Influence of microsurgical varicocelectomy on human sperm mitochondrial DNA copy number: a pilot study

Gabriel, Maria San; Chan, Sam W.; Alhathal, Naif; Chen, Junjian Z.; Zini, Armand

doi:10.1007/s10815-012-9785-z

Cited by 37 publications

(21 citation statements)

References 60 publications

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“…Indeed, mtDNA may serve as a sensitive surrogate for precise quantification of oxidative DNA damage locally in diseased tissues and systemically in circulating blood of cancer patients. We have developed a comprehensive strategy to measure multiple mtDNA end-points in circulating lymphocytes to study systemic stress in clinical investigations [47] and to study the influence of microsurgical varicocelectomy on human sperm mtDNA copy number [48]. Finally, this method also has the potential to quantify specific oxidative base lesions accumulated in supercoiled mtDNA when coupled with lesion-specific repair enzymes.…”

Section: A New Paradigm Of Oxidative Injury and Its Implicationsmentioning

confidence: 99%

Oxidative Stress Induces Mitochondrial DNA Damage and Cytotoxicity through Independent Mechanisms in Human Cancer Cells

Han

Chen

2013

BioMed Research International

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Intrinsic oxidative stress through increased production of reactive oxygen species (ROS) is associated with carcinogenic transformation, cell toxicity, and DNA damage. Mitochondrial DNA (mtDNA) is a natural surrogate to oxidative DNA damage. MtDNA damage results in the loss of its supercoiled structure and is readily detectable using a novel, supercoiling-sensitive real-time PCR method. Our studies have demonstrated that mtDNA damage, as measured by DNA strand breaks and copy number depletion, is very sensitive to exogenous H2O2 but independent of endogenous ROS production in both prostate cancer and normal cells. In contrast, aggressive prostate cancer cells exhibit a more than 10-fold sensitivity to H2O2-induced cell toxicity than normal cells, and a cascade of secondary ROS production is a critical determinant to the differential response. We propose a new paradigm to account for different mechanisms governing cellular oxidative stress, cell toxicity, and DNA damage with important ramifications in devising new techniques and strategies in prostate cancer prevention and treatment.

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Section: A New Paradigm Of Oxidative Injury and Its Implicationsmentioning

confidence: 99%

Oxidative Stress Induces Mitochondrial DNA Damage and Cytotoxicity through Independent Mechanisms in Human Cancer Cells

Han

Chen

2013

BioMed Research International

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“…mtDNA is maintained at different copy numbers in different tissues, the two extremes of this spectrum being mammalian erythrocytes and sperm which have no mtDNA and ~5 copies of mtDNA per cell [19], respectively, and oocytes, which may contain >500,000 copies [20]. In Drosophila, mtDNA is eliminated from sperm in the male genital tract prior to fertilization, so that fertilizing sperm may contain no mtDNA at all [21].…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial DNA: A disposable genome?

Shokolenko

Alexeyev

2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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In mammalian cells, mitochondria are the only organelles besides the nucleus that house genomic DNA. The mammalian mitochondrial genome is represented by prokaryotic-type, circular, highly compacted DNA molecules. Today, more than a half-century after their discovery, the biology of these small and redundant molecules remains much less understood than that of their nuclear counterparts. One peculiarity of the mitochondrial genome that emerged in recent years is its disposable nature, as evidenced by cells abandoning a fraction of their mitochondrial DNA (mtDNA) in response to various stimuli with little or no physiological consequence. Here, we review some recent developments in the field of mtDNA biology and discuss emerging questions on the disposability and indispensability of mtDNA.

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“…5 Blumer et al proposed that varicocele leads to a reduction in mitochondrial activity 6,7 , which may also be coupled with a modification in the copy number of mitochondrial DNA (mtDNA). 8 Mitochondrial functionality was assessed by the diaminobenzidine (DAB) assay which categorized the rate of mitochondrial activity as grades I-IV. The group with varicocele presented a greater percentage of sperm with inactive mitochondria (class III or most inactive mitochondria) and a lower percentage of sperm with active mitochondria (class I).…”

Section: Introductionmentioning

confidence: 99%

Varicocele Negatively Affects Sperm Mitochondrial Respiration

Ferramosca

Albani

Coppola

et al. 2015

Urology

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Influence of microsurgical varicocelectomy on human sperm mitochondrial DNA copy number: a pilot study

Abstract: These findings support the concept that correction of a varicocele can improve spermatogenesis and sperm function, as mitochondrial DNA copy number has been suggested to reflect the efficiency of spermatogenesis and has been inversely related to sperm motility.

Cited by 37 publications

References 60 publications

Oxidative Stress Induces Mitochondrial DNA Damage and Cytotoxicity through Independent Mechanisms in Human Cancer Cells

Oxidative Stress Induces Mitochondrial DNA Damage and Cytotoxicity through Independent Mechanisms in Human Cancer Cells

Mitochondrial DNA: A disposable genome?

Varicocele Negatively Affects Sperm Mitochondrial Respiration

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