Abstract

During the recent years, alteration of mitochondrial function has been associated with an increasing numbers of phenotypes (Wallace 1992; Munnich et al. 1996). Although alteration of mtDNA is only rarely identified in patients, mtDNA has been claimed to be at the origin of aging (Wallace et al. 1995), several degenerative disorders (Wallace et al. 1995), and more recently male infertility (Cummins et al. 1994; St. Johns et al. 1997). Thus, some authors have suggested that some forms of infertility may be explained as premature aging of the testis (Cummins et al. 1994). Frank and Hurst (1996) have also hypothesized that a germ-line mutation of the mtDNA with severe effects on males but only mild effects on females might increase to a relatively high frequency because natural selection of mitochondria occurs only in females. Thus, the strictly maternal inheritance of mtDNA could create an important male-female asymmetry in the expected severity of mitochondrial disease. However, althrough in plants there is a direct role of mtDNA mutations in the phenotype of cytoplasmic male sterility (Hanson 1991), in mammals the evidence is not so convincing.

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