A Critical Balance Between Oxidative Stress and Antioxidant Defense in Cardiovascular System Under Hyperglycemia: A Summary of Experimental Studies

Ayaz, Murat; Turan, Belma

doi:10.1007/978-1-4614-9317-4_7

Cited by 2 publications

(2 citation statements)

References 99 publications

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“…As discussed above, a 10 kDa fragment of OPA1 keeps cristae junctions tightly closed, preventing the release of cytochrome c and apoptosis. Dysfunctional mitochondria have been frequently found to have disruption and loss of cristae, such as reported with ischemic heart failure (32;109), with reduction in OPA1 expression (31;152), in Huntington’s disease (36), and with reduction in Crif1, as occurs with Alzheimer’s disease (9;23). …”

Section: Mitochondrial Structure and Mitochondrial Traffickingmentioning

confidence: 99%

Mitochondrial Dynamics and Heart Failure

Knowlton

Liu

2015

Comprehensive Physiology

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Mitochondrial dynamics, fission and fusion, were first identified in yeast with investigation in heart cells beginning only in the last 5–7 years. In the ensuing time it has become evident that these processes are not only required for healthy mitochondria, but also, that derangement of these processes contributes to disease. The fission and fusion proteins have a number of functions beyond the mitochondrial dynamics. Many of these functions are related to their membrane activities, such as apoptosis. However, other functions involve other areas of the mitochondria, such as OPA1’s role in maintaining cristae structure and preventing cytochrome c leak, and its essential (at least a 10 kDa fragment of OPA1) role in mtDNA replication. In heart disease, changes in expression of these important proteins can have detrimental effects on mitochondrial and cellular function.

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Section: Mitochondrial Structure and Mitochondrial Traffickingmentioning

confidence: 99%

Mitochondrial Dynamics and Heart Failure

Knowlton

Liu

2015

Comprehensive Physiology

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“…Majority of the researches dealing with the OS have concluded that it is the primarily cause and/or the major contributor to the etiology of severe pathologies with serious public health implications such as DM and its complications [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Experimental Diabetic Neuropathy: Electrophysiological Changes & Antioxidant Supplementations

Ayaz¹,

Yanardag²,

Ugurlutan³

2015

J. Adv. Neurosci. Res.

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Diabetic neuropathy is the one of the serious secondary complications of diabetes mellitus in which an alteration or a damage in nerve cells is observed. The nerve disorders can be developed at any time, but the possibility of the development increases with the longer duration of diabetes. The damage can be occurred in the sensory, motor, and autonomic nervous system, therefore the damage is observed in the innervated organs and systems. As a result, diabetic neuropathy is the most common cause of non-traumatic amputations and autonomic failure. In their lifetime, diabetic patients with diabetic neuropathy have a 15% incidence of undergoing one or more amputations. Due to the similarities of the presented pathologies to the human diseases and its the easiness, diabetes induced animal models are widely used in studies. Since diabetes and therefore diabetic neuropathy is a worldwide problem, it is necessary to examine the effects of diabetes mellitus on the neural system. The recorded compound action potentials revealed that diabetes is the reason of the significant increase in time to peak, rheobase and chronaxie values. Furthermore, the maximum depolarization, area, kinetics and the conduction velocities of both the fast and slow nerve fibers were found to be decreased. In addition to the decline of the conduction velocities, a shift from faster fibers to the slower ones was observed. Since the oxidant agents are unavoidable, the aim should be to minimize it as much as possible. For minimization, the antioxidant agents are crucial. It is also shown that beyond the inhibition of the oxidation agents, some of them also restore the damaged nerves. Currently to avoid diabetic neuropathy it is suggested to keep the glucose levels as close as possible to the normal values. If it is necessary pain therapy can be used to minimize the pain. The promising results of the animal studies show that the treatment strategies should be renewed by including the antioxidants to the daily diet to the diabetic patients.

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A Critical Balance Between Oxidative Stress and Antioxidant Defense in Cardiovascular System Under Hyperglycemia: A Summary of Experimental Studies

Cited by 2 publications

References 99 publications

Mitochondrial Dynamics and Heart Failure

Mitochondrial Dynamics and Heart Failure

Experimental Diabetic Neuropathy: Electrophysiological Changes & Antioxidant Supplementations

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