Reproductive system toxicity spermatogenesis

In addition to their endocrine disrupting properties, it must be appreciated that many of the chemicals in question possess more general toxic properties, which may be potentiated by metabolism by the organism. Several PAHs, PCBs and PCDDs are carcinogenic, while certain phthalate esters can enhance the excretion of zinc, potentially leading to zinc deficiency. Zinc, an essential element, plays a vital role in spermatogenesis and mature T-cell production. Deficiency may result in abnormalities of the male reproductive system, depletion of spermatogenesis and suppression of the immune system. 

The direct effect of inhalation exposure to 1,2-dibromoethane on spermatogenesis in animals has not been studied. Nonetheless, the available data from animal studies indicate that the male reproductive system in rats is affected by exposure to 1,2-dibromoethane at high doses. In all studies discussed below, however, rats had high mortality associated with chemical toxicity and/or chemically-induced neoplasia. It is therefore difficult to attribute effects on the reproductive organs to... 

Two major systems have been identified as toxicity targets for 1,3-DNB the red blood cell and the male reproductive system (see Section 2.2.2). In the red blood cell, 1,3-DNB induces formation of methemoglobin leading to cyanosis (Blackburn et al. 1988 Linder et al. 1988, 1990 Reader et al. 1991). In the male reproductive system, 1,3-DNB causes disruption of spermatogenesis resulting in hypospermia, poor sperm quality, and infertility (Blackburn et al. 1988 Hess et al. 1988 Linder et al. 1988). Whether adverse hematological and reproductive effects are caused by the same mechanism of action remains unresolved. 

In a continuous breeding study in mice reproductive and fertility parameters were not affected by gavage administration of ONCB even in the presence of systemic toxicity (significant methemoglobinemia and increased spleen and liver weights). Decreased spermatogenesis has been reported after inhalation exposure in rats and mice. 

Alkaloids are active bioagents in animal tissues. There is clear scientific evidence of this. Crawford and Kocan" " have tested the toxicity of steroidal alkaloids from the potato Solanum tuberosum), such as a-chaconine, a-solanine, solanidine and solasodine, and Veratrum alkaloid, jervine on fish. The results of Crawford and Kocan s research proved that rainbow trout exhibited a toxic response to chaconine, solasidine and solanine, while medaka only did so to chaconine and solanine. Embryo mortality was observed as an effect of toxicity in both species. Many other alkaloids are known to disturb or cause disorder in animal reproductive systems. For example, gossypol from cotton-seed oil is known as a clear reducer of spermatogenesis and premature abortion of the embryo. 

Endocrine and Reproductive Effects. Because the male and female reproductive organs are under complex neuroendocrine and hormonal control, any toxicant that alters any of these processes can affect the reproductive system (see Chapters 17 and 20). In addition metals can act directly on the sex organs. Cadmium is known to produce testicular injury after acute exposure, and lead accumulation in the testes is associated with testicular degeneration, inhibition of spermatogenesis, and Leydig-cell atrophy. 

Studies in animals have shown that sulfur mustard may induee developmental and reproductive effects (reviewed in NRC, 1999, 2003). Acute exposures resulting in systemic uptake may have effects on reproductive organs, including inhibition of spermatogenesis. Fetal anomalies were observed in tests with rats given sulfur mustard during gestation but only at maternally toxic doses. 

Intermediate-Duration. No human data on the toxicity of di- -butyl phthalate following intermediate-duration exposure were identified. Systemic, reproductive, and developmental effects have been observed in animals following oral exposure. The liver appears to be the most sensitive systemic target in rats and mice exposed to di- -butyl phthalate in the diet for 13 weeks (NTP 1995 Schilling et al. 1992). The reproductive effects consist of testicular atrophy with decreases in spermatogenesis (Murakami et al. 

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