Site of Mitochondrial Reactive Oxygen Species Production in Skeletal Muscle of Chronic Obstructive Pulmonary Disease and Its Relationship with Exercise Oxidative Stress

Puente-Maestu, Luís; Tejedor, Alberto; Lázaro, Alberto; Miguel, Javier de; Álvarez-Sala, L.; González-Aragoneses, Federico; Simón, Carlos; Agustí, Àlvar

doi:10.1165/rcmb.2011-0382oc

Cited by 47 publications

(60 citation statements)

References 38 publications

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“…As downregulation of free flavin concentrations in leaves by RfBP induces the production of the H 2 O 2 signal and its translocation from the apoplast to the cytosol [11], the signal may act in turn to promote flowering [61,62]. Alternatively, H 2 O 2 may be generated through electron leakage from the mitochondrial electron transport chain due to shortage of FMN and FAD, which serve as redox centers in the chain [65–68]. …”

Section: Discussionmentioning

confidence: 99%

Downregulation of leaf flavin content induces early flowering and photoperiod gene expression in Arabidopsis

Zhu

Tian

et al. 2014

BMC Plant Biol

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BackgroundRiboflavin is the precursor of flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), essential cofactors for many metabolic enzymes that catalyze a variety of biochemical reactions. Previously we showed that free flavin (riboflavin, FMN, and FAD) concentrations were decreased in leaves of transgenic Arabidopsis plants expressing a turtle riboflavin-binding protein (RfBP). Here, we report that flavin downregulation by RfBP induces the early flowering phenotype and enhances expression of floral promoting photoperiod genes.ResultsEarly flowering was a serendipitous phenomenon and was prudently characterized as a constant phenotype of RfBP-expressing transgenic Arabidopsis plants in both long days and short days. The phenotype was eliminated when leaf free flavins were brought back to the steady-state levels either by the RfBP gene silencing and consequently nullified production of the RfBP protein, or by external riboflavin feeding treatment. RfBP-induced early flowering was correlated with enhanced expression of floral promoting photoperiod genes and the florigen gene FT in leaves but not related to genes assigned to vernalization, autonomous, and gibberellin pathways, which provide flowering regulation mechanisms alternative to the photoperiod. RfBP-induced early flowering was further correlated with increased expression of the FD gene encoding bZIP transcription factor FD essential for flowering time control and the floral meristem identity gene AP1 in the shoot apex. By contrast, the expression of FT and photoperiod genes in leaves and the expression of FD and AP1 in the shoot apex were no longer enhanced when the RfBP gene was silenced, RfBP protein production canceled, and flavin concentrations were elevated to the steady-state levels inside plant leaves.ConclusionsToken together, our results provide circumstantial evidence that downregulation of leaf flavin content by RfBP induces early flowering and coincident enhancements of genes that promote flowering through the photoperiod pathway.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-014-0237-z) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Downregulation of leaf flavin content induces early flowering and photoperiod gene expression in Arabidopsis

Zhu

Tian

et al. 2014

BMC Plant Biol

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“…Mitochondria are also a major endogenous source of reactive oxygen species, either under normal (Rigoulet et al, 2011) or pathological (Puente-Maestu et al, 2012;Reale et al, 2012) conditions. Macromolecular oxidative damage in mitochondria induces a decline in the efficiency of oxidative phosphorylation, and result in the induction of the mitochondrial permeability transition and in the release of pro-apototic factors that trigger apoptosis (Pereira et al, 2009a).…”

Section: Introductionmentioning

confidence: 99%

Resveratrol affects differently rat liver and brain mitochondrial bioenergetics and oxidative stress in vitro: Investigation of the role of gender

Moreira

Silva

Santos

et al. 2013

Food and Chemical Toxicology

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a b s t r a c tResveratrol (3,5,4 0 -trihydroxy-trans stilbene) is commonly recognized by its antioxidant properties. Despite its beneficial qualities, the toxic effects of this natural compound are still unknown. Since mitochondria are essential to support the energy-dependent regulation of several cell functions, the objective of this study was to evaluate resveratrol effects on rat brain and liver mitochondrial fractions from male and females regarding oxidative stress and bioenergetics. No basal differences were observed between mitochondrial fractions from males and females, except in liver mitochondria, the generation of H 2 O 2 by the respiratory chain is lower for female preparations. Resveratrol inhibited lipid peroxidation in preparations from both genders and organs. Furthermore, brain mitochondria in both gender groups appeared susceptible to resveratrol as seen by a decrease in state 3 respiration and alterations in mitochondrial membrane potential fluctuations during ADP phosphorylation. As opposed, liver mitochondria were less affected by resveratrol. Our data also demonstrates that resveratrol inhibits complex I activity in all mitochondrial preparations. The results suggest that brain mitochondria appear to be more susceptible to resveratrol effects, and gender appears to play a minor role. It remains to be determined if resveratrol effects on brain mitochondria contribute to deterioration of mitochondrial function or instead to mediate hormesis-mediated events.

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“…In the last decade, it has been proposed that oxidative stress is a major contributor to muscle dysfunction in COPD patients, especially in those with a severe disease [14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30]. Several investigations have consistently demonstrated that under resting and exercise conditions, COPD patients exhibit higher levels of lipid peroxidation, oxidized glutathione, and protein carbonylation and nitration in their blood and both respiratory and limb muscles [14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30].…”

Section: Protein Carbonylation In Skeletal Muscle Dysfunction and mentioning

confidence: 99%

“…Oxidative stress, defined as the imbalance between oxidants and antioxidants in favor of the former (Figure 1), was shown to be a key contributing factor to the respiratory and limb muscle dysfunction of patients with COPD [14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30], muscles of animals with experimental cancer cachexia [31,32,33], and sepsis [34,35,36,37,38,39,40], and in elderly subjects [41,42,43]. High levels of oxidants may alter the function and structure of key cellular molecules such as proteins, DNA, and lipids, eventually leading to cellular injury and cell death (Figure 2) Moreover, protein oxidation including protein carbonylation was demonstrated to modify enzyme activity and DNA binding of transcription factors, while also rendering proteins more prone to proteolytic degradation (Figure 2) [44,45,46,47].…”

Section: Introductionmentioning

confidence: 99%

Role of Protein Carbonylation in Skeletal Muscle Mass Loss Associated with Chronic Conditions

Barreiro

2016

Proteomes

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Muscle dysfunction, characterized by a reductive remodeling of muscle fibers, is a common systemic manifestation in highly prevalent conditions such as chronic heart failure (CHF), chronic obstructive pulmonary disease (COPD), cancer cachexia, and critically ill patients. Skeletal muscle dysfunction and impaired muscle mass may predict morbidity and mortality in patients with chronic diseases, regardless of the underlying condition. High levels of oxidants may alter function and structure of key cellular molecules such as proteins, DNA, and lipids, leading to cellular injury and death. Protein oxidation including protein carbonylation was demonstrated to modify enzyme activity and DNA binding of transcription factors, while also rendering proteins more prone to proteolytic degradation. Given the relevance of protein oxidation in the pathophysiology of many chronic conditions and their comorbidities, the current review focuses on the analysis of different studies in which the biological and clinical significance of the modifications induced by reactive carbonyls on proteins have been explored so far in skeletal muscles of patients and animal models of chronic conditions such as COPD, disuse muscle atrophy, cancer cachexia, sepsis, and physiological aging. Future research will elucidate the specific impact and sites of reactive carbonyls on muscle protein content and function in human conditions.

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Site of Mitochondrial Reactive Oxygen Species Production in Skeletal Muscle of Chronic Obstructive Pulmonary Disease and Its Relationship with Exercise Oxidative Stress

Cited by 47 publications

References 38 publications

Downregulation of leaf flavin content induces early flowering and photoperiod gene expression in Arabidopsis

Downregulation of leaf flavin content induces early flowering and photoperiod gene expression in Arabidopsis

Resveratrol affects differently rat liver and brain mitochondrial bioenergetics and oxidative stress in vitro: Investigation of the role of gender

Role of Protein Carbonylation in Skeletal Muscle Mass Loss Associated with Chronic Conditions

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