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Znečištění životního prostředí a endokrinně podmíněná neplodnost samců ryb
GOLSHAN, Mahdi
There are a large number of natural and synthetic environmental contaminants (ECs) known or suspected to mimic or interfere with male reproductive endocrine functions. Our current knowledge is largely addressed to ECs that induce oestrogen-induced feminization. However, there are several ECs that cause alternations in androgen production similar to oestrogenic ECs, but they do not induce vitellogenin-induced feminization. The mechanisms of action of these chemicals are still unclear due to the fact that androgen receptor (AR) functions in androgen-mediated male reproductive physiology are largely unknown. In the present study, we examined the effects of vinclozolin (VZ) (100, 400 and 800 ?g/L) and di-(2-ethylhexyl)-phthalate (DEHP) (1, 10 and 100 ?g/L) on male reproductive performance in goldfish following 30 days of exposure. Since both VZ and DEHP act as agonists and/or antagonists of hormonal receptors, estrogen receptor subtypes (er) and androgen receptor (ar) mRNA levels were studied. For studying their oestrogenic activity, one group of goldfish were exposed to 17?-estradiol (E2). In DEHP treated goldfish, sperm production, motility and velocity were decreased at 1, 100 and 10 ?g/L, respectively. Our previous study has shown that sperm production, motility and velocity were decreased in goldfish exposed to 800 ?g/L VZ. These suggest that DEHP and VZ are capable of interfering with spermatogenesis and sperm maturation. In E2 treated goldfish, none of the males produced sperm, indicating E2-suppressed spermatogenesis. Similar to E2 treated goldfish, 11-KT levels were decreased in goldfish exposed to ?10 and ?1 ?g/L DEHP at day 15 and 30, respectively. In VZ treated goldfish, 11-KT levels were decreased in goldfish exposed to 800 ?g/L VZ following 7 d, but increased in goldfish exposed to 100 ?g/L VZ following 30 d of exposure. E2 levels remained unchanged and increased in DEHP and E2 treated goldfish, respectively. In VZ treated goldfish, LH levels were increased at 100 ?g/L. In contrast, LH levels were decreased in DEHP and E2 treated goldfish following 15 d of exposure. There were also positive relationships between LH and 11-KT levels suggesting that inhibition or stimulation of androgen production were mediated by DEHP- or VZ-induced alternations in pituitary function. In VZ treated goldfish, gnrh3 mRNA levels were decreased following 7 d of exposure and increased at low dose following 30 d of exposure. kiss1 or kiss2 mRNA levels were also increased in VZ treated goldfish, while gpr54 mRNA remained unchanged. In DEHP treated goldfish, gnrh3, kiss1 and its receptor (gpr54) mRNA levels did not change during the period of exposure. In E2 treated goldfish, gnrh3 mRNA levels were decreased at day 7, but kiss1 and gpr54 mRNA levels were increased at day 30 of exposure. These results suggest that, in contrast to DEHP, VZ effects on pituitary and testicular functions are mediated by disruption of hypothalamus function and upstream neuroendocrine regulators. The brain ar and testicular lhr mRNA levels were changed in VZ and E2 treated goldfish depending on dose and period of treatment, however they remained unchanged in DEHP treated goldfish. These differences suggest that DEHP may act through an independent hormonal receptor pathway, while VZ acts through a receptor pathway. vtg, er and cyp19a1b remained unchanged in DEHP and VZ treated goldfish but increased in E2 treated goldfish. These indicate that neither VZ nor DEHP acts as oestrogenic compound to impair male fertility. In conclusion, DEHP and VZ reduced sperm quality in goldfish due to stimulation and inhibition of 11-KT production which were mediated by alternations in pituitary function to produce LH or by disruption of the transfer of Cholesterol to steroidogenesis. Upstream neuroendocrine regulators (gnrh3 and kiss-1/gpr54) were disrupted in VZ treated goldfish. Taken together, VZ and DEHP differentially act on brain and testis to impair fertility endpoints.
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