The Mitochondrial Free Radical Theory of Aging

Barja, Gustavo

doi:10.1016/b978-0-12-394625-6.00001-5

Cited by 169 publications

(140 citation statements)

References 98 publications

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“…Our results revealed that age was statistically significantly correlated with free radical levels and thus supports a previous report [18] that aging is closely related to the activity of free radicals. Meanwhile, age had no significant correlation with sleep or fatigue, which may be because sleep and fatigue fluctuate widely within the same age groups and are also strongly related to an individual's lifestyle, health, and economic status.…”

Section: Discussionsupporting

confidence: 92%

An Analysis of Influencing Factors on Free Radicals among Women

Lee¹,

Song

2016

IJBSBT

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Section: Discussionsupporting

confidence: 92%

An Analysis of Influencing Factors on Free Radicals among Women

Lee¹,

Song

2016

IJBSBT

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“…However there is a threshold above which ROS become harmful and induce oxidative stress (Dai et al 2014;Genova and Lenaz 2015;Orr et al 2013;Rigoulet et al 2011). Mitochondria are the main generators of ROS, and complex I is considered as the major source of ROS involved in aging (Barja 2014;Genova and Lenaz 2015;Holzerova and Prokisch 2015;Orr et al 2013;Scialo et al 2013). Indeed, longlived animals have species-specific low mitochondrial ROS generation rates at complex I, and the extension of longevity by caloric restriction can be mimicked by inhibition of this ETC complex [reviewed in (Barja 2014;Genova and Lenaz 2015;Schmeisser 2011, 2014;Scialo et al 2013)].…”

Section: Introductionmentioning

confidence: 99%

Drosophila melanogaster mitochondrial Hsp22: a role in resistance to oxidative stress, aging and the mitochondrial unfolding protein response

2015

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Aging is characterized by the accumulation of dysfunctional mitochondria. Since these organelles are involved in many important cellular processes, different mechanisms exist to maintain their integrity. Among them is the mitochondrial unfolding protein response, which triggers the expression of a set of proteins aimed at re-establishing mitochondrial homeostasis. The induction of mitochondrial chaperones expression, particularly of Hsp60 and Hsp70, is a hallmark of this pathway. In Drosophila melanogaster, Hsp22 is also up-regulated by mitochondrial stress. This small heat shock protein is one of the members of the family to be localized inside mitochondria. One characteristic of Drosophila Hsp22 is its preferential up-regulation during aging and in oxidative stress conditions. It is a beneficial protein since its over-expression increases lifespan and resistance to stress while its down-regulation is detrimental. This review focuses on Drosophila Hsp22 and its links with the mitochondrial unfolding protein response and the aging process, in addition to highlight the important role of this sHSP in mitochondrial homeostasis.

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“…In fact, the mitochondrial electron transfer chain is a major production site in adipocytes from mice (Wang et al, 2010a,b) and from isolated mitochondria showing that 0.2%-2% of consumed O 2 is reduced by single electrons, generating O 2˙-as a byproduct (Brand, 2010) especially by complex I (NADH dehydrogenase) and complex III (cytochrome bc1 complex) (Fisher-Wellman and Neufer, 2012). High ROS levels produced by dysfunctional mitochondria have been suggested as the main cause of aging (Barja, 2014), resulting from error accumulation impinged on biomolecules. Interestingly, the aging process has been shown to share similar features with dysfunctional adipose tissue; for example, obesity contributes to reduced life span and the clinical outcomes closely resemble those usually found in aging (Ahima, 2009).…”

Section: Role Of Ros In Adipogenesismentioning

confidence: 99%

The two faces of reactive oxygen species (ROS) in adipocyte function and dysfunction

Castro

Grune

Speckmann

2016

Biological Chemistry

126

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White adipose tissue (WAT) is actively involved in the regulation of whole-body energy homeostasis via storage/release of lipids and adipokine secretion. Current research links WAT dysfunction to the development of metabolic syndrome (MetS) and type 2 diabetes (T2D). The expansion of WAT during oversupply of nutrients prevents ectopic fat accumulation and requires proper preadipocyte-to-adipocyte differentiation. An assumed link between excess levels of reactive oxygen species (ROS), WAT dysfunction and T2D has been discussed controversially. While oxidative stress conditions have conclusively been detected in WAT of T2D patients and related animal models, clinical trials with antioxidants failed to prevent T2D or to improve glucose homeostasis. Furthermore, animal studies yielded inconsistent results regarding the role of oxidative stress in the development of diabetes. Here, we discuss the contribution of ROS to the (patho)physiology of adipocyte function and differentiation, with particular emphasis on sources and nutritional modulators of adipocyte ROS and their functions in signaling mechanisms controlling adipogenesis and functions of mature fat cells. We propose a concept of ROS balance that is required for normal functioning of WAT. We explain how both excessive and diminished levels of ROS, e.g. resulting from over supplementation with antioxidants, contribute to WAT dysfunction and subsequently insulin resistance.

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The Mitochondrial Free Radical Theory of Aging

Cited by 169 publications

References 98 publications

An Analysis of Influencing Factors on Free Radicals among Women

An Analysis of Influencing Factors on Free Radicals among Women

Drosophila melanogaster mitochondrial Hsp22: a role in resistance to oxidative stress, aging and the mitochondrial unfolding protein response

The two faces of reactive oxygen species (ROS) in adipocyte function and dysfunction

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