Proteasome 20S and Rab5 Alteration after 24 h and 14 Days Chlorpyrifos Exposure Lead to β-Amyloid and Tau Protein Level Increases and SN56 Neuronal Cell Death

被引:3
作者
Moyano, Paula [1 ]
Manuel Garcia, Jose [2 ]
Teresa Frejo, Maria [1 ]
Lobo, Margarita [1 ]
Garcia, Jimena [3 ]
del Pino, Javier [1 ]
机构
[1] Univ Complutense Madrid, Sch Vet, Dept Pharmacol & Toxicol, Madrid 28040, Spain
[2] Univ Complutense Madrid, Sch Med, Dept Legal Med Psychiat & Pathol, Madrid 28040, Spain
[3] Alfonso X Univ, Sch Hlth Sci, Dept Pharmacol, Madrid 28691, Spain
关键词
OXIDATIVE STRESS; AMPA RECEPTORS; ACTIVATION; RATS; DYSFUNCTION; INHIBITION; DISEASE; DRIVES; DAMAGE;
D O I
10.1021/acs.chemrestox.9b00216
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
The biocide chlorpyrifos (CPF) was shown to produce cognition impairment following single and long-term exposure. The complete mechanisms that lead to the CPF induced cognitive disorders remain to be discovered. A beta and tau proteins production was induced in basal forebrain SN56 cholinergic cells, by CPF, through proteasome 20S inhibition and Rab5 overexpression, leading to cell death both after acute and repeated administration, which was related with cognitive disorders induction. The results obtained in our study procure novel information related to the mechanisms involved in CPF neurodegeneration, which could be responsible for cognitive dysfunction and may lead to a promising alternative treatment of these effects.
引用
收藏
页码:1920 / 1924
页数:5
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