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Defective Repair Of Oxidative Damage In The Mitochondrial DNA Of A ... - Cancerres Aacrjournals
Get Defective Repair Of Oxidative Damage In The Mitochondrial DNA Of A ... - Cancerres Aacrjournals
Rma Wesley J. Driggers, Valentina I. Grishko, Susan P. LeDoux, and Glenn L. Wilson2 Department of Simriurul anil Cellular Biology. University of South Alabama. Mobile. Alabama JftfiHK ABSTRACT Recent evidence has linked mitochondria! DNA (mtl)NA) damage to several disease processes, including cancer and aging. An important source of such damage is reactive oxygen species. These molecules can be generated endogenous!) via the electron transport system or may arise from a host of exogenous sour.
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Except for mutations, deletion of mtDNA is another important factor that causes diseases, including Alzheimer's disease (AD), myopathy, Kearns-Sayre syndrome (KSS), Pearson syndrome, and human colorectal cancer [29].
Base excision repair (BER) of 8-oxo-7,8-dihydroguanine (8-oxoG). Oxidative DNA damage is repaired via several repair intermediates by base excision repair (BER).
Abnormalities in mtDNA may affect all organs of the body, but cause symptoms primarily in tissues that are dependent on high energy production. Deficient mtDNA maintenance contributes to conditions as diverse as normal aging, neurodegenerative disease, diabetes, cardiovascular disease, and cancer.
Mitochondrial disease can cause a vast array of health concerns, including fatigue, weakness, metabolic strokes, seizures, cardiomyopathy, arrhythmias, developmental or cognitive disabilities, diabetes mellitus, impairment of hearing, vision, growth, liver, gastrointestinal, or kidney function, and more.
BASE EXCISION REPAIR IS A BONA FIDE REPAIR PATHWAY IN THE MITOCHONDRIA. BER is involved in the repair of various types of DNA damage affecting the nuclear genome, including small non-bulky adducts, oxidized bases, as well as deaminated and hydrolyzed bases.
Oxidative stress is characterized by the overproduction of reactive oxygen species, which can induce mitochondrial DNA mutations, damage the mitochondrial respiratory chain, alter membrane permeability, and influence Ca2+ homeostasis and mitochondrial defense systems.
mtDNA damage has been frequently shown to be involved in initiation and progression of several diseases including various types of neurodegenerative disorders, cancer, stroke, heart-diseases, and diabetes.
Conditions caused by variants in mitochondrial DNA often involve multiple organ systems. The effects of these conditions are most pronounced in organs and tissues that require a lot of energy (such as the heart, brain, and muscles).
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