Abstract
BackgroundAlthough not fully understood, oxidative stress has been implicated in the pathogenesis of different autoimmune diseases such as systemic sclerosis. Accumulating evidence indicates that oxidative stress can induce mitochondrial DNA (mtDNA) damage and variations in mtDNA copy number (mtDNAcn). ObjectiveThe aim of this study was to explore mtDNAcn and oxidative DNA damage byproducts in peripheral blood of patients with systemic sclerosis and healthy controls. MethodsForty six patients with systemic sclerosis and forty nine healthy subjects were studied. Quantitative real-time PCR used to measure the relative mtDNAcn and the oxidative damage (oxidized purines) of each sample. ResultsThe mean mtDNAcn was lower in patients with systemic sclerosis than in healthy controls whereas the degree of mtDNA damage was significantly higher in cases as compared to controls. Moreover, there was a negative correlation between mtDNAcn and oxidative DNA damage. Study limitationsThe lack of simultaneous analysis and quantification of DNA oxidative damage markers in serum or urine of patients with systemic sclerosis and healthy controls. ConclusionThese data suggest that alteration in mtDNAcn and increased oxidative DNA damage may be involved in the pathogenesis of systemic sclerosis.
Highlights
Systemic Sclerosis (SSc) is a rare chronic disease of connective tissue characterized by a vasculopathy and fibrosis in the skin and various internal organs.[1,2] The exact cause of disease is unknown, but its occurrence can be influenced by a complicated interplay of genetic, epigenetic and environmental factors.[3]
To study the existence of oxidative damage, the presence of oxidized purine bases that are FPG-sensitive sites were determined in DNA of peripheral blood samples from patients with SSc and normal controls
No association was found between oxidative DNA damage and age, sex, and disease duration
Summary
Systemic Sclerosis (SSc) is a rare chronic disease of connective tissue characterized by a vasculopathy and fibrosis in the skin and various internal organs.[1,2] The exact cause of disease is unknown, but its occurrence can be influenced by a complicated interplay of genetic, epigenetic and environmental factors.[3]. Mitochondria are the major endogenous source of ROS. They have their own genome [mitochondrial DNA (mtDNA)] and are indispensable organelles for normal cellular physiology. MtDNA is prone to oxidative stress damage because of its high exposure to the ROS that are produced by mitochondria.[7]. Objective: The aim of this study was to explore mtDNAcn and oxidative DNA damage byproducts in peripheral blood of patients with systemic sclerosis and healthy controls. Results: The mean mtDNAcn was lower in patients with systemic sclerosis than in healthy controls whereas the degree of mtDNA damage was significantly higher in cases as compared to controls. Study limitations: The lack of simultaneous analysis and quantification of DNA oxidative damage markers in serum or urine of patients with systemic sclerosis and healthy controls
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