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目的探讨以外周血单个核细胞线粒体功能失调作为锰神经毒性早期效应标志的可能性。方法选取已脱离锰接触的锰中毒病人18名作为中毒脱离接触组,选取锰作业工人73名作为锰接触组,选取无职业性锰接触人群63名作为对照组,对锰作业现场进行劳动卫生学监测,对中毒脱离接触组、接触组及对照组人群进行一般健康状况及神经系统检查,并对接触组和对照组进行神经行为功能核心组合测试(NCBT),检测3组人群外周血单个核细胞线粒体功能(呼吸控制率、ATP生成、线粒体膜电位),并对接触组神经行为指标与线粒体功能失调进行相关性分析。结果锰作业现场中拌粉机旁及其二层投料口粉尘浓度严重超标,高达16.3和38.0 mg/m3,分别超标1.63和3.8倍(卫生标准为10 mg/m3,TJ36-79),其中MnO2浓度为0.84和1.51 mg/m3,超标4.2和7.6倍(卫生标准为0.2 mg/m3,TJ36-79);一般健康状况及神经检查发现,中毒脱离接触组和接触组均有头晕、头痛、记忆力减退、注意力分散等植物神经紊乱等症状,中毒脱离接触组中有震颤及共济运动失调等锥体外系损害体征,接触组未见锥体外系神经系统损害体征;接触组与对照组NCBT神经行为功能检测发现,接触组易出现疲倦感,简单反应时较对照组显著增加,数字跨度、视觉记忆和目标追踪试验与对照组比较,差异有统计学意义;接触组血单个核细胞线粒体功能指标RCR、ATP生成及线粒体膜电位较对照组均显著降低,差异均有统计学意义(P<0.05),而中毒脱离接触组与对照组比较,差异无统计学意义(P>0.05);相关分析表明,接触组简单反应时、数字跨度与线粒体功能指标改变具有相关性(P<0.05或P<0.01)。结论锰接触可导致外周血单个核细胞线粒体功能失调,对于锰接触者外周血单个核细胞线粒体功能失调可作为潜在的锰神经毒性早期效应生物标志。
Objective To investigate the possibility of using mitochondrial dysfunction of peripheral blood mononuclear cells as a marker of early signs of neurotoxicity in manganese. Methods Totally 18 manganese poisoning patients who had been separated from manganese exposure were selected as poisoning disengagement group. Totally 73 manganese workers were selected as manganese exposure group, and 63 non-occupational manganese exposure groups were selected as control group. (NCBT) .Three groups of peripheral blood mononuclear cells (PBMCs) were detected in three groups: control group, exposure group, contact group and control group. Mitochondrial function (respiratory control rate, ATP production, mitochondrial membrane potential), and the correlation between neurobehavioral indicators and mitochondrial dysfunction in the contact group. Results The concentration of dust in the manganese operation site beside the powder feeding machine and on the second floor exceeded the standard seriously, up to 16.3 and 38.0 mg / m3, exceeding the standards of 1.63 and 3.8 times (the standard of health was 10 mg / m3 and TJ36-79) respectively. The concentration of MnO2 Were 0.84 and 1.51 mg / m3 respectively, exceeding the standards of 4.2 and 7.6 times (the standard of health was 0.2 mg / m3 and TJ36-79). The general health status and neurological examination showed that both the exposure group and the exposure group had dizziness, headache and memory loss , Attention deficit disorder and other symptoms of autonomic disorders, poisoning disengagement group with tremor and ataxia and other extrapyramidal signs of damage, no signs of extrapyramidal neurological damage in the contact group; contact group and control group NCBT nerve behavior The functional test found that the contact group was prone to fatigue, simple response significantly increased compared with the control group, the digital span, visual memory and target tracking test compared with the control group, the difference was statistically significant; contact group blood mononuclear cells mitochondrial function index RCR , ATP production and mitochondrial membrane potential were significantly lower than those in the control group (P <0.05), but there was no significant difference between the exposure group and the control group (P> 0.05) It shows that the reaction is simple contact group, digit span and change indicator of mitochondrial function correlated (P <0.05 or P <0.01). Conclusion Manganese exposure can lead to mitochondrial dysfunction in peripheral blood mononuclear cells. Mitochondrial dysfunction of peripheral blood mononuclear cells may be potential biomarker of early signs of manganese neurotoxicity in manganese exposure.