Mitochondrial reactive oxygen species: Do they extend or shorten animal lifespan?

Abstract

Testing the predictions of the Mitochondrial Free Radical Theory of Ageing (MFRTA) has provided a deep understanding of the role of reactive oxygen species (ROS) and mitochondria in the aging process. However those data, which support MFRTA are in the majority correlative (e.g. increasing oxidative damage with age). In contrast the majority of direct experimental data contradict MFRTA (e.g. changes in ROS levels do not alter longevity as expected). Unfortunately, in the past, ROS measurements have mainly been performed using isolated mitochondria, a method which is prone to experimental artifacts and does not reflect the complexity of the in vivo process. New technology to study different ROS (e.g. superoxide or hydrogen peroxide) in vivo is now available; these new methods combined with state-of-the-art genetic engineering technology will allow a deeper interrogation of, where, when and how free radicals affect aging and pathological processes. In fact data that combine these new approaches, indicate that boosting mitochondrial ROS in lower animals is a way to extend both healthy and maximum lifespan. In this review, I discuss the latest literature focused on the role of mitochondrial ROS in aging, and how these new discoveries are helping to better understand the role of mitochondria in health and disease. This article is part of a Special Issue entitled 'EBEC 2016: 19th European Bioenergetics Conference, Riva del Garda, Italy, July 2-6, 2016', edited by Prof. Paolo Bernardi.

A flavone-polysaccharide based prescription attenuates the mitochondrial dysfunction induced by duck hepatitis A virus type 1

“…Among these inflammatory cells, phagocytes such as neutrophils and mononuclear phagocytes can also be recruited and produce ROS to kill the pathogens during the so-called “respiration burst” [28]. However, ROS are not just helpful weapons of phagocytes but are harmful agents causing oxidative stress and damage nearby cells and molecules at exorbitant concentration [29]. …”

N-Acetyl-L-cysteine Protects the Enterocyte against Oxidative Damage by Modulation of Mitochondrial Function

“…In this study, H 2 O 2 exposure induced oxidative stress evidenced by decreased cell viability, inhibited T-AOC, and increased leakage of LDH, while NAC treatment markedly improved antioxidant system. Mitochondria are the powerhouses of the cell, producing a considerable share of cellular ATP and playing a central role in cellular function and metabolism [28]. Our previous report showed that mitochondrial dysfunction was observed with decrease in the basal respiration, maximal respiration, and nonmitochondrial respiration after LPS treatment [1].…”

Mitochondria and aging: A role for the mitochondrial transition pore?

“…Similarly, mice deleted for the gene of the p66shc adaptor protein have reduced ROS generation and delayed aging (Migliaccio et al., 1999; Napoli et al., 2003). However, new recent data challenged this hypothesis as they show that ROS can be beneficial and extend lifespan at least in lower organisms such as flies and worms (Sanz, 2016; Sena & Chandel, 2012). Accumulating evidence suggests that other aspects of mitochondrial physiology must be considered to explain the contribution of mitochondria to aging (Gonzalez‐Freire et al., 2015; Payne & Chinnery, 2015).…”