Oxidative damage to mitochondrial DNA in atrial muscle of patients with atrial fibrillation

Increased oxidative DNA damage, 8-hydroxydeoxy- guanosine, in human pterygium

“…[21][22][23] As a reliable biomarker of oxidative DNA damage, higher levels of 8-OHdG have been observed in the lungs of cigarette smokers, 24 the liver of patients with chronic hepatitis, 25 the breast tissue of benign and malignant tumors, 26 the trabecular meshwork of glaucoma patients, 27 the renalcell carcinoma, 28 the urine of patients with dystrophinopathy, 29 the leucocytes of patients with Leber's hereditary optic neuropathy 30 and patients on chronic hemodialysis, 31 and heart mitochondrial DNA of patients with atrial fibrillation. 32 To our knowledge, this is the first study to explore the increase of 8-OHdG content in pterygium tissue.…”

Increased oxidative DNA damage, lipid peroxidation, and reactive oxygen species in cultured orbital fibroblasts from patients with Graves’ ophthalmopathy: evidence that oxidative stress has a role in this disorder

“…23 Total DNA from orbital tissues and cultured orbital fibroblasts was isolated by phenol/ chloroform extraction with butylated hydroxyl toluene (freshly prepared in ethanol) as previously described. 24 After precipitating with ice-cold 75% ethanol, we air-dried and dissolved isolated DNA in distilled water. An aliquot of 50 mg DNA was then first digested with 6 U of nuclease P1 (Roche, Mannheim, Germany) in a solution of 200 mM sodium acetate (pH 5.3) at 371C for 2 h, followed by reaction with 2 U of calf intestine alkaline phosphatase (Roche) at 371C for 2 h. The hydrolysate was filtered through the Millipore Ultra free C3LGC (Millipore, Billerica, MA, USA) at 10 000 g for 10 min to remove enzymes and other macromolecules.…”

Oxidative Mitochondrial DNA Damage and Deletion in Hepatocytes of Rejecting Liver Allografts in Rats: Role of TNF-α *

“…The oxidation of deoxyguanosine to 8-hydroxy-2Ј-deoxyguanosine (8-OHdG) and subsequent mutations of mtDNA are reported to be involved in the pathogenesis of many chronic conditions. [9][10][11][12][13][14] We hypothesized that severe oxidative mtDNA damage in hepatocytes occurs acutely by the release of inflammatory cytokines such as TNF-␣ during acute rejection, and that this damage is not repaired completely, leading to deletions that contribute to liver failure after transplantation. To test this hypothesis, we first measured the levels of 8-OHdG in mtDNA, the frequency of 4,834-bp deletions of mtDNA, and the levels of TNF-␣ in rats receiving syngeneic liver grafts, grafts destined to rejected, and grafts accepted despite a major histocompatibility barrier.…”