Mitochondrial DNA mutation and depletion are associated with decline of fertility and motility of human sperm

被引:0
作者
Wei, YH [1 ]
Kao, SH
机构
[1] Natl Yang Ming Univ, Dept Biochem, Taipei 112, Taiwan
[2] Natl Yang Ming Univ, Ctr Cellular & Mol Biol, Taipei 112, Taiwan
关键词
mitochondria; DNA mutation; sperm motility; infertility;
D O I
暂无
中图分类号
Q95 [动物学];
学科分类号
071002 ;
摘要
Sperm motility is one of the most important determinants of male fertility. In this review, we discuss recent findings that mutation and depletion of mitochondrial DNA (mtDNA) are associated with poor motility and diminished fertility in human sperm. The mtDNA mutations were identified and characterized by polymerase chain reaction (PCR) techniques and DNA sequencing, and the copy number of mtDNA was determined as the ratio between the amount of mtDNA and that of nuclear DNA in sperm. By use of these molecular techniques we first established that the common 4977-bp deletion and 2 novel deletions of 7345 bp and 7599 bp of mtDNA occur more frequently and in higher proportions in spermatozoa with poorer motility and lower fertility. On the other hand, we found that the copy number of mtDNA is lower for sperm with poorer motility. Scores of several motility parameters of sperm assessed by a computer-assisted semen analyzer are positively correlated with the copy number of mtDNA. Moreover, with a transmission electron microscope we examined spermatozoa with low levels of mtDNA from infertile patients. We found that more than 70% of spermatozoa exhibited normal helicoidal morphology of mitochondria packed in the midpiece. These results indicate that depletion of mtDNA in these spermatozoa is not due to a decrease in the number of mitochondria but is a result of the paucity of the mitochondrial genome per se. On the basis of these recent findings, we suggest that mutation and depletion of mtDNA in spermatozoa may play an important role in the pathophysiology of some male infertility.
引用
收藏
页码:1 / 12
页数:12
相关论文
共 96 条
  • [1] REACTIVE OXYGEN SPECIES AND HUMAN SPERMATOZOA - ANALYSIS OF THE CELLULAR MECHANISMS INVOLVED IN LUMINOL-DEPENDENT AND LUCIGENIN-DEPENDENT CHEMILUMINESCENCE
    AITKEN, RJ
    BUCKINGHAM, DW
    WEST, KM
    [J]. JOURNAL OF CELLULAR PHYSIOLOGY, 1992, 151 (03) : 466 - 477
  • [2] AITKEN RJ, 1989, BIOL REPROD, V40, P183
  • [3] MITOCHONDRIAL GENE-EXPRESSION IN MALE GERM-CELLS OF THE MOUSE
    ALCIVAR, AA
    HAKE, LE
    MILLETTE, CF
    TRASLER, JM
    HECHT, NB
    [J]. DEVELOPMENTAL BIOLOGY, 1989, 135 (02) : 263 - 271
  • [4] SEQUENCE AND ORGANIZATION OF THE HUMAN MITOCHONDRIAL GENOME
    ANDERSON, S
    BANKIER, AT
    BARRELL, BG
    DEBRUIJN, MHL
    COULSON, AR
    DROUIN, J
    EPERON, IC
    NIERLICH, DP
    ROE, BA
    SANGER, F
    SCHREIER, PH
    SMITH, AJH
    STADEN, R
    YOUNG, IG
    [J]. NATURE, 1981, 290 (5806) : 457 - 465
  • [5] BIOGENESIS OF MITOCHONDRIA
    ATTARDI, G
    SCHATZ, G
    [J]. ANNUAL REVIEW OF CELL BIOLOGY, 1988, 4 : 289 - 333
  • [6] REGULATION OF MITOCHONDRIAL GENE-EXPRESSION IN MAMMALIAN-CELLS
    ATTARDI, G
    CHOMYN, A
    KING, MP
    KRUSE, B
    POLOSA, PL
    MURDTER, NN
    [J]. BIOCHEMICAL SOCIETY TRANSACTIONS, 1990, 18 (04) : 509 - 513
  • [7] MITOCHONDRIAL DIABETES REVISITED
    BALLINGER, SW
    SHOFFNER, JM
    GEBHART, S
    KOONTZ, DA
    WALLACE, DC
    [J]. NATURE GENETICS, 1994, 7 (04) : 458 - 459
  • [8] Oxidative decay of DNA
    Beckman, KB
    Ames, BN
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (32) : 19633 - 19636
  • [9] Relationship of genotype to phenotype in fibroblast-derived transmitochondrial cell lines carrying the 3243 mutation associated with the MELAS encephalomyopathy: Shift towards mutant genotype and role of mtDNA copy number
    Bentlage, HACM
    Attardi, G
    [J]. HUMAN MOLECULAR GENETICS, 1996, 5 (02) : 197 - 205
  • [10] METABOLIC-REGULATION IN MAMMALIAN SPERM - MITOCHONDRIAL VOLUME DETERMINES SPERM LENGTH AND FLAGELLAR BEAT FREQUENCY
    CARDULLO, RA
    BALTZ, JM
    [J]. CELL MOTILITY AND THE CYTOSKELETON, 1991, 19 (03): : 180 - 188