Mitochondrial Impairment Mechanism in D-galactose-induced Senescence in Experimental Fibroblast Cell Model
- DOI
- 10.2991/bst-16.2016.18How to use a DOI?
- Keywords
- D-galactose, Mitochondria, Oxidative Stress, Oxidative Phosphorylation.
- Abstract
To establish an effective model for cellular senescence, human embryo lung fibroblast cells (MRC-5) were cultured in D-galactose (D-Gal) medium respectively, as control, same concentration of D-glucose (D-Glu) was used. Decrease in cell proliferation, increase in senescence associated -galactosidase activity, up-expression of p21 protein, and cell cycle arrest at S-phage were observed in D-Gal-treated cells. Meanwhile, D-Gal-treated cells showed the significant increased ROS and MDA level and decreased SOD activity. Furthermore, mitochondrial impairment and decrease in efficiency of oxidative phosphorylation (OXPHOS) was induced by D-Gal as evidenced by the decreased transmembrane potential, reduction of ATP production and changes of respiration function. Additionally, the significant decrease of mitochondrial quantity, mitochondrial DNA (mtDNA) copy number and increased mtDNA damage were detected in D-Gal-treated cells. Our data demonstrate that D-Gal induces mitochondrial oxidative impairment associated with increased generation of ROS, ultimately inhibiting the ATP synthesis which contributes to premature cellular senescence.
- Copyright
- © 2016, the Authors. Published by Atlantis Press.
- Open Access
- This is an open access article distributed under the CC BY-NC license (http://creativecommons.org/licenses/by-nc/4.0/).
Cite this article
TY - CONF AU - Wei Ye AU - Jian-Ming Cao AU - Xiao-Jun Tang AU - Chu Liu AU - Dong-Jie Hao AU - Jing Jin AU - Jian-Xin Lu PY - 2016/01 DA - 2016/01 TI - Mitochondrial Impairment Mechanism in D-galactose-induced Senescence in Experimental Fibroblast Cell Model BT - Proceedings of the 2016 International Conference on Biological Sciences and Technology PB - Atlantis Press SP - 113 EP - 124 SN - 2468-5747 UR - https://doi.org/10.2991/bst-16.2016.18 DO - 10.2991/bst-16.2016.18 ID - Ye2016/01 ER -