Mitochondrial response to oxidative and nitrosative stress in early stages of diabetes

Noriega‐Cisneros, Ruth; Cortés‐Rojo, Christian; Manzo‐Ávalos, Salvador; Clemente‐Guerrero, Mónica; Calderón-Cortés, Elizabeth; Salgado‐Garciglia, Rafael; Montoya‐Pérez, Rocío; Boldogh, István; Saavedra‐Molina, Alfredo

doi:10.1016/j.mito.2013.05.012

Cited by 18 publications

(13 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Definitely less investigated than OS, the NS-related endpoints, as 3-nitrotyrosine and NO bioactivity, have been reported to be associated with other redox-related anomalies in some diseases, such as diabetes [127, 128], bladder cancer [191], autism [169], schizophrenia [183], and Sjøgren's syndrome [271]. Albeit relatively unexplored, the subject of nitrosative damage deserves higher attention in further studies, as NS-related endpoints might provide precious insights in the pathogenesis of several OS/MDF-related disorders.…”

Section: Discussionmentioning

confidence: 99%

“…Diabetic patients displayed excess oxidation of proteins, lipids, and DNA, that is, increased levels of 15-F2t-iso-prostaglandin and 4-HNE, as products of lipid oxidation, and advanced oxidation protein products, advanced glycation end products (AGEs), excess oxidative DNA damage (8-OHdG), upregulated NADPH oxidase, Trx and HSP70, and decreased GSH : GSSG ratio [125–128]. Downregulation of Complex I and/or IV, and of SOD-2 point to MDF occurrence in diabetic patients [129–133].…”

Section: Ageing and Ageing-related Degenerative Disordersmentioning

confidence: 99%

See 1 more Smart Citation

Oxidative Stress and Mitochondrial Dysfunction across Broad-Ranging Pathologies: Toward Mitochondria-Targeted Clinical Strategies

Pagano

Talamanca

Castello

et al. 2014

Oxidative Medicine and Cellular Longevity

115

View full text Add to dashboard Cite

Beyond the disorders recognized as mitochondrial diseases, abnormalities in function and/or ultrastructure of mitochondria have been reported in several unrelated pathologies. These encompass ageing, malformations, and a number of genetic or acquired diseases, as diabetes and cardiologic, haematologic, organ-specific (e.g., eye or liver), neurologic and psychiatric, autoimmune, and dermatologic disorders. The mechanistic grounds for mitochondrial dysfunction (MDF) along with the occurrence of oxidative stress (OS) have been investigated within the pathogenesis of individual disorders or in groups of interrelated disorders. We attempt to review broad-ranging pathologies that involve mitochondrial-specific deficiencies or rely on cytosol-derived prooxidant states or on autoimmune-induced mitochondrial damage. The established knowledge in these subjects warrants studies aimed at elucidating several open questions that are highlighted in the present review. The relevance of OS and MDF in different pathologies may establish the grounds for chemoprevention trials aimed at compensating OS/MDF by means of antioxidants and mitochondrial nutrients.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Ageing and Ageing-related Degenerative Disordersmentioning

confidence: 99%

Oxidative Stress and Mitochondrial Dysfunction across Broad-Ranging Pathologies: Toward Mitochondria-Targeted Clinical Strategies

Pagano

Talamanca

Castello

et al. 2014

Oxidative Medicine and Cellular Longevity

115

View full text Add to dashboard Cite

show abstract

“…In addition, almost all the existing reports used young rats (3 months of age) as biological models (Noriega-Cisneros et al 2013). For this reason and because of the high incidence of diabetes in the elderly and the lack of studies on oxidative and nitrosative stress in rat kidney mitochondria, we were interested in evaluating these processes.…”

Section: Discussionmentioning

confidence: 99%

Effects of diabetes on oxidative and nitrosative stress in kidney mitochondria from aged rats

Pérez-Gallardo

Noriega‐Cisneros

Esquivel‐Gutiérrez

et al. 2014

J Bioenerg Biomembr

Self Cite

View full text Add to dashboard Cite

Diabetes mellitus (DM) is characterized by chronic hyperglycemia resulting from defects in the secretion and/or action of insulin. Diabetic nephropathy (DN) develops in diabetic patients and is characterized by a progressive deterioration of renal function. The mitochondrial electron transport chain (ETC) produces most of the reactive oxygen species (ROS) that are involved in diabetic nephropathy. Due to the high incidence of DM in the elderly, the aim of this study was to evaluate oxidative and nitrosative stress in kidney mitochondria from aged rats. We evaluated lipid peroxidation (LPO), nitric oxide (NO(•)) production, S-nitrosylation profiles, glutathione levels, and glutathione reductase and aconitase activities under streptozotocin (STZ)-induced experimental diabetes in kidney mitochondria from aged rats. The results showed an increase in LPO, NO(•) production, and S-nitrosylated proteins in rats with STZ-induced diabetes. A decrease in glutathione (GSH) levels and glutathione reductase (GR) and aconitase activities in the rats that received the STZ-induced diabetes treatment was also observed, when compared with the age-related controls. The data suggest that oxidative and nitrosative stresses promote mitochondrial oxidative dysfunction in the more advanced age rat kidney in STZ-induced diabetes.

show abstract

“…Exposure of glucolipotoxicity to pancreatic β -cells promotes oxidative stress and mitochondrial dysfunction with cytochrome c release, caspase activation, and apoptosis [ 141 ]. Mitochondrial dysfunction leads to the opening of the mitochondrial membrane permeability transition pore, release of cytochrome c, and subsequent caspase activation [ 27 , 78 , 80 , 82 , 127 , 141 , 142 ].…”

Section: Diabetes Mellitus Oxidative Stress and Programmed Cell mentioning

confidence: 99%

New Insights for Oxidative Stress and Diabetes Mellitus

Maiese

2015

Oxidative Medicine and Cellular Longevity

197

123

View full text Add to dashboard Cite

The release of reactive oxygen species (ROS) and the generation of oxidative stress are considered critical factors for the pathogenesis of diabetes mellitus (DM), a disorder that is growing in prevalence and results in significant economic loss. New therapeutic directions that address the detrimental effects of oxidative stress may be especially warranted to develop effective care for the millions of individuals that currently suffer from DM. The mechanistic target of rapamycin (mTOR), silent mating type information regulation 2 homolog 1 (S. cerevisiae) (SIRT1), and Wnt1 inducible signaling pathway protein 1 (WISP1) are especially justified to be considered treatment targets for DM since these pathways can address the complex relationship between stem cells, trophic factors, impaired glucose tolerance, programmed cell death pathways of apoptosis and autophagy, tissue remodeling, cellular energy homeostasis, and vascular biology that greatly impact the biology and disease progression of DM. The translation and development of these pathways into viable therapies will require detailed understanding of their proliferative nature to maximize clinical efficacy and limit adverse effects that have the potential to lead to unintended consequences.

show abstract

Mitochondrial response to oxidative and nitrosative stress in early stages of diabetes

Cited by 18 publications

References 47 publications

Oxidative Stress and Mitochondrial Dysfunction across Broad-Ranging Pathologies: Toward Mitochondria-Targeted Clinical Strategies

Oxidative Stress and Mitochondrial Dysfunction across Broad-Ranging Pathologies: Toward Mitochondria-Targeted Clinical Strategies

Effects of diabetes on oxidative and nitrosative stress in kidney mitochondria from aged rats

New Insights for Oxidative Stress and Diabetes Mellitus

Contact Info

Product

Resources

About