The goal of the Oxidative Damage and Mitochondrial Function Core is two-fold. First, we will continue to provide measurement of oxidative damage to lipid, DNA and protein in cells and tissues using the latest and most sensitive methods and technologic approaches. The second and new function of the Core is to provide several key assays of mitochondrial function including measures of reactive oxygen species generation, respiration and ATP production in isolated mitochondria and in cultured cells. Compromised mitochondrial function and accumulation of oxidative damage to cell components with age have been proposed as primary factors underlying age-associated alterations in physiologic function and pathology. A number of recent studies have suggested that the relation between mitochondrial dysfunction, oxidative damage and aging may not be as straightforward as originally proposed by Hamian more than 50 years ago. However, measures of oxidative damage and mitochondrial function continue to be important components of many studies on the underlying mechanisms of aging and age-related disease, and it is critical that these measures are done with the highest possible sensitivity and accuracy. The measurements offered by the Core require costly equipment and technologic expertise that prevent these types of analyses as routine measures in individual laboratories.
The Specific Aims of the Oxidative Damage and Mitochondrial Function Core are as follows: 1. To provide sensitive and accurate measurements of oxidative damage to lipids, DNA and protein through analysis of F2-isoprostanes/isofurans (lipid oxidation), 8-oxo-2-deoxyguanosine (oxo8dG) (DNA oxidation), and oxidative modifications to proteins (carbonyls, disulfide content and alterations in protein hydrophobicity). 2. To provide high quality sensitive measurement of mitochondrial function in isolated mitochondria and cell culture using state-of-the-art techniques. 3. To provide education and consultation regarding methodology for assessing oxidative damage and mitochondrial function.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Center Core Grants (P30)
Project #
5P30AG013319-19
Application #
8572594
Study Section
Special Emphasis Panel (ZAG1-ZIJ-2)
Project Start
Project End
Budget Start
2013-07-01
Budget End
2014-06-30
Support Year
19
Fiscal Year
2013
Total Cost
$98,534
Indirect Cost
$32,624
Name
University of Texas Health Science Center San Antonio
Department
Type
DUNS #
800772162
City
San Antonio
State
TX
Country
United States
Zip Code
78229
Branch, Sarah Y; Sharma, Ramaswamy; Beckstead, Michael J (2014) Aging decreases L-type calcium channel currents and pacemaker firing fidelity in substantia nigra dopamine neurons. J Neurosci 34:9310-8
Ratnam, Sarayu; Engler, Peter; Bozek, Grazyna et al. (2014) Identification of Ssm1b, a novel modifier of DNA methylation, and its expression during mouse embryogenesis. Development 141:2024-34
Zhang, Yiqiang; Bokov, Alex; Gelfond, John et al. (2014) Rapamycin extends life and health in C57BL/6 mice. J Gerontol A Biol Sci Med Sci 69:119-30
Edrey, Yael H; Salmon, Adam B (2014) Revisiting an age-old question regarding oxidative stress. Free Radic Biol Med 71:368-78
Boiko, Nina; Kucher, Volodymyr; Wang, Bin et al. (2014) Restrictive expression of acid-sensing ion channel 5 (asic5) in unipolar brush cells of the vestibulocerebellum. PLoS One 9:e91326
Liu, Yuhong; Diaz, Vivian; Fernandez, Elizabeth et al. (2014) Rapamycin-induced metabolic defects are reversible in both lean and obese mice. Aging (Albany NY) 6:742-54
Elbourkadi, Najoua; Austad, Steven N; Miller, Richard A (2014) Fibroblasts from long-lived species of mammals and birds show delayed, but prolonged, phosphorylation of ERK. Aging Cell 13:283-91
Hasty, Paul; Livi, Carolina B; Dodds, Sherry G et al. (2014) eRapa restores a normal life span in a FAP mouse model. Cancer Prev Res (Phila) 7:169-78
Fok, Wilson C; Bokov, Alex; Gelfond, Jonathan et al. (2014) Combined treatment of rapamycin and dietary restriction has a larger effect on the transcriptome and metabolome of liver. Aging Cell 13:311-9
Strong, Randy; Miller, Richard A; Astle, Clinton M et al. (2013) Evaluation of resveratrol, green tea extract, curcumin, oxaloacetic acid, and medium-chain triglyceride oil on life span of genetically heterogeneous mice. J Gerontol A Biol Sci Med Sci 68:6-16

Showing the most recent 10 out of 144 publications