Effects of age and dietary antioxidants on cerebral electron transport chain activity

Abstract

Aging is a pleiotropic process involving genetic and environmental factors. Recently it has been demonstrated that dietary constituents may affect senescence. In the present study, adult (3 month-old) mice were fed diets supplemented with ubiquinone (coenzyme Q 10 ), ␣-lipoic acid, melatonin or ␣-tocopherol for a six-month period to determine if antioxidants may reverse or inhibit the progression of certain age-associated changes in cerebral mitochondrial electron transport chain (ETS) enzyme activities. The control consisted of a group of mice maintained on a basal diet for the same period. The activity of cytochrome c oxidase (Complex IV) increased with age but melatonin supplementation restored the activity to levels of 3 month-old animals. The activity of succinate dehydrogenase (Complex II) showed no age-related changes. However, this enzyme complex was elevated, in animals supplemented with coenzyme Q 10 , ␣-lipoic acid and ␣-tocopherol, above corresponding values obtained with basal diet. NADH-ubiquinone oxidoreductase (Complex I) and ubiquinol: ferricytochrome-c oxidoreductase (Complex III) activities remained unchanged.

Dietary melatonin selectively reverses age-related changes in cortical cytokine mRNA levels, and their responses to an inflammatory stimulus

“…Since melatonin can prolong survival time of mice [2,31] albeit associated with increased spontaneous tumor incidence according to one report [2] -this is likely to be relevant to the aging process [36], even if the exact mechanism is incompletely understood [54]. We have found dietary melatonin can prevent age-related changes in both cerebral mitochondrial function [42] and in levels of production of nitric oxide and reactive oxygen species (ROS) [9]. This agent has also been reported to reverse age-related behavioral changes [4].…”

Metabolic syndrome and mitochondrial function: Molecular replacement and antioxidant supplements to prevent membrane peroxidation and restore mitochondrial function

“…For example, in rodents fed diets supplemented with antioxidants the antioxidants were found to inhibit the progression of certain age-associated changes in cerebral mitochondrial electron transport chain enzyme activities [Sugiyama et al, 1995;Sharman and Bondy, 2001]. The dietary use of antioxidants has also been shown to inhibit the age-associated decline in immune and other functions and prolong the lifespan of laboratory animals [De and Darad, 1991;Sugiyama et al, 1995;Arivazhagen et al, 2001;Sharman and Bondy, 2001]. In addition, antioxidant administration has certain neuroprotective effects, such as prevention of age-related hearing loss [Seidman et al, 2002].…”

Melatonin and the aging brain

“…While electron transport is a very efficient process, it has been estimated that around 2% of oxygen utilized escapes complete reduction to water and can form transient reactive intermediates (Boveris and Chance, 1973). There is evidence that the efficiency of mitochondrial respiration may diminish with age with a consequent increase in the production of superoxide and other oxidant species (Kokoszka et al, 2001;Sharman and Bondy, 2001). Following chemical stress, mitochondria from aged mice are more prone to produce reactive oxygen species than are mitochondria from young mice (Liu and Ames, 2005).…”