Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center, San Antonio, TX, USA.
Dose Response. 2006 Aug 19;5(2):163-73. doi: 10.2203/dose-response.06-005.Masoro.
Caloric restriction (CR) markedly extends the life of rats, mice and several other species, and it also modulates age-associated physiological deterioration and delays the occurrence and/or slows progression of age-associated diseases. The level of CR that retards the aging processes is a low-intensity stressor, which enhances the ability of rats and mice of all ages to cope with intense stressors. CR thus exhibits a hormetic action in these species, and therefore it is hypothesized that hormesis plays a role in the life-extending and anti-aging actions of CR. Both the findings in support of this hypothesis and those opposing it are critically considered. However, it is likely that hormesis is not the only process contributing to CR-induced life extension. It is proposed that two general processes are involved in CR-induced life extension. One is the reduced endogenous generation of damaging agents, such as reactive oxygen species. The second is hormesis, which enhances processes that protect against the action of damaging agents and also promotes processes that repair the damage once it occurs.
热量限制（CR）显著延长了大鼠、小鼠和其他几种物种的寿命，它还调节与年龄相关的生理恶化，并延迟与年龄相关的疾病的发生和/或减缓其进展。延缓衰老过程的 CR 水平是一种低强度应激源，它增强了所有年龄段大鼠和小鼠应对强烈应激源的能力。因此，CR 在这些物种中表现出一种兴奋效应，因此假设兴奋效应在 CR 的延长寿命和抗衰老作用中发挥作用。支持和反对这一假设的发现都被批判性地考虑。然而，很可能兴奋效应不是导致 CR 诱导寿命延长的唯一过程。有人提出，CR 诱导的寿命延长涉及两个一般过程。一种是减少内源性损伤性物质的产生，如活性氧。第二种是兴奋效应，它增强了对抗损伤性物质作用的过程，也促进了一旦发生损伤就修复损伤的过程。
