Oxidative Stress and Mitochondrial Dysfunction in Cardiovascular Diseases

Hernández‐Reséndiz, Sauri; Buelna‐Chontal, Mabel; Correa, Francisco; Zazueta, Cecilia

doi:10.5772/35005

Cited by 4 publications

(2 citation statements)

References 164 publications

(141 reference statements)

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“…In addition, changes in energy metabolism can also increase oxidative stress in various metabolic disorders. The catabolism of substances such as glucose and fatty acids promotes the accumulation of reduced coenzymes (NADPH and FAD), which transfer their electrons to the respiratory chain [5], allowing the production of ATP by oxidative phosphorylation. The relative contribution of each of these substances as energy sources depends on their presence in the cell.…”

Section: Introductionmentioning

confidence: 99%

“…With increased peroxidation of membrane lipids also increases the viscosity of the lipid bilayer by reducing the degree of saturation of fatty acids. Excess lipoperoxides inactivate sulfhydryl groups of proteins -enzymes, inhibits oxidative phosphorylation, which leads to impaired membrane permeability [5,10]. One of the main end products of lipid peroxidation is malonic dialdehyde.…”

Section: Introductionmentioning

confidence: 99%

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Changes of lipid oxidation products content in ventricles of the rat heart as a result of electrolyte-steroid cardiomyopathy and correction of this condition

Sverediuk¹,

Pelykh²

2020

J Educ Health Sport

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Cardiovascular disease is one of the leading causes of death in the world. One of such pathologies is metabolic cardiomyopathy. This pathology includes dysfunction of amino acids, lipids, mitochondria, and disease of products accumulation. Conditions that can cause such changes include congenital and acquired hormone levels. A good example is the longterm use of dexamethasone for the treatment of patients with allergies or rheumatology diseases. Electrolyte disturbances are often a concomitant consequence of disease or lifestyle. They also contribute to heart damage under these conditions. Cell damage often begins with damage to cell lipid membranes and is accompanied by accumulation of lipid peroxidation products. The purpose of our study was to investigate diene, triene conjugates and thiobarbituric acid reactive substances levels in the animal ventriculs heart tissue of both sex in conditions of long-term action of dexamethasone and high concentration (4%) solution of 273 sodium chloride in drink water. L-carnitine, as an antioxidant and having the ability to influence to energetic metabolism, apoptosis and transcription of DNA may be a promising means for correction disorders. The experiment was performed with the use of 96 mature white nonlinear rats. Dexamethasone with long-term use promotes the accumulation of diene, triene conjugates and thiobarbituric acid reactive substances (malondialdehyde is main) in the ventricular myocardium of rats of both sexes, more in animals with high content (4%) of NaCl in drinking water, and in males, compared with females. L-carnitine has the ability to significantly offset the negative effects of dexamethasone on the content of lipoperoxidation products in the ventricular myocardium of rats of both sexes, including against the background of increased salt content in drinking water.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Changes of lipid oxidation products content in ventricles of the rat heart as a result of electrolyte-steroid cardiomyopathy and correction of this condition

Sverediuk¹,

Pelykh²

2020

J Educ Health Sport

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Mitochondrial Dysfunction and Oxidative Stress: Focusing on Cardiac Hypertrophy and Heart Failure

Katare

Nizami

Banerjee

2019

Oxidative Stress in Heart Diseases

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Targeting Mitochondria for Cardiac Protection

Hernández‐Reséndiz¹,

Buelna‐Chontal²,

Correa³

et al. 2013

CDT

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The critical role of mitochondria in cardiomyocyte survival and death has become an exciting field of research in cardiac biology. Indeed, it is accepted that mitochondrial dysfunction plays a crucial role in the pathogenesis of multiple cardiac diseases. Besides the obvious relevance of mitochondria in energy production, calcium homeostasis, and reactive oxygen species (ROS) production, new processes like mitochondrial fusion/fission, phosphorylation and nitrosylation modifications in mitochondrial proteins have been suggested to form part of a cast of key players in cardiac disease. This review describes currently studied drugs and compounds that target mitochondria in the scenario of cardiovascular diseases.

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Oxidative Stress and Mitochondrial Dysfunction in Cardiovascular Diseases

Cited by 4 publications

References 164 publications

Changes of lipid oxidation products content in ventricles of the rat heart as a result of electrolyte-steroid cardiomyopathy and correction of this condition

Changes of lipid oxidation products content in ventricles of the rat heart as a result of electrolyte-steroid cardiomyopathy and correction of this condition

Mitochondrial Dysfunction and Oxidative Stress: Focusing on Cardiac Hypertrophy and Heart Failure

Targeting Mitochondria for Cardiac Protection

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