Occupational acute dimethylformamide poisoning: an analysis of 16 cases / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To analyze the clinical features and diagnostic points of occupational acute dimethylformamide (DMF) poisoning and to explore the mechanism of occupational acute DMF poisoning.</p><p><b>METHODS</b>A comprehensive analysis was performed on the clinical data of 16 cases of occupational acute DMF poisoning, including symptoms, signs, and laboratory testing results.</p><p><b>RESULTS</b>The main clinical features of occupational acute DMF poisoning were digestive system impairments, especially abdominalgia. Hemorrhagic gastroenteritis was not found by gastroscopy. There was no significant correlation between the degree of abdominalgia and alanine aminotransferase level (r(s) = 0.109, P>0.05).</p><p><b>CONCLUSION</b>Abdominalgia is recommended to be one of the reference indices for the diagnosis and degrading of occupational acute DMF poisoning, The mechanism of DMF poisoning remains unclear but it is considered to be related to methyl isocyanate, the intermediate product of DMF metabolism.</p>

The effects of benzene poisoning on expression of multidrug resistance 1 gene and P-glycoprotein in bone marrow mononuclear cells of C57BL/6 mice / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effects of benzene poisoning on the expression of multidrug resistance 1 (MDR1) gene and P-glycoprotein (P-gp) in the bone marrow mononuclear cells (BMMNCs) of C57BL/6 mice.</p><p><b>METHODS</b>C57BL/6 mice were randomly divided into control group (n = 24), low-dose group (n = 24), medium-dose group (n = 24), and high-dose group (n = 24) to receive corn oil, 25 mg/kg benzene, 50 mg/kg benzene, or 100 mg/kg benzene by gavage, once daily, 5 days/weeks, for 4 weeks. The mice were sacrificed on day 12, 26, or 29 of poisoning. Peripheral blood routine test was performed; real-time quantitative PCR was used to measure the MDR1 gene expression in BMMNCs; Western blot was used to measure the P-gp expression in BMMNCs.</p><p><b>RESULTS</b>On day 12, the red blood cell count and hemoglobin level in the high-dose group were significantly lower than those in the control group, low-dose group, and medium-dose group (P < 0.01 or P < 0.05). On day 26, the white blood cell count in the high-dose group was significantly lower than those in the control group, low-dose group, and medium-dose group (P < 0.01 or P < 0.05). At each time point, the mRNA expression of MDR1 gene in the low-dose group, medium-dose group, and high-dose group was significantly lower than that in the control group (P < 0.01). On day 26, the P-gp expression in the high-dose group was significantly lower than those in the control group, low-dose group, and medium-dose group, and the P-gp expression in the medium-dose group was significantly lower than that in the low-dose group (P < 0.01 or P < 0.05). On day 29, the P-gp expression in the low-dose group, medium-dose group, and high-dose group was significantly lower than that in the control group (P < 0.05).</p><p><b>CONCLUSION</b>Benzene poisoning can affect the expression of MDR1 gene and P-gp, which may be one of the mechanisms of benzene hematotoxicity.</p>

Influence of MDR1 gene C3435T on peripheral white blood cell counts in workers exposed to benzene / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the effects of MDR1 C3435T on the peripheral white blood cell counts in workers exposed to benzene.</p><p><b>METHODS</b>One hundred and twenty-one benzene-exposed workers and 110 healthy controls without benzene exposure were enrolled in this study. White blood cell counts influenced by the polymorphism of MDR1 gene were analyzed.</p><p><b>RESULTS</b>The frequency of MDR1 3435 C/C, C/T, T/T in healthy controls was 37.27%, 46.36%, 16.37%, respectively, and it was 38.84%, 41.33%, 19.83% in the benzene-exposed workers, respectively. The frequency of the MDR1 gene was also not significantly different between benzene exposed workers and controls. Subjects exposed to benzene with MDR1 3435 mutation genotype (T/T) had the significantly lower WBC [(5.46 ± 1.51) × 10(9)/L] than those carrying wild type (C/C) and heterozygous (C/T), whose WBC were (6.08 ± 1.28) × 10(9)/L (P = 0.044).</p><p><b>CONCLUSION</b>P-glycoprotein encoded by MDR1 gene may be implicated into the hematotoxicity of benzene. Subjects carrying MDR1 3435 T/T genotype may have a higher risk of benzene poisoning.</p>

High-resolution melting: a analysis for genotyping of MDR1 C3435T in benzene-exposed workers / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>Using high resolution melting (HRM) to analysis MDR1 C3435T in people exposed to benzene.</p><p><b>METHODS</b>Restriction fragment length polymorphism (RFLP) was utilized to detect the polymorphism of MDR1 3435 in 121 benzene-exposed workers, and the results were compared with the HRM in 10% samples and were confirmed with direct sequencing for six people in them.</p><p><b>RESULTS</b>By direct sequencing, consistent results of benzene-exposed workers with RFLP or HRM were got. The new high resolution melting curve analysis is more efficient, more convenient, and cheaper than RFLP.</p><p><b>CONCLUSION</b>High-resolution melting analysis provides a valid approach to efficiently detect DNA genetic diagnosis, which is suitable for detect susceptible genes in occupational surveillance.</p>

Effects of acrylonitrile on the activities of antioxidant enzymes and levels of lipid peroxidation in rat testes / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the mechanism of male reproductive toxicity induced by acrylonitrile (ACN).</p><p><b>METHODS</b>Male Sprague-Dawley rats were daily administrated ACN by intraperitoneal injection 5 times a week for 13 weeks at the dose of 0, 7.5, 15.0 and 30.0 mg/kg body weight, respectively. The rats were sacrificed and testes were removed at the end of 4, 8, 13 or 15 weeks, respectively. The activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and glutathione S-transferase (GST) and the levels of glutathione (GSH) and malonaldehyde (MDA) were detected in testes.</p><p><b>RESULTS</b>Following ACN treatment of 4 weeks, the levels of GSH in ACN 15.0 mg/kg and 30.0 mg/kg group were (7.44 +/- 0.77) mg/g pro and (6.95 +/- 0.77) mg/g pro respectively, and the activity of GSH-Px was (70.89 +/- 4.01) U/mg pro in 30.0 mg/kg group, all of which were significantly higher than the control group (P < 0.05, P < 0.01). After 8 weeks, the levels of GSH decreased to (2.50 +/- 0.94) mg/g pro in ACN 30.0 mg/kg group (P < 0.01); the activities of SOD increased to (102.08 +/- 16.08) NU/mg pro and (113.30 +/- 17.20) NU/mg pro in ACN 15.0 mg/kg and 30.0 mg/kg group (P < 0.01). After 13 weeks, the levels of GSH declined in ACN 15.0 mg/kg and 30.0 mg/kg group, and the activities of GST decreased in ACN 30.0 mg/kg group, and of GSH-Px decreased in both doses group. However, the level of MDA [(0.68 +/- 0.16) nmol/mg pro] were significantly higher in 30.0 mg/kg group than that in control group [(0.38 +/- 0.12) nmol/mg pro] (P < 0.01). 2 weeks after stopping ACN treatment, the level of GSH restored to normal but the levels of MDA or the activity of GSH-Px in 30.0 mg/kg group were still higher or lower respectively than those of control (P < 0.05).</p><p><b>CONCLUSION</b>ACN may impair the balance of antioxidant system, thus induce lipid peroxidation damage to rat testes.</p>