The effect of chronic alcohol consumption on mitochondrial DNA mutagenesis in human blood

Wurmb‐Schwark, Nicole von; Ringleb, A.; Schwark, Thorsten; Broese, Thomas; Weirich, Steffen; Schlaefke, Detlef; Wegener, R.; Oehmichen, M.

doi:10.1016/j.mrfmmm.2007.07.003

Cited by 17 publications

(13 citation statements)

References 35 publications

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“…Mansouri et al [66] found in the liver tissue and white blood cells from patients with ALD a significantly decreased mtDNA copy number and an increased level of mtDNA deletion, similar to the data obtained by Tsuchishima et al [67] who also found an acquired mutation of mtDNA, at least in the encoding ATPase region, that may be reversed by stopping drinking. In addition, von Wurmb-Schwark et al [68] investigated mitochondrial mutagenesis in patients with a chronic and moderate alcoholic disease, and found a relative amount of 4,977 bp deleted in mtDNA in alcoholics compared to controls.…”

Section: Effects Of Alcohol On Mitochondrial Biomoleculesmentioning

confidence: 99%

Cellular and Mitochondrial Effects of Alcohol Consumption

Manzo‐Ávalos

Saavedra‐Molina

2010

IJERPH

219

155

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Alcohol dependence is correlated with a wide spectrum of medical, psychological, behavioral, and social problems. Acute alcohol abuse causes damage to and functional impairment of several organs affecting protein, carbohydrate, and fat metabolism. Mitochondria participate with the conversion of acetaldehyde into acetate and the generation of increased amounts of NADH. Prenatal exposure to ethanol during fetal development induces a wide spectrum of adverse effects in offspring, such as neurologic abnormalities and pre-and post-natal growth retardation. Antioxidant effects have been described due to that alcoholic beverages contain different compounds, such as polyphenols as well as resveratrol. This review analyzes diverse topics on the alcohol consumption effects in several human organs and demonstrates the direct participation of mitochondria as potential target of compounds that can be used to prevent therapies for alcohol abusers.

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Section: Effects Of Alcohol On Mitochondrial Biomoleculesmentioning

confidence: 99%

Cellular and Mitochondrial Effects of Alcohol Consumption

Manzo‐Ávalos

Saavedra‐Molina

2010

IJERPH

219

155

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“…Due to limited study size, we may not exclude minor associations. The level of mtDNA-CN is determined by heredity, in addition to the influence on one's lifestyle habits such as physical activity, smoking, and alcohol consumption [21][22][23][24][25]35]. Poor self-rated health is also associated with low levels of mtDNA-CN [19].…”

Section: Discussionmentioning

confidence: 99%

Mitochondria-DNA copy-number and incident venous thromboembolism among middle-aged women: a population-based cohort study

Nymberg

Memon

Sundquist

et al. 2021

J Thromb Thrombolysis

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Venous thromboembolism (VTE) is the third most common cardiovascular disease. Low amount of mitochondrial DNA copy number (mtDNA-CN) has been associated with arterial cardiovascular disease (CVD) and reflects mitochondrial dysfunctions. However, whether mtDNA-CN is associated with VTE has not been determined. To examine the association between mtDNA-CN and incident VTE among middle-aged women. 6917 women aged 50–64 years, followed for 20 years in the Women’s Health In the Lund Area (WHILA) study. DNA samples for mtDNA quantification were available from 2521 women. Quantification of mtDNA-CN was performed using a well-optimized droplet digital PCR method. After exclusions of women with anticoagulant treatment, women living in nursing homes, and women who were diagnosed with cancer, stroke, VTE, or coronary heart disease at baseline, a cohort of 2117 women remained for analysis. Cox regression was used to analyze the relationship between mtDNA-CN and time to VTE (hazard ratio = HR). In total, 87 women were diagnosed with VTE during follow-up, corresponding to an incidence rate of 2.8 per 1000 person-years. Neither crude nor adjusted HR for mtDNA-CN were significantly associated with incident VTE. A sensitivity analysis with inclusion of excluded women did not change the results. MtDNA-CN was not significantly associated with VTE. The present study suggests that mtDNA-CN, reflecting mitochondrial dysfunction, should not be considered a biomarker that plays a major role for developing VTE. However, due to limited study size we may not exclude minor associations.

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“…As there was no significant difference between AZT-exposed and AZT-unexposed newborns (p = 0.55), we suggest that our findings could be explained by the influence of external factors other than AZT. It is well known that mitochondrial mutagenesis depends on many different factors such as alcohol [38], [50] or nicotine [51]. While these stressors are known to damage mitochondrial DNA there are also findings on protective factors, e. g. green tea [52] or other dietary components.…”

Section: Discussionmentioning

confidence: 99%

“…Nuclear DNA was quantified as previously described [38]. Briefly, a 98 bp fragment of the telomerase gene (forward primer: 5′-GGC ACA CGT GGC TTT TCG-3′, reverse primer: 5′-GGT GAA CCT CGT AAG TTT ATG CAA-3′) was used to specifically amplify nuclear DNA.…”

Section: Methodsmentioning

confidence: 99%

Zidovudine Exposure in HIV-1 Infected Tanzanian Women Increases Mitochondrial DNA Levels in Placenta and Umbilical Cords

et al. 2012

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BackgroundZidovudine (AZT) constitutes part of the recommended regimens for prevention and treatment of HIV-1 infection. At the same time, AZT as well as HIV-1 infection itself may induce mitochondrial damage. In this study, we analyzed the impact of prenatal AZT-exposure on mitochondrial alterations in HIV-infected women and their infants.MethodsMitochondrial DNA (mtDNA) levels in placentas of HIV-1 infected Tanzanian women with and without prenatal AZT exposure, and in the umbilical cords of their AZT-exposed/unexposed infants were quantified using real-time PCR. Furthermore, we checked for the most common mitochondrial deletion in humans, the 4977 base pair deletion (dmtDNA4977) as a marker for mitochondrial stress.Results83 women fulfilled the inclusion criteria. 30 women had been treated with AZT (median duration 56 days; IQR 43–70 days) while 53 women had not taken AZT during pregnancy. Baseline maternal characteristics in the two groups were similar. The median mtDNA levels in placentas and umbilical cords of women (311 copies/cell) and infants (190 copies/cell) exposed to AZT were significantly higher than in AZT-unexposed women (187 copies/cell; p = 0.021) and infants (127 copies/cell; p = 0.037). The dmtDNA4977 was found in placentas of one woman of each group and in 3 umbilical cords of AZT-unexposed infants but not in umbilical cords of AZT-exposed infants.ConclusionsAntenatal AZT intake did not increase the risk for the common mitochondrial deletion dmtDNA4977. Our data suggests that AZT exposure elevates mtDNA levels in placentas and umbilical cords possibly by positively influencing the course of maternal HIV-1 infection.

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The effect of chronic alcohol consumption on mitochondrial DNA mutagenesis in human blood

Cited by 17 publications

References 35 publications

Cellular and Mitochondrial Effects of Alcohol Consumption

Cellular and Mitochondrial Effects of Alcohol Consumption

Mitochondria-DNA copy-number and incident venous thromboembolism among middle-aged women: a population-based cohort study

Zidovudine Exposure in HIV-1 Infected Tanzanian Women Increases Mitochondrial DNA Levels in Placenta and Umbilical Cords

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