Male Reproductive Effects

Mammalian male reproductive function can be affected through a direct effect on the testis, resulting in decreased or altered sperm production, through impairment of the accessory sex gland secretions, and/or indirectly through the neuroendocrine system, causing hormonal imbalance. Adverse effects on male fertility include altered genetic material of sperm, contributing to altered spermatogenesis, pregnancy loss, or genetic disease in offspring. Common endpoints for assessment of male reproductive function include size of testis, semen quality, secretory function of the prostate and seminal vesicles, reproductive endocrine function, impotence or reduced libido, and fertility. When evaluating reproductive effects of a certain metal on human males, one must take into account possible influences of concomitant exposures to other toxic and essential metals; these may act addi-tively, synergistically, or antagonistically. Moreover, the influence of age and lifestyle factors particularly stress, smoking habits, and alcohol consumption must be considered. In addition, certain toxic metals such as lead and cadmium are pervasive in the human environment and accumulate in the human body over a lifetime; biomarkers of lead and cadmium exposure commonly correlate with age, smoking habits, and/ or alcohol consumption. Quantitative assessment of the body status of certain essential elements, especially zinc and selenium, is relevant, because they can reduce or protect from the adverse male reproductive effects of several metals.

Recent evidence indicates that the human male reproductive capacity has deteriorated considerably during the past five decades. In industrialized countries, a substantial number of couples seek in vitro fertilization (IVF) or intracytoplasmic sperm injection (ICSI) because of poor semen quality.

Furthermore, large differences in mean sperm concentration between countries, and between different locations within a country, have been observed. The possible role of environmental and lifestyle factors in contributing to these trends and differences has been suggested and is widely debated, because consideration must be given to many potentially confounding factors. Because the underlying causes are likely to be multiple and complex, it is important to identify the factors contributing to the deterioration of human male fertility to prevent further decline in fertility potential.

The human male has a relatively low fertility potential compared with other mammals. For example, the number of sperm per human ejaculate is typically only twofold to fourfold higher than the number at which fertility is significantly reduced, whereas the number of sperm in rat, rabbit, or bull ejaculate is many times (up to 1400-fold) the number that will produce maximum fertility (Working, 1988). Human males have markedly smaller relative testis size and the lowest rate of daily sperm production per gram of testis, by a factor of more than 3, compared with mouse, rat, or monkey. The percentages of progressively motile sperm and morphologically normal sperm in human semen are also considerably lower than in experimental animals (Working, 1988). Certain rodent species and strains, commonly used in experimental studies, seem to be resistant to the male reproductive toxicity of lead (Apostoli et al., 1998) and cadmium (Gunn et al., 1965; Liu et al., 2001). The human male may be more susceptible than the rat to metal toxicity, possibly because of poorer efficacy of the antioxidant defense system and greater vulnerability to oxidative damage to sperm DNA and sulfhydryl (-SH) groups required for the maintenance of sperm maturation and motility. Because of differences among species in reproductive endpoints and in the route, level, and duration of metal exposure, the experimental animal data may be useful for estimates of allowable human exposure.

Although experimental animal and in vitro studies have indicated adverse reproductive effects of high doses of many metals and beneficial or protective effects of some essential metals (particularly zinc, selenium, and magnesium), the internal metal dose was often not measured, and relatively few studies have evaluated the effects of long-term moderate oral exposure. For most metals, data relevant to humans are scanty and are usually limited by inadequate controls and adjustments for the influence of potentially confounding variables.

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