Dietary Restriction Downregulates Free Radical and Lipid Peroxide Production: Plausible Mechanism for Elongation of Life Span.

Abstract

SummaryDietary restriction elongates life span by suppressing age-related diseases in experimental animals. It has received a great deal of attention in connection with the rela tionship between aging, nutrition, and oxidative stress because oxidative injury in several tissues is a prominent feature in the aging process. Although the oxidative stress theory of aging has currently gained popularity, the premise from which this hypothesis was derived is paradoxical because the same oxygen, that supports life in one hand threatens survival and promotes aging in the other. Until recently, no single experimental paradigm could offer satisfactory mechanistic explanations for this complex issue. Recent investigations using the life-extending dietary restriction regimen could offer satisfactory mechanistic explanations for this apparent self contradiction to life. The modulation of free radical-induced oxidative stress provided sufficient data to support the notion that dietary restriction's antiaging ef fect may come from its ability to tightly regulate the oxidative status of an organism. The re sult is the maintenance of cellular homeostasis, a hallmark of dietary restriction's action in the extension of life span. To date, we reported that dietary restriction (maintained on 60% of ad libitum feeding) suppresses age-related oxidative damage by modulating the amount as well as the fatty acid composition of tissue phospholipids. These remarkable findings have been incorporated into the new "membrane peorxidation cycle" concept. The intervention of this cycle appears to be an evolutionary process that the dietary restricted rats have adapted as a strategy to protect the membrane in an oxidative environment.

The influence of dietary fat source on liver and skeletal muscle mitochondrial modifications and lifespan changes in calorie-restricted mice

“…Of note, only two traits currently correlate inversely with maximal longevity among animal species: both the rate of reactive oxygen species (ROS) generation in mitochondria and the degree of fatty acid unsaturation of tissue membranes (Pamplona and Barja, 2011; Barja 2014). In accordance, a decrease in long-chain PUFA in mitochondrial membrane phospholipids may be a mechanism contributing to the anti-aging effects of CR (Laganiere and Yu 1989; 1993; Yu et al 2002). Interestingly, the drug atenolol, a β1-blocker that decreases fatty acid unsaturation in heart and skeletal muscle mitochondria and changes the lipid profile towards that found in long-lived mammals, reverted several age-associated detrimental alterations in mice but did not extend longevity, possibly due to unwanted side effects of the drug (Sánchez-Román et al 2010; 2014; Gómez et al.…”

Effects of weight loss on erythrocyte membrane composition and fluidity in overweight and moderately obese women

“…This reduction might be the result of one or more of the following factors: first, changes in nutritional habits as a result of the suggestion to increase the intake of fruit and vegetables (rich in antioxidants) and reduce that of fried foods (rich in lipoperoxides); second, a reduction in the lipid peroxides of various tissues due to the well-known effect of caloric restriction [26,27] and consequent decreased exchange of these lipoperoxides between tissues and blood lipoproteins and erythrocytes; third, the decrease in membrane cholesterol in the erythrocytes: in fact, in a previous study, we showed that increased membrane cholesterol has a prooxidant action on the erythrocytes of overweight and moderately obese women [9].…”

Mitochondrial ultrastructure and markers of dynamics in hepatocytes from aged, calorie restricted mice fed with different dietary fats

“…The assumption has been made that polyunsaturated fatty acids are more susceptible to peroxidation and other modifications that result in the accumulation of oxidative injury in membranes containing these fatty acids. This idea is supported by a decreased content of long-chain polyunsaturated fatty acids in mitochondria isolated from different organs after CR (Yu et al, 2002). As one of the major ROS-producing constituents of the cell, special attention has been paid to the role of the mitochondria on these phenomena, and the proposal has been made that a combination of both “mitochondrial” and “membrane” theories of aging (Zs.-Nagy, 1978) can explain the life-span extension effect of CR (Bevilacqua et al, 2004; Hagopian et al, 2005).…”