Mitochondrial metabolism of reactive oxygen species

Venditti, Paola; Stefano, Lisa Di; Meo, S. Di

doi:10.1016/j.mito.2013.01.008

Cited by 268 publications

(179 citation statements)

References 142 publications

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“…Although the main sites involved in mitochondrial ROS production are believed to be localized at Complexes I and III, succinate-dependent ROS production by Complex II from rat skeletal muscle and glycerol 3-phosphate-dependent production by Complex II from several rat tissues have also been reported (Venditti et al 2013).…”

Section: Mitochondria-derived H 2 Omentioning

confidence: 99%

“…This idea is based on a series of observations. Normally, the rate of mitochondrial ROS generation is rather low and results in minimal damage, because mitochondria have a highly efficient antioxidant defence system able to scavenge a large number of the ROS produced (Venditti et al 2013). However, when in several circumstances, high rates of ROS production occur, a substantial part of oxidants may escape the scavenging systems.…”

Section: Mitochondrial Dysfunction and Oxidant Productionmentioning

confidence: 99%

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Skeletal muscle insulin resistance: role of mitochondria and other ROS sources

Meo

Iossa

Venditti

2017

Journal of Endocrinology

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207

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At present, obesity is one of the most important public health problems in the world because it causes several diseases and reduces life expectancy. Although it is well known that insulin resistance plays a pivotal role in the development of type 2 diabetes mellitus (the more frequent disease in obese people) the link between obesity and insulin resistance is yet a matter of debate. One of the most deleterious effects of obesity is the deposition of lipids in non-adipose tissues when the capacity of adipose tissue is overwhelmed. During the last decade, reduced mitochondrial function has been considered as an important contributor to 'toxic' lipid metabolite accumulation and consequent insulin resistance. More recent reports suggest that mitochondrial dysfunction is not an early event in the development of insulin resistance, but rather a complication of the hyperlipidemia-induced reactive oxygen species (ROS) production in skeletal muscle, which might promote mitochondrial alterations, lipid accumulation and inhibition of insulin action. Here, we review the literature dealing with the mitochondria-centered mechanisms proposed to explain the onset of obesity-linked IR in skeletal muscle. We conclude that the different pathways leading to insulin resistance may act synergistically because ROS production by mitochondria and other sources can result in mitochondrial dysfunction, which in turn can further increase ROS production leading to the establishment of a harmful positive feedback loop.

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Section: Mitochondria-derived H 2 Omentioning

confidence: 99%

Section: Mitochondrial Dysfunction and Oxidant Productionmentioning

confidence: 99%

Skeletal muscle insulin resistance: role of mitochondria and other ROS sources

Meo

Iossa

Venditti

2017

Journal of Endocrinology

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207

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“…A critical function of the mitochondria is to metabolize ROS generated by mitochondrial oxidative phosphorylation and other cellular sources (Venditti et al 2013). Since we have found evidence of mitochondrial dysfunction and elevated mPTP opening in sel-12 mutants ( Figure 6B), which enhances ROS production (Brookes et al 2004), we investigated ROS levels in sel-12 mutants.…”

Section: Sel-12 Deficiency Leads To Defects In Mitochondrial Functionmentioning

confidence: 99%

“…Similarly, MitoTracker CMXRos labeling is greatly reduced in all sel-12 mutants compared to wild-type animals ( Figure S5, A and B). These data indicate that the mitochondrial membrane potential in sel-12 mutants is reduced and suggest that mitochondrial function is abrogated.A critical function of the mitochondria is to metabolize ROS generated by mitochondrial oxidative phosphorylation and other cellular sources (Venditti et al 2013). Since we have found evidence of mitochondrial dysfunction and elevated mPTP opening in sel-12 mutants ( Figure 6B), which enhances ROS production (Brookes et al 2004), we investigated ROS levels in sel-12 mutants.…”

mentioning

confidence: 99%

A γ-Secretase Independent Role for Presenilin in Calcium Homeostasis Impacts Mitochondrial Function and Morphology in Caenorhabditis elegans

Sarasija¹,

Norman

2015

Genetics

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Mutations in the presenilin (PSEN) encoding genes (PSEN1 and PSEN2) occur in most early onset familial Alzheimer's Disease. Despite the identification of the involvement of PSEN in Alzheimer's Disease (AD) 20 years ago, the underlying role of PSEN in AD is not fully understood. To gain insight into the biological function of PSEN, we investigated the role of the PSEN homolog SEL-12 in Caenorhabditis elegans. Using genetic, cell biological, and pharmacological approaches, we demonstrate that mutations in sel-12 result in defects in calcium homeostasis, leading to mitochondrial dysfunction. Moreover, consistent with mammalian PSEN, we provide evidence that SEL-12 has a critical role in mediating endoplasmic reticulum (ER) calcium release. Furthermore, we found that in SEL-12-deficient animals, calcium transfer from the ER to the mitochondria leads to fragmentation of the mitochondria and mitochondrial dysfunction. Additionally, we show that the impact that SEL-12 has on mitochondrial function is independent of its role in Notch signaling, g-secretase proteolytic activity, and amyloid plaques. Our results reveal a critical role for PSEN in mediating mitochondrial function by regulating calcium transfer from the ER to the mitochondria.KEYWORDS Caenorhabditis elegans; calcium; endoplasmic reticulum; mitochondria; presenilin M ITOCHONDRIA are highly dynamic organelles that are responsible for a myriad of functions including ATP production, generation and metabolism of reactive oxygen species (ROS), and apoptosis (Detmer and Chan 2007). Thus cells, in particular muscle cells and neurons due to their highenergy demands, are extremely reliant on mitochondrial function. Mitochondria also play a critical role in calcium homeostasis by acting as a calcium buffer. Calcium, in turn, regulates mitochondrial morphology, activity, and movement. The relevance of mitochondria is highlighted by the fact that many neurodegenerative diseases, such as Parkinson's and Alzheimer's Disease (AD) are characterized by abnormal mitochondrial activity and morphology (Cali et al. 2012).Mutations in the genes encoding presenilins (PSENs), PSEN1 and PSEN2, are the most common cause of early onset familial Alzheimer's Disease (FAD). PSENs are 50-kDa multipass transmembrane proteins that reside predominantly on the endoplasmic reticulum (ER) (Bezprozvanny and Mattson 2008) and have been shown to be enriched in an ER subcompartment that is in contact with mitochondria (Area-Gomez et al. 2009). Although altered PSEN function has been known to have a role in AD for 20 years (Sherrington et al. 1995), the functional consequences of mutations in PSENs are controversial and not understood. The prevailing model for the pathogenesis of AD is the "amyloid hypothesis," which states that an increase in b amyloid (Ab) 42 peptide is the major cause of neuronal degradation in AD (Hardy and Selkoe 2002); support for this hypothesis stems from the accumulation of amyloid plaques in the brains of AD patients (Hardy 2006). In addition to the "amyloid hypot...

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“…Cell proliferation can facilitate a series of biochemical metabolic reactions, along with providing energy and materials for cell growth (Venditti et al 2013), such as chlorogenic acid contents, PPO, and cellulose content. Germin-like proteins can bind carbohydrates such as cellulose to participate in cell wall modification, and, on the other hand, can prevent cell growth through negative (Dunwell et al 2008;Caliskan et al 2004), which can be cleared by SOD and CAT (Liu et al 2014a).…”

Section: Mapk Signaling Pathway In Callus Proliferation During the Camentioning

confidence: 99%

Signaling pathway in development of Camellia oleifera nurse seedling grafting union

Feng

Yang

Chen

et al. 2017

Trees

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Key message The anatomical and physiological signaling pathways associated with successful scion-rootstock union in nurse seedling grafting of Camellia oleifera propagation are illustrated. Abstract Grafting, the successful union between scion and rootstock, has practical and biological importance. Nurse seedling grafting, as those practiced for Camellia oleifera, often results in high cell division activity and affinity, and is usually associated with significant rootstock and scion anatomical structures changes. However, a comprehensive explanation of signaling pathways, and how they affect graft union development, is still largely unknown. The present study investigates the union formation process in C. oleifera nurse seedling grafts and determines that it consists of six stages, namely, isolation layer formation, rootstock callus differentiation, scion callus differentiation, callus proliferation and connection, cambium differentiation and connection, and conducting tissue differentiation and connection, extending over a period of 35 days. Principal components analyses of the observed changes in physiology and protein expression identified three main factors contributing to the union formation process: cell proliferation, cell differentiation, and vascular bundle development. Further analysis showed that the regulation of the union formation process can be divided into two signaling pathways, namely, calcium and MAPK, which occur during vascular bundle development and cell proliferation and differentiation, respectively.

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Mitochondrial metabolism of reactive oxygen species

Cited by 268 publications

References 142 publications

Skeletal muscle insulin resistance: role of mitochondria and other ROS sources

Skeletal muscle insulin resistance: role of mitochondria and other ROS sources

A γ-Secretase Independent Role for Presenilin in Calcium Homeostasis Impacts Mitochondrial Function and Morphology in Caenorhabditis elegans

Signaling pathway in development of Camellia oleifera nurse seedling grafting union

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