Life-long caloric restriction reduces oxidative stress and preserves nitric oxide bioavailability and function in arteries of old mice
Article first published online: 2 JUL 2013
© 2013 The Anatomical Society and John Wiley & Sons Ltd
Volume 12, Issue 5, pages 772–783, October 2013
How to Cite
Donato, A. J., Walker, A. E., Magerko, K. A., Bramwell, R. C., Black, A. D., Henson, G. D., Lawson, B. R., Lesniewski, L. A. and Seals, D. R. (2013), Life-long caloric restriction reduces oxidative stress and preserves nitric oxide bioavailability and function in arteries of old mice. Aging Cell, 12: 772–783. doi: 10.1111/acel.12103
- Issue published online: 11 SEP 2013
- Article first published online: 2 JUL 2013
- Accepted manuscript online: 29 MAY 2013 12:21AM EST
- Manuscript Accepted: 13 MAY 2013
- NIH. Grant Numbers: HL107120, AG013038, AG033196, AG033755, AG000279, AG040297, AG029337
Fig. S1 Vasodilation of carotid arteries to acetylcholine (ACh) alone or after pretreatment with TEMPOL (A), vasodilation to ACh after TEMPOL pretreatment in the absence or presence of the NOS inhibitor, L-NAME (B) (A&B: n = 8–10 per group) and aortic nitrotyrosine, an oxidative stress marker, abundance (C) in young, old ad libitum (AL) and old life-long caloric restricted (CR) B6D2F1 mice; (n = 6–8 per group) Nitrotyrosine is expressed relative to GAPDH to account for differences in protein loading and presented normalized to the Young mean. Representative blots shown below the summary graph (C,D). Values are means ± SEM. *P < 0.05 vs. Young. †P < 0.05 vs. Old AL.
Fig. S2 Dietary composition of the normal chow (NIH-31) for young and old ad libitum mice or fortified chow utilized for the old life-long caloric restricted B6D2F1 mice (NIA Fortified).
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