Abstract

Reactive oxygen species (ROS) are considered responsible of ageing in animal and humans. Mitochondria are both source and target of ROS. Various strategies to reduce ROS production have been considered to extend lifespan. Caloric restriction, exercise, and antioxidants are thought to be able to protect cells from structural and functional damage. However, there is evidence that ROS production has a detrimental effect on health, but at physiological levels are necessary to stimulate longevity. They play an important effect on secondary signal transduction stimulating innate immunology and mitochondriogenesis. During exercise at moderate intensity, skeletal muscles generate ROS that are necessary for the remodelling of the muscular cells. Physical inactivity determines excessive ROS production and muscle atrophy. Caloric restriction (CR) can reduce ROS generation and improve longevity while antioxidant supplementation has shown a negative effect on longevity reducing the muscle adaptation to exercise and increasing mortality risk in patients with chronic diseases. The role of ROS in chronic diseases in also influenced by sex steroids that decrease in aging. The physiology of longevity is the result of integrated biological mechanisms that influence mitochondrial function and activity. The main objective of this review is to evaluate the effects of ROS on mitochondriogenesis and lifespan extension.

Highlights

  • Longevity is a physiological process depending more than 90% on the genotype and is a species-specific characteristic [1]

  • The most implicated factors correlated with longevity in vertebrate animals and mammals at the cellular level are the rate of mitochondrial Reactive oxygen species (ROS) production [4,5,6,7] and the degree of fatty acid unsaturation of tissue cellular membranes, including the mitochondrial ones [8,9,10]

  • An excess ROS production has been largely accepted to be responsible for ageing process and for promoting chronic diseases, cardiovascular mortality [223] and bone marrow mesenchymal stem cells apoptosis [224]

Read more

Summary

Introduction

Longevity is a physiological process depending more than 90% on the genotype and is a species-specific characteristic [1]. Molecular oxygen (O2) can generate partially reduced molecules such as superoxide anion (O2−∙), hydrogen peroxide (H2O2) and the hydroxyl radical (OH.), which represent the incomplete reduction of oxygen due to the acquisition of one, two or three electrons, respectively [14] These products of partial oxygen reduction are highly reactive and in the absence of an adequate protective system, can cause damage to biological structures. The main objective of this review is to discuss the biological mechanisms affecting ROS production, given that these reactive species are involved in both pathological and physiological processes. Both these processes can be exploited in efforts to extend lifespan

The determinants of longevity
The role of mitochondria and ROS in aging
Mitochondrial hormesis
Hormonal control of mitochondrial genome
The relationship between ROS and diseases
Muscle exercise and ROS
Effect of nutrition on ROS production
The risk of undernutrition
10. Caloric excess
11. Nutritional prevention
12. Effect of polyphenols
13. Vitamin C and E
Findings
14. Conclusions
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call