scholarly journals The Role of Physical Exercise on Lipid Peroxidation in Diabetic Complications

10.5772/46182 ◽  
2012 ◽  
Author(s):  
Yaar Gl
Keyword(s):  
Lipid Peroxidation ◽  
Physical Exercise ◽  
Diabetic Complications

Pulmonary Lipid Peroxidation and Antioxidant Defenses During Exhaustive Physical Exercise: The Role of Vitamin E and Selenium

Nutrition ◽  
1998 ◽  
Vol 14 (5) ◽  
pp. 448-451 ◽  
Author(s):  
Konda Veera Reddy ◽  
Todeti Charles Kumar ◽  
Munagunura Prasad ◽  
Pallu Reddanna
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Physical Exercise ◽  
Antioxidant Defenses

Role of dyslipidaemia and lipid peroxidation in pregnancy induced hypertension

2015 ◽  
Vol 4 (3) ◽  
pp. 205 ◽  
Author(s):  
Shikha Saxena ◽  
KV Thimmaraju ◽  
PremC Srivastava ◽  
AyazK Mallick ◽  
Biswajit Das ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Pregnancy Induced Hypertension ◽  
Induced Hypertension ◽  
In Pregnancy

scholarly journals Physical Exercise and Cardiac Repair: The Potential Role of Nitric Oxide in Boosting Stem Cell Regenerative Biology

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1002
Author(s):  
Fabiola Marino ◽  
Mariangela Scalise ◽  
Eleonora Cianflone ◽  
Luca Salerno ◽  
Donato Cappetta ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Stem Cell ◽  
Physical Exercise ◽  
Cell Biology ◽  
Molecular Mechanisms ◽  
Heart Function ◽  
Stem Cell Biology ◽  
Myocardial Repair ◽  
Beneficial Effects

Over the years strong evidence has been accumulated showing that aerobic physical exercise exerts beneficial effects on the prevention and reduction of cardiovascular risk. Exercise in healthy subjects fosters physiological remodeling of the adult heart. Concurrently, physical training can significantly slow-down or even reverse the maladaptive pathologic cardiac remodeling in cardiac diseases, improving heart function. The underlying cellular and molecular mechanisms of the beneficial effects of physical exercise on the heart are still a subject of intensive study. Aerobic activity increases cardiovascular nitric oxide (NO) released mainly through nitric oxidase synthase 3 activity, promoting endothelium-dependent vasodilation, reducing vascular resistance, and lowering blood pressure. On the reverse, an imbalance between increasing free radical production and decreased NO generation characterizes pathologic remodeling, which has been termed the “nitroso-redox imbalance”. Besides these classical evidence on the role of NO in cardiac physiology and pathology, accumulating data show that NO regulate different aspects of stem cell biology, including survival, proliferation, migration, differentiation, and secretion of pro-regenerative factors. Concurrently, it has been shown that physical exercise generates physiological remodeling while antagonizes pathologic remodeling also by fostering cardiac regeneration, including new cardiomyocyte formation. This review is therefore focused on the possible link between physical exercise, NO, and stem cell biology in the cardiac regenerative/reparative response to physiological or pathological load. Cellular and molecular mechanisms that generate an exercise-induced cardioprotective phenotype are discussed in regards with myocardial repair and regeneration. Aerobic training can benefit cells implicated in cardiovascular homeostasis and response to damage by NO-mediated pathways that protect stem cells in the hostile environment, enhance their activation and differentiation and, in turn, translate to more efficient myocardial tissue regeneration. Moreover, stem cell preconditioning by and/or local potentiation of NO signaling can be envisioned as promising approaches to improve the post-transplantation stem cell survival and the efficacy of cardiac stem cell therapy.

scholarly journals Insights in the Role of Lipids, Oxidative Stress and Inflammation in Rheumatoid Arthritis Unveiled by New Trends in Lipidomic Investigations

Antioxidants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 45
Author(s):  
Helena Beatriz Ferreira ◽  
Tânia Melo ◽  
Artur Paiva ◽  
Maria do Rosário Domingues
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Lipid Profile ◽  
Inflammatory Responses ◽  
Molecular Level ◽  
Lipid Hydroperoxides ◽  
Lipid Species ◽  
Inflammatory Autoimmune Disease

Rheumatoid arthritis (RA) is a highly debilitating chronic inflammatory autoimmune disease most prevalent in women. The true etiology of this disease is complex, multifactorial, and is yet to be completely elucidated. However, oxidative stress and lipid peroxidation are associated with the development and pathogenesis of RA. In this case, oxidative damage biomarkers have been found to be significantly higher in RA patients, associated with the oxidation of biomolecules and the stimulation of inflammatory responses. Lipid peroxidation is one of the major consequences of oxidative stress, with the formation of deleterious lipid hydroperoxides and electrophilic reactive lipid species. Additionally, changes in the lipoprotein profile seem to be common in RA, contributing to cardiovascular diseases and a chronic inflammatory environment. Nevertheless, changes in the lipid profile at a molecular level in RA are still poorly understood. Therefore, the goal of this review was to gather all the information regarding lipid alterations in RA analyzed by mass spectrometry. Studies on the variation of lipid profile in RA using lipidomics showed that fatty acid and phospholipid metabolisms, especially in phosphatidylcholine and phosphatidylethanolamine, are affected in this disease. These promising results could lead to the discovery of new diagnostic lipid biomarkers for early diagnosis of RA and targets for personalized medicine.

Ferroptosis and cardiovascular disease: role of free radical-induced lipid peroxidation

2021 ◽  
pp. 1-11
Author(s):  
Xin Chen ◽  
Xuan Li ◽  
Xiaodong Xu ◽  
Luxiao Li ◽  
Ningning Liang ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Lipid Peroxidation ◽  
Free Radical

Modulation of collagen synthesis by growth factors: The role of ascorbate-stimulated lipid peroxidation

1991 ◽  
Vol 289 (1) ◽  
pp. 6-11 ◽  
Author(s):  
Jeffrey C. Geesin ◽  
Laura J. Hendricks ◽  
Joel S. Gordon ◽  
Richard A. Berg
Keyword(s):  
Lipid Peroxidation ◽  
Growth Factors ◽  
Collagen Synthesis

scholarly journals Role of vitamin E in glutathione-induced oxidant stress: methemoglobin, lipid peroxidation, and hemolysis

1977 ◽  
Vol 18 (5) ◽  
pp. 635-644
Author(s):  
N R Brownlee ◽  
J J Huttner ◽  
R V Panganamala ◽  
D G Cornwell
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Oxidant Stress

scholarly journals 4-Hydroxynonenal Contributes to Fibroblast Senescence in Skin Photoaging Evoked by UV-A Radiation

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 365 ◽  
Author(s):  
Audrey Swiader ◽  
Caroline Camaré ◽  
Paul Guerby ◽  
Robert Salvayre ◽  
Anne Negre-Salvayre
Keyword(s):  
Lipid Peroxidation ◽  
Dermal Fibroblasts ◽  
Connective Tissues ◽  
Hairless Mice ◽  
Cultured Fibroblasts ◽  
Γh2ax Foci ◽  
Skin Photoaging ◽  
Actinic Elastosis

Solar ultraviolet A (UV-A) radiation promotes a huge variety of damages on connective tissues and dermal fibroblasts, including cellular senescence, a major contributor of skin photoaging. The mechanisms of skin photoaging evoked by UV-A partly involve the generation of reactive oxygen species and lipid peroxidation. We previously reported that 4-hydroxynonenal (HNE), a lipid peroxidation-derived aldehyde, forms adducts on elastin in the skins of UV-A irradiated hairless mice, possibly contributing to actinic elastosis. In the present study, we investigated whether and how HNE promotes fibroblast senescence in skin photoaging. Dermal fibroblasts of skins from UV-A-exposed hairless mice exhibited an increased number of γH2AX foci characteristic of cell senescence, together with an accumulation of HNE adducts partly colocalizing with the cytoskeletal protein vimentin. Murine fibroblasts exposed to UV-A radiation (two cycles of 15 J/cm2), or HNE (30 µM, 4 h), exhibited senescence patterns characterized by an increased γH2AX foci expression, an accumulation of acetylated proteins, and a decreased expression of the sirtuin SIRT1. HNE adducts were detected on vimentin in cultured fibroblasts irradiated by UV-A or incubated with HNE. The HNE scavenger carnosine prevented both vimentin modification and fibroblast senescence evoked by HNE in vitro and in the skins of UV-A-exposed mice. Altogether, these data emphasize the role of HNE and lipid peroxidation-derived aldehydes in fibroblast senescence, and confirm the protective effect of carnosine in skin photoaging.

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