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作 者:贾飞飞[1] 姜慧[2] 申旭波[3] 熊云刚[3] 邹焰[3]
机构地区:[1]中国石油大学(华东)校医院,山东东营257061 [2]中国疾病预防控制中心疾控应急办,北京102206 [3]遵义医学院预防医学教研室,贵州遵义563003
出 处:《工业卫生与职业病》2011年第1期17-21,共5页Industrial Health and Occupational Diseases
基 金:贵州省科技计划课题(SY20093067)
摘 要:目的探讨锰接触工人神经行为改变与Parkin基因4号外显子S/N167多态性的相关性。方法选工龄在半年以上的职业性锰暴露工人200名和劳动强度相似,但工作环境不接触锰工人94名,按累积暴露指数将其分为高、低暴露组和对照组。利用沟槽稳定试验和拼板试验进行神经行为改变检测;利用PCR-RFLP法对Parkin基因4号外显子多态性位点进行基因分型。结果高暴露组中,Parkin基因4号外显子AA型工人的划痕长度、集合试验得分均低于GG基因型和GA基因型,而碰撞次数高于GG基因型和GA基因型,其差异有统计学意义(P<0.05);低暴露组中,Parkin基因4号外显子AA基因型工人的划痕长度、集合试验得分均低于GG基因型和GA基因型,其差异有统计学意义(P<0.05),3个基因型工人碰撞次数间差异无统计学意义(P>0.05);对照组中,Parkin基因4号外显子3个基因型划痕长度、碰撞次数、集合试验得分之间差异无统计学意义(P>0.05)。结论环境因素和遗传因素共同作用更易导致锰引起神经行为改变;携带Parkin基因4号外显子AA基因型的工人是锰损伤的易感者;Parkin基因4号外显子G601A突变导致的Ser167Asn多态性有可能作为检测锰致神经行为改变以及锰中毒风险评估的指标。Objective To study the relationship between neurobehavioral changes and Parkin gene polymorphism in manganese exposed workers. Methods 200 Mn exposed workers having working age 90.5 year and 94 Mn unexposed workers were chosen and divided into high and low exposed groups and control group according to cumulated exposure index(CEI). Every worker was detected by neurobehavioral detective equipment. The genetic DNA was extracted from every worker; the genotypes of exon 4 polymorphism were detected by PCR--RFI.P. Results In high exposed group, the subjects with AA genotype were significantly lower in the length of drawing and the scores of Pegboard test than those with GG and GA genotypes(P〈 0.05), while collision frequencies were significantly higher(P〈0.05). In low exposed group, the subjects with AA genotype were significantly lower in the length of drawing and the scores of Pegboard test than those with GG and GA genotypes(P〈0.05), but there was no significant difference in collision frequency(P〉 0.05). In the control group, there was no significant difference in subjects with different genotypes of exon 4 in three neurobehavioral detection(P〉0.05). Conclusions The common environmental and genetic effects might facilitate the neurobehavioral changes induced by manganese. The workers with AA genotype of exon 4 are susceptible to be injured by Mn. The S/N167 polymorphism of exon 4 of Parkin gene might be used as an indicator to detect the manganeseinduced neurobehavioral changes, and also as the risk assessment in manganese poisoning.
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