Lipid peroxidation injury and endoplasmic reticulum stress in Al-induced apoptosis.
- Author:
Qin-li ZHANG
1
;
Fang WANG
;
Ying-tao SHI
;
Lin-ping WANG
;
Ling ZHANG
;
Hong-mei ZHANG
;
Jing WANG
;
Qiu-ying LI
;
Qiao NIU
Author Information
- Publication Type:Journal Article
- MeSH: Aluminum; toxicity; Animals; Apoptosis; drug effects; Cells, Cultured; Endoplasmic Reticulum Stress; physiology; Lipid Peroxidation; physiology; Neurons; drug effects; metabolism; pathology; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Industrial Hygiene and Occupational Diseases 2008;26(3):143-146
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the role of lipid peroxidation injury and endoplasmic reticulum stress in Al-induced apoptosis.
METHODSNeurons from 0-3 day rats were cultured and treated with different concentrations of AlCl3.6H2O. Morphologic changes of neurons and endoplasmic reticulum were observed under fluorescent and transmission electron microscope; activities of superoxide dismutase (SOD), malondialdehyde (MDA) and ATP enzymes were detected.
RESULTSTypical morphologic changes in neurons apoptosis and endoplasmic reticulum were found under fluorescent and transmission electron microscope; SOD enzyme viability and ATP enzyme viability were significantly increased in the low-dosage group, but reduced in mid and high-dosage group (P < 0.01), whereas MDA levels decreased in the low-dosage group, but increased in mid and high-dosage group (P < 0.01).
CONCLUSIONAluminum may induce neurons apoptosis, and lipid peroxidation injury in endoplasmic reticulum plays an important role in the apoptosis progression.
