摘要
目的探讨乙体氯氰菊酯(β-CP)的亚急性神经毒性,为该类农药的中毒防治提供理论依据。方法选取昆明种雄鼠40只,分为对照组和染毒组,每组20只。染毒组经口灌胃5 mg/kg·bw β-CP 1次/d,连续30 d,对照组给予等量溶剂。观察小鼠一般情况及体重,并应用分光光度法检测2组小鼠海马与颞叶皮质谷氨酸(Glu)、谷氨酰胺(Gln)水平、谷氨酰胺合成酶(GS)、谷氨酰胺酶(PAG)和谷氨酸脱羧酶(GAD)活性,应用Real-time PCR与Western blot法检测GLAST、GLT-1转录、翻译水平。结果乙体氯氰菊酯染毒组小鼠偶见舔身、多动等症,未见死亡;2组小鼠体重均增加。染毒组海马与颞叶皮质Glu含量升高,Gln含量降低;海马与颞叶皮质GS活性降低,海马PAG活性升高、GAD活性降低;海马与颞叶皮质GLAST、GLT-1转录及翻译水平未见明显改变。结论 5 mg/kg·bwβ-CP亚急性染毒后可能通过扰乱谷氨酸代谢,导致兴奋性神经毒性,具体机制有待进一步研究。
Objective To investigate the neurotoxicity of beta-cypermethrin, and provide theoretical basis for the prevention and treatment of beta-cypermethrin poisoning. Methods Forty Kunming male mice were divided into control group and beta-cypermethrin group. Mice in beta-cypermethrin group were treated with 5 mg/kg·bw beta-cypermethrin by oral gavage daily for 30 days, and mice in control group were gavaged with equivalent distilled oil. The general condition and bodyweight of mice were observed and recorded. The level of glutamate and glutamine and activities of glutamine synthetase, phosphate-activated glutaminase and glutamate decarboxylase in the hippocampus and temporal cortex of mice were evaluated by spectrophotometry while GLAST, GLT-1 mRNA and protein levels were detected by Real-time PCR and Western blot. Results Mice in beta-cypermethrin group showed licking and hyperactivity occasionally, and there were no deaths. The bodyweights of the two groups both increased. Compared with the control ones, the mice in beta-cypermethrin group exhibited increased levels of glutamate and decreased levels of glutamine in both hippocampus and temporal cortex. Furthermore, the activities of glutamine synthetase in both hippocampus and temporal cortex were down-regulated compared with those of control ones. The activity of phosphate-activated glutaminase was higher while the activity of glutamate decarboxylase was lower in hippocampus of beta-cypermethrin treated mice. Conclusion Beta-cypermethrin(5 mg/kg·bw) may lead to excitatory neurotoxicity via disrupting glutamate metabolism, and its mechanism needed to further study.
作者
姜波
王斌
王晓
彭楠
和祯泉
张瑞
JIANG Bo;WANG Bin;WANG Xiao;PENG Nan;HE Zhen-quan;ZHANG Rui(Key Laboratory of Cerebrocranial Disease,Ningxia Medical University,Yinchuan Ningxia 750004,China;Traditional Chinese Medicine Hospital of Guyuan,Guyuan Ningxia 756000,China;School of Public Health and Management,Ningxia Medical University,Yinchuan Ningxia 750004,China)
出处
《毒理学杂志》
CAS
CSCD
2020年第5期400-404,共5页
Journal of Toxicology
基金
宁夏教育厅优秀青年教师培育基金项目(NGY2017087)
宁夏自治区“十三五”重大科技项目(2016BZ07)
地方高校国家级大学生创新创业训练计划(201710752011)。
