| Literature DB >> 22886955 |
Zhengde Du1,2, Yujuan Hu1, Yang Yang1, Yu Sun1, Sulin Zhang1, Tao Zhou1, Lingling Zeng1, Wenjuan Zhang1, Xiang Huang1, Weijia Kong3, Honglian Zhang4.
Abstract
Mitochondrial DNA (mtDNA) common deletion (CD) plays a significant role in aging and age-related diseases. In this study, we used D-galactose (D-gal) to generate an animal model of aging and the involvement and causative mechanisms of mitochondrial damage in such a model were investigated. Twenty 5-week-old male Sprague-Dawley rats were randomly divided into two groups: D-gal group (n=10) and control group (n=10). The quantity of the mtDNA CD in the hippocampus was determined using a TaqMan real-time PCR assay. Transmission electron microscopy was used to observe the mitochondrial ultrastructure in the hippocampus. Western blot was used to detect the protein levels of NADPH oxidase (NOX) and uncoupling protein 2 (UCP2). We found that the level of mtDNA CD was significantly higher in the hippocampus of D-gal-induced aging rats than in control rats. In comparison with the control group, the mitochondrial ultrastructure in the hippocampus of D-gal-treated rats was damaged, and the protein levels of NOX and UCP2 were significantly increased in the hippocampus of D-gal-induced aging rats. This study demonstrated that the levels of mtDNA CD and NOX protein expression were significantly increased in the hippocampus of D-gal-induced aging rats. These findings indicate that NOX-dependent reactive oxygen species generation may contribute to D-gal-induced mitochondrial damage.Entities:
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Year: 2012 PMID： 22886955 DOI： 10.1007/s11596-012-0081-z
Source DB: PubMed Journal: J Huazhong Univ Sci Technolog Med Sci ISSN： 1672-0733