Large-scale mitochondrial DNA deletions in skeletal muscle of patients with end-stage renal disease

Lim, Paik‐Seong; Cheng, Ya-Ming; Wei, Yau‐Huei

doi:10.1016/s0891-5849(00)00334-8

Cited by 50 publications

(58 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Generally, age-dependent oxidative mtDNA damage has been detected previously in liver (Yen et al 1991), testis (Lee et al 1994), muscle (Lee et al 1994;Lim et al 2000), heart (Katsumata et al 1994), and lung (Lee et al 1999) tissues of healthy elderly subjects. Lim et al (Lim et al 2000) clearly demonstrated that the frequency of oxidative mtDNA damage in the human skeletal muscle of end-stage renal disease (ESRD) patients was higher than in age-matched non--ESRD subjects and the increase in oxidative stress may lead to premature oxidative damage of the mitochondrial genome in diseased tissues. Suzuki et al (Suzuki et al 1999) reported that both the mtDNA deletion and the 8-OHdG levels correlated not only with age, but also with the duration of disease.…”

Section: Discussionmentioning

confidence: 90%

Increased salivary level of 8-hydroxydeoxyguanosine is a marker of premature oxidative mitochondrial DNA damage in gingival tissue of patients with periodontitis

Çanakçı

Tatar

et al. 2009

Arch. Immunol. Ther. Exp.

View full text Add to dashboard Cite

Introduction: Oxidative stress may contribute to the pathogenesis of periodontitis. However, the detailed molecular mechanism remains unclear. Both 8-hydroxydeoxyguanosine (8-OHdG) and mitochondrial DNA (mtDNA) deletion have been reported as early oxidative DNA damage markers. In this study, 8-OHdG levels in saliva and mtDNA deletions in gingival tissue of patients with chronic periodontitis (CP) were evaluated. Materials and Methods: Gingival tissue and whole saliva samples were collected from 32 patients with CP and 32 healthy control subjects. To determine the clinical condition of each subject, the plaque index, gingival index, clinical attachment level (CAL), and probing depth (PD) were measured. Using the ELISA and polymerase chain reaction methods, the salivary 8-OHdG levels and the 7.4-kbp and 5-kbp mtDNA deletions were examined. Results: The 5-kbp mtDNA deletion was detected in 20 of the 32 periodontitis patients (62.5%), but was not detected in the healthy controls. The mean value of 8-OHdG in the saliva of the periodontitis patients with deleted mtDNA was significantly higher than in the patients with non-deleted mtDNA (p<0.01). Also, significant correlation was found between the occurrence of the 5-kbp mtDNA deletion and salivary 8-OHdG levels (p<0.01). Similar correlations were detected between salivary 8-OHdG levels and age, PD, and CAL (p<0.01, p<0.05). Conclusion: Increased oxidative stress may lead to premature oxidative DNA damage in the gingival tissue of periodontitis patients and the salivary 8-OHdG level may signify premature oxidative mtDNA damage in diseased gingival tissue.

show abstract

Section: Discussionmentioning

confidence: 90%

Increased salivary level of 8-hydroxydeoxyguanosine is a marker of premature oxidative mitochondrial DNA damage in gingival tissue of patients with periodontitis

Çanakçı

Tatar

et al. 2009

Arch. Immunol. Ther. Exp.

View full text Add to dashboard Cite

show abstract

“…The 4977 bp deletion and other deletion events are induced by external factors like UV radiation (Berneburg et al, 2004), ionising radiation (Prithivirajsingh et al, 2004) deuterium oxide (Berneburg et al, 1999) or by pathologic conditions like chronic hypoxia/reperfusion (Merril et al, 1996;Bagenholm et al, 1998), ischemia (CorralDebrinski et al, 1992b) or end-stage renal disease (Lim et al, 2000). All of these factors are associated with an increased generation of free radicals.…”

Section: Discussionmentioning

confidence: 99%

The 4977bp deletion of mitochondrial DNA in human skeletal muscle, heart and different areas of the brain: A useful biomarker or more?

Meißner

Bruse

Mohamed

et al. 2008

Experimental Gerontology

144

119

View full text Add to dashboard Cite

It has been suggested that deletions of mitochondrial DNA (mtDNA) are important players with regard to the ageing process. Since the early 1990s, the 4977 bp deletion has been studied in various tissues, especially in postmitotic tissues with high energy demand. Unfortunately, some of these studies included less than 10 subjects, so the aim of our study was to quantify reliable the deletion amount in nine different regions of human brain, heart and skeletal muscle in a cohort of 92 individuals. The basal ganglia contain the highest deletion amounts with values up to 2.93% and differences in deletion levels between early adolescence and older ages were up to three orders of magnitude. Values in frontal lobe were on average an order of magnitude lower, but lowest in cerebellar tissue where the amount was on average only 5 x 10 -3 of the basal ganglia. The deletion started to accumulate in iliopsoas muscle early in the fourth decade of life with values between 0.00019% and 0.0035% and was highest in a 102 year-old woman with 0.14%. In comparison to skeletal muscle, the overall abundance in heart muscle of the left ventricle was only one third. The best linear logarithmic correlation between amount of the deletion and age was found in substanta nigra with r=0.87 (p<0.0005) followed by anterior wall of the left ventricle (r=0.82; p<0.0005). With regard to mitochondrial DNA damage, we propose to use the 4977 bp deletion as an ideal biomarker to discriminate between physiological ageing and accelerated ageing. The biological meaning of mitochondrial deletions in the process of ageing is under discussion, but there is experimental evidence that large-scale deletions impair the oxidative phosphorylation in single cells and sensitize these cells to undergo apoptosis.

show abstract

“…[20] The retention of potentially toxic substances, such as organic compounds in uremic plasma, may be responsible for clinical toxicity, as these compounds tend to generate organic free radicals during oxidative metabolism. [19] A reduced activity of antioxidant enzyme superoxide dismutase and an increase of total malondialdehyde (i.e., the product of lipid peroxidation in erythrocytes of chronic renal failure patients undergoing continuous ambulatory peritoneal dialysis) have been demonstrated. [22,23] The imbalance between antioxidation and oxidation occurs early in the course of CKD, gradually increasing as the disease progresses, and is exacerbated by dialysis.…”

Section: Discussionmentioning

confidence: 99%

“…[25] This is due to mtDNA's proximity to free radicals on the inner mitochondrial membrane, the lack of histone protection, and poor DNA repair mechanisms. [9,12] Previously, a study that analyzed mtDNA extracted of skeletal muscle [19] and in hair follicles [15] showed the accumulation of mtDNA deletion 4977bp in patients with ESRD. Lim et al [19] demonstrated 4977bp deletion in 77% of patients in end stage renal disease, compared with only 22% of age-paired normal controls.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Prevalence of 4977bp Deletion in Mitochondrial DNA from Patients with Chronic Kidney Disease Receiving Conservative Treatment or Hemodialysis in Southern Brazil

et al. 2008

View full text Add to dashboard Cite

Large-scale mitochondrial DNA deletions in skeletal muscle of patients with end-stage renal disease

Cited by 50 publications

References 44 publications

Increased salivary level of 8-hydroxydeoxyguanosine is a marker of premature oxidative mitochondrial DNA damage in gingival tissue of patients with periodontitis

Increased salivary level of 8-hydroxydeoxyguanosine is a marker of premature oxidative mitochondrial DNA damage in gingival tissue of patients with periodontitis

The 4977bp deletion of mitochondrial DNA in human skeletal muscle, heart and different areas of the brain: A useful biomarker or more?

Prevalence of 4977bp Deletion in Mitochondrial DNA from Patients with Chronic Kidney Disease Receiving Conservative Treatment or Hemodialysis in Southern Brazil

Contact Info

Product

Resources

About