Morphological effects of the catechol estrogens on rat epididymal epithelia

Seegers, J.C.; Nieuwoudt, Luan; Joubert, W. S.

doi:10.1016/0960-0760(91)90083-h

Cited by 6 publications

(5 citation statements)

References 9 publications

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“…Mammalian adult male germ cells and supporting gonadal tissues are highly susceptible to the toxic effects of ROS (9)(10)(11)(12), and catechol estrogens seem to be involved in some of these toxic effects (13,14). Catechol estrogens and/or oxidative damage resulting from maternal sources could also contribute to testicular carcinogenesis in utero.…”

Section: Introductionmentioning

confidence: 99%

Risk of Testicular Germ Cell Cancer in Relation to Variation in Maternal and Offspring CytochromeP450 Genes Involved in Catechol Estrogen Metabolism

Starr

Chen

Doody

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

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The incidence of testicular germ cell carcinoma (TGCC) is highest among men ages 20 to 44 years. Exposure to relatively high circulating maternal estrogen levels during pregnancy has long been suspected as being a risk factor for TGCC. Catechol (hydroxylated) estrogens have carcinogenic potential, thought to arise from reactive catechol intermediates with enhanced capability of forming mutation-inducing DNA adducts. Polymorphisms in maternal or offspring genes encoding estrogenmetabolizing enzymes may influence prenatal catechol estrogen levels and could therefore be biomarkers of TGCC risk. We conducted a population-based, case-parent triad study to evaluate TGCC risk in relation to maternal and/or offspring polymorphisms in CYP1A2, CYP1B1, CYP3A4, and CYP3A5. We identified 18-to 44-year-old men diagnosed with invasive TGCC from 1999 to 2004 through a population-based cancer registry in Washington State and recruited cases and their parents (110 case-parent triads, 50 case-parent dyads). Maternal or offspring carriage of CYP1A2 À163A was associated with reduced risk of TGCC [maternal heterozygote relative risk (RR), 0.6; 95% confidence interval (95% CI), 0.2-1.7; offspring heterozygote RR, 0.7; 95% CI, 0.3-1.5)]. Maternal CYP1B1 48Gly homozygosity was associated with a 2.7-fold increased risk of TGCC (95% CI, 0.9-7.9), with little evidence that Leu 432 Val or Asn 453Ser genotypes were related to risk. Men were also at increased risk of TGCC if they carried the CYP3A4 À392G (RR, 7.0; 95% CI, 1.6-31) or CYP3A5 6986G (RR, 2.4; 95% CI, 1.1-5.6) alleles. These results support the hypothesis that maternal and/or offspring catechol estrogen activity may influence sons' risk of TGCC. (Cancer Epidemiol Biomarkers Prev 2005;14(9): 2183-90)

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Section: Introductionmentioning

confidence: 99%

Risk of Testicular Germ Cell Cancer in Relation to Variation in Maternal and Offspring CytochromeP450 Genes Involved in Catechol Estrogen Metabolism

Starr

Chen

Doody

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…The dependency of E expression on the GTW dose suggests it might play a direct role in affecting fertility. E is considered to be a fundamental chemical in the toxicologic evaluation of chemicals with estrogenic properties (Seegers et al, 1991;Ikegawa et al, 1995;Iwase et al, 1995). The epididymal toxicity of estrogen on the number and motility of sperm may play a role in the onset of infertility (Kaneto et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

“…Enhancing activity of estrogens in Leydig cells may be an important mechanism of GTW antifertility, as there were no changes in the expression of T and AR. Although some estrogenic compounds have been found to affect epididymal tissue or spermatozoa (Rao and Chinoy, 1983;Robaire et al, 1987;Seegers et al, 1991), further studies into whether the testis and epididymis damage induced by GTW resulted from the activity of estrogens are needed. Although using GTW provides a promising approach for the control of rodent fecundity, the detrimental effects of longer-term GTW treatment and their reversibility need to be assessed before GTW can be considered an appropriate male contraceptive in human.…”

Section: Discussionmentioning

confidence: 99%

Effects of Tripterygium wilfordii multiglycosides on sex hormones and receptors in mandarin vole Leydig cells

Wang

Tai

2012

Animal Biol

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Multiglycosides of Tripterygium wilfordii (GTW) have been found to exhibit reversible antifertility effects through complex mechanisms. The positive expression of sex hormones and receptors in Leydig cells were investigated following GTW treatment to determine the impact of GTW on male mandarin vole (Microtus mandarinus) fertility. Compared to the control group, body weight, testis and epididymis weight were not affected by GTW, but the number of sperm sharply declined. There were significant decreases in the thickness of seminifeous epithelium and epididymal epithelium, and the diameter of seminiferous tubules. The expression of estrogen receptor alpha (ERα) in Leydig cells significantly decreased and estradiol (E) expression significantly increased. Testosterone (T) and androgen receptor (AR) expression were not affected. These results show that GTW may impair fertility in male mandarin voles via interference with spermatogenesis. This may be associated with an alteration in estrogen activation rather than suppression of T and AR in Leydig cells and suggests the estrogen system of Leydig cells is of major importance for the GTW's antifertility effects.

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“…Previous work in our laboratory showed that the 2-/4-OHE, metabolites act as mitogens when administered at low levels (Seegers et al, 1989b), and as cytotoxins when administered at high levels in in vitro studies (Seegers et al, 1989a). In vivo studies showed that very low levels (40 ng/rat/week) of 2-OHE, and especially 4-OHE, were very toxic to the rat epididymal epithelia (Seegers et al, 1991), but at these very low levels no effect on the morphology of the rat testis was seen with weekly doses. Morphological lesions were observed by others in the testis of rats, only after continuous exposure to E, at high dosage levels (50 pg/rat; Rao & Chinoy, 1984;Kalla, 1987).…”

Section: Introductionmentioning

confidence: 86%

“…In conclusion it is proposed that the cytotoxic effects of continuously administered E, may be caused by the formation and subsequent actions of the catecholestrogens. The male infertility observed when patients are exposed to excess E, may therefore be attributed to the effects of catecholestrogens on developing spermatids, on testosterone production and on epididymal epithelia (Seegers et al, 1991).…”

Section: -Ohe Metabolites In the Present Study Appears Tomentioning

confidence: 99%

Morphological effects of the catecholestrogens on cells of the seminiferous tubules of Sprague-Dawley rats

et al. 2009

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Estradiol-17P (E,) and rhe two catecholestrogens 2-OHE, and 4-OHE2, when daily administered at low doses of 10-40 ng/rat, were cytotoxic to the seminiferous epithelium. The structural changes seen after seven days exposure included abnormal meiotic type I1 cells with uneven chromosome distribution, the formation of binucleated and multinucleated giant cells, of which many were sloughed into the lumina of the seminiferous tubules. The effect of the 4-OHE, metabolites were always more pronounced than that of 2-OHE, or E,. After 21 daily exposures, 4-OHE2 proved to be very toxic, the seminiferous tubules were markedly denuded and numerous giant cells were present in the lumina. The catecholestrogens also caused a significant lowering ( P < 0.02) of testosterone serum levels after eight days exposure. E, at 40 ng/rat/day had no effect on testosterone production. At these low doses the catecholestrogens did not affect gonadotropin release after eight days exposure. Our results indicate that the morphological lesions could not exclusively be attributed to testosterone withdrawal and that a direct effect on developing spermatids is also indicated.

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Morphological effects of the catechol estrogens on rat epididymal epithelia

Cited by 6 publications

References 9 publications

Risk of Testicular Germ Cell Cancer in Relation to Variation in Maternal and Offspring CytochromeP450 Genes Involved in Catechol Estrogen Metabolism

Risk of Testicular Germ Cell Cancer in Relation to Variation in Maternal and Offspring CytochromeP450 Genes Involved in Catechol Estrogen Metabolism

Effects of Tripterygium wilfordii multiglycosides on sex hormones and receptors in mandarin vole Leydig cells

Morphological effects of the catecholestrogens on cells of the seminiferous tubules of Sprague-Dawley rats

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