Effect of chronic lead exposure on expression of autophagy-associated proteins in rat hippocampus.
- Author:
Wei-feng YE
1
;
Yun TIAN
;
Ji-yun HUANG
;
Mei-hua LIAO
;
Rong-rong TAO
;
Gen-sheng ZHANG
;
Yi-jia LOU
;
Feng HAN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis Regulatory Proteins; metabolism; Autophagy; drug effects; physiology; Beclin-1; Cathepsin B; metabolism; Chronic Disease; Disease Models, Animal; Female; Hippocampus; drug effects; metabolism; pathology; Lead Poisoning; metabolism; pathology; Lysosomal-Associated Membrane Protein 2; metabolism; Male; Microtubule-Associated Proteins; metabolism; Rats; Rats, Sprague-Dawley; Signal Transduction; drug effects
- From: Journal of Zhejiang University. Medical sciences 2012;41(4):402-409
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of chronic lead exposure on expression of autophagy-associated proteins in rat hippocampus.
METHODSSD rats were randomly divided into three groups: control group was given distilled water, lead-exposed groups were given 0.5 g/L (low-dose) or 2.0 g/L(high-dose) lead acetate solution in drinking water. The rat pups started to drink the lead content water until 60 d maturity. The lead contents in blood and brain samples were analyzed by graphite furnace atomic absorption spectrophotometry. The expressions of Beclin 1, LC3, LAMP2 and cathepsin B proteins were detected by Western blot and immunohistochemistry.
RESULTSCompared with control group, the contents of lead were significantly higher in blood and hippocampus samples in chronic lead-exposed rats (P<0.01). Western blot showed that the expression of Beclin 1 and LC3-II/LC3-I increased significantly in high dose lead-exposed group compared with control group (P<0.05 or P<0.001). The confocal laser immunostaining results demonstrated that increased immunofluorescence staining of cathepsin B in hippocampal neurons compared with control animals.
CONCLUSIONThe disturbance of autophagy-lysosome signaling molecules might be partially contribute to neurotoxicity of chronic lead exposure.
