brain, or kidney after DMF exposure.

Animals ; Brain ; drug effects ; pathology ; DNA Damage ; drug effects ; Dimethylformamide ; toxicity ; Female ; Gastric Lavage ; HSP70 Heat-Shock Proteins ; metabolism ; Kidney ; drug effects ; pathology ; Liver ; drug effects ; pathology ; Lymphocytes ; drug effects ; Rats ; Rats, Wistar ; Toxicity Tests

OBJECTIVETo assess the value of blood N-methylcarbamoylated haemoglobin (NMHb) as a biomarker of N, N-dimethylformamide (DMF) exposure.

METHODSSeventy-two DMF processing workers in a synthetic leather factory were included in the DMF exposure group, and 12 workers in a food factory without exposure to DMF were included in the control group. Long-time individual sampling in workplace was performed among 45 workers in the exposure group, accompanied by a questionnaire survey. Blood and urine were collected for the determination of urinary N-methylformamide (NMF), urinary creatinine, and blood NMHb. Air DMF and urinary NMF were determined by gas chromatography. NMHb in blood was degraded to 3-methyl-5-isopropylhydantoin by Edman degradation before it could be determined by gas chromatography/mass spectrometry.

RESULTSAir DMF in workplace and NMF in post-shift urine were both correlated with NMHb in blood, and the respective regression equations were LgNMHb (nmol/g globin) = 0.32×LgDMF (mg/m(3))+1.8 (r = 0.60, P < 0.005), and LgNMHb (nmol/g globin) = 0.47×LgNMF (mg/g Cr) + 1.4 (r = 0.56, P < 0.005).

CONCLUSIONNMHb can be used as a biomarker of long-term exposure to DMF.

Adult ; Biomarkers ; blood ; Dimethylformamide ; analysis ; Hemoglobins ; analysis ; Humans ; Middle Aged ; Occupational Exposure ; Workplace ; Young Adult

Dimethylformamide ; poisoning ; Fatal Outcome ; Humans ; Male ; Occupational Exposure ; Young Adult

OBJECTIVETo explore the effect of N,N-dimethylformamide (DMF) on oxidation or antioxidation status among occupational exposed workers.

METHODSA total of 104 DMF exposed workers and 101 controls were recruited in this study in May 2012. The information of occupational history, age, gender, smoking and alcohol habits of all subjects were collected by questionnaire. DMF concentration in the air of workplace was tested. N-methyl-carbamoylated haemoglobin adduct (NMHb) in blood was chosen as an inner-dose biomarker, which was expressed as 3-methyl-5-isopropylhydantoin(MVH), the degeneration product of NMHb. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) levels were detected to reflect liver function. Serum superoxide dismutase (SOD) activity, glutathione-S-transferase (GST) activity, malondialdehyde (MDA) levels, 3- nitrotyrosine (3-NT) levels were detected to reflect oxidative/antioxidative status.

RESULTSDMF concentration in workplace air was within the range of 3.3-12.4 mg/m(3), which did not exceed our national standard. The MVH level in exposed workers was (19.69 ± 12.52) mg/kg, but was not detectable in control group. The activity of SOD in exposed workers ((125.30 ± 21.23) U/ml) was significantly higher than the control group ((118.35 ± 18.48) U/ml, t = -2.47, P = 0.014). However, the activity of SOD showed different trends with the increasing of MVH level. When MVH ≤ 24 mg/kg, the SOD activity increased with the increasing of MVH level (r = 0.356, P = 0.002). However, when MVH> 24 mg/kg, SOD activity expressed decreasing trend with the increasing of MVH level (r = -0.260, P = 0.150). No significant differences were observed in GST, MDA, 3-NT, ALT, AST levels among the two groups.

CONCLUSIONDMF exposure might have stimulatory effect on antioxidation system of the body under low concentration; within the range of compensatory defense, DMF exposure did not cause obvious lipid and/or protein peroxidative damage.

Adult ; Antioxidants ; metabolism ; Case-Control Studies ; Dimethylformamide ; Female ; Glutathione Transferase ; blood ; Humans ; Male ; Occupational Exposure ; Oxidation-Reduction ; Superoxide Dismutase ; blood ; Workplace ; Young Adult