Changes of pathologic feature and microtubulin associated protein 2 in nervous system of hens with organophosphate-induced delayed neuropathy induced by 2,4,6-trimethylbenzoyl phenylphosphonate / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To develop the organophosphate-induced delayed neuropathy (OPIDN) hen model with 2,4,6-trimethylbenzoyl phenylphosphonate (TOCP), and observe the change of pathology and investigate the alterations of microtubulin associated protein 2 (MAP2).</p><p><b>METHODS</b>48 adult hens were randomly divided into four groups, including three experimental groups and control group (n = 12 each group). The hens in three experimental groups were treated with TOCP by gavage at single dosages of 250, 500 and 750 mg/kg respectively while the control hens received an equivalent volume of corn oil by gavage. All hens were sacrificed after 21 days of treatment. Half hens in each group were dissected for HE examination and myelin straining of brain, spinal cord and sciatic nerve while brains of another half hens were dissected for the determination of MAP2 by western blotting.</p><p><b>RESULTS</b>The delayed neurotoxicity symptoms of hens both in 500 and 750 mg/kg groups were consistently observed. The pathological changes of brain, spinal cord and sciatic nerve in 500 and 750 mg/kg groups showed nerve cells difference necrosis, increased cytoplasm basophilia, microglia proliferation, mono-nuclear and lymphocyte infiltration, myelin sheath extensive up to part of them disaggregation deletion. Compared with the control group, at 500 and 750 mg/kg respectively the increase of MAP2 was 25% and 23% (P < 0.01 and P < 0.05).</p><p><b>CONCLUSIONS</b>The histopathologic changes of OPIDN caused by TOCP have dose-response relationship. The changes of MAP2 in nervous system may contribute to the occurrence and development of TOCP induced delayed neurotoxicity.</p>

Study on malignant transformation of human bronchial epithelial cells induced by glycidyl methacrylate / 中华预防医学杂志

<p><b>OBJECTIVE</b>To study the malignant transformation of human bronchial epithelial cells induced by glycidyl methacrylate (GMA).</p><p><b>METHODS</b>16HBE cells were treated multiple times with GMA at concentrations of 1, 2, 4 and 8 microg/ml. Cellular biological characteristics of malignant transformation were identified by the tests of conA, colony forming frequency on soft agar, scanning electron microscope and tumorigenesis in nude mice. Test of immunocytochemical detection was also applied to confirm the derivation of cell and tumor. Groups of solvent control (DMSO) and positive control (MCA) were also performed at the same time.</p><p><b>RESULTS</b>Transformed foci could be observed after the cells were treated by GMA at concentrations from 1 to 8 microg/ml. The number of transformation foci increased with the concentration of GMA. Transforming rate in 8 microg/ml group (8.48 x 10(-6)) was significantly higher (P < 0.01) than that of solvent control group (4.5 x 10(-7)). The transformed cells lost contact inhibition and exhibited a crossover growth in culture dish. They also could grow in semi-solid agar and showed dose-reaction relations with the concentration of GMA. The colony forming frequency in 2, 4 and 8 microg/ml group was 1.20 per thousand, 2.35 per thousand and 5.70 per thousand respectively, which were higher than that of solvent control group (P < 0.01). The transformed cells could be agglutinated by low concentration of conA. Microvilli on the surface of transformed cells increased and became strong and long under scanning electron microscope. The transformed cells could form subcutaneous tumor in nude mice which was diagnosed as squamous cell carcinoma in morphology. Expression of cytokeratin (CK) was detected in both 16HBE cells and tumor formed in nude mice.</p><p><b>CONCLUSION</b>GMA could induce the malignant transformation of 16HBE cells. This research system might provide a potential tool and lay a foundation for the study of the molecular mechanism of carcinogenesis induced by GMA.</p>

Experimental study on protective effects of HupA in the treatment of isocarbophos poisoning / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the therapeutic and prophylactic efficiency of HupA in mice with acute isocarbophos poisoning, and the protective effects of the HupA on AChE inhibited by isocarbophos.</p><p><b>METHODS</b>Mice were randomizedly divided into the non-treatment group, the atropine control group, the HupA treatment group and the atropine and HupA combined treatment group. Toxic signs and survival rates were observed and compared among these groups. The AChE activity was monitored in the whole blood, the red cells and brain tissue exposed to isocarbophos in the either treated with HupA or non-treated groups.</p><p><b>RESULTS</b>In HupA treatment group compared with the non-treatment group, toxic signs were significantly decreased and the survival rate was increased. The therapeutic efficiency in the atropine and HupA combined treatment group was better than other groups. After isocarbophos was administered, the AChE activity in the HupA treatment group and the non-treatment group was decreased. However, the AChE activity in the whole blood (1.096 +/- 0.111), (1.262 +/- 0.146), (1.181 +/- 0.353) U/ml, the red cells (0.798 +/- 0.063), (1.000 +/- 0.176), (0.837 +/- 0.331) and the brain tissue (13.739 +/- 2.970), (18.507 +/- 3.466), (10.764 +/- 2.212) U/g in HupA treatment group 0.5, 1 and 2 hours after isocarbophos was administered was significantly higher than those in the non-treatment group (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>HupA has therapeutic effect on mice with acute isocarbophos poisoning. The protective effect of HupA on blood and brain AChE inhibited by isocarbophos may be one of the mechanisms of the therapeutic effect of HupA in acute Isocarbophos poisoning.</p>