Epididymal sperm motion as a parameter of male reproductive toxicity: sperm motion, fertility, and histopathology in ethinylestradiol-treated rats

Kaneto, Masako; Kanamori, Shuichi; Hishikawa, Atsuko; Kishi, Kurajiro

doi:10.1016/s0890-6238(99)00021-0

Cited by 42 publications

(41 citation statements)

References 25 publications

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“…These discrepancies between the results from relative ratios and absolute counts demonstrate that the evaluation with absolute counts is essential in precisely assessing the cytotoxic changes in cases in which more than two different kinds of cells are affected simultaneously. The results from our FCM analysis are in accordance with the histopathological evaluation by Iwase et al (1995), Kaneto et al (1999b) Miyamoto et al (2000) and Kinomoto et al (2000). Kaneto et al (1999b) showed that dosages of 10 mg/kg EE resulted in a decrease of spermatocytes primarily, but spermatogonia was well-preserved for 2 weeks.…”

Section: Discussionsupporting

confidence: 86%

“…The results from our FCM analysis are in accordance with the histopathological evaluation by Iwase et al (1995), Kaneto et al (1999b) Miyamoto et al (2000) and Kinomoto et al (2000). Kaneto et al (1999b) showed that dosages of 10 mg/kg EE resulted in a decrease of spermatocytes primarily, but spermatogonia was well-preserved for 2 weeks. However, after 3 weeks of dosing, quantitative morphometric evaluation was reported to be impossible due to severe atrophic changes in almost all tubules.…”

Section: Discussionsupporting

confidence: 86%

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Assessment of quantitative dual-parameter flow cytometric analysis for the evaluation of testicular toxicity using cyclophosphamide- and ethinylestradiol-treated rats.

Katoh

Kitajima²,

Saga³

et al. 2002

J. Toxicol. Sci.

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-In the drug discovery process, effects to the human spermatogenesis must be fully evaluated before the first human trial. To estimate testicular toxicity, histopathological evaluation has been recommended in addition to the traditional mating procedure. However, it is laborious and time-consuming. Flow cytometric analysis (FCM) has also been applied to estimate testicular toxicity because of its speed, simplicity, and the objectivity of the data. Using cyclophosphamide (CP)-and ethinylestradiol (EE)-treated rat testis, we attempted to validate our dual-parameter, DNA ploidy and cell-size FCM, in a high-throughput toxicity study. Our results showed that CP damaged some spermatogonia and some early meiotic spermatocytes and EE caused severe decrease of spermatogenic cells except for spermatogonia as well as marked decrease of somatic cells, most probably Leydig cells. This is the first report discriminating between the changes of spermatogonia and that of somatic cells with FCM analysis. These results demonstrate that this method is a very useful and powerful tool to assess testicular toxicity, especially in high-throughput toxicological studies.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionsupporting

confidence: 86%

Assessment of quantitative dual-parameter flow cytometric analysis for the evaluation of testicular toxicity using cyclophosphamide- and ethinylestradiol-treated rats.

Katoh

Kitajima²,

Saga³

et al. 2002

J. Toxicol. Sci.

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“…Alterations in these parameters are suggested as optional procedures for confirmation of histopathologic findings or to better characterize adverse effects (Kaneto et al, 1999). In the present investigation, an adverse impact on sperm parameters were noticed which provides sufficient evidence in favor of reproductive toxicity.…”

Section: Discussionsupporting

confidence: 51%

Assessment of Molybdenum Induced Alteration in Oxidative Indices, Biochemical Parameters and Sperm Quality in Testis of Wistar Male Rats

Pandey¹,

Jain²

2015

Asian J. of Biochemistry

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The present study was carried out to investigate the effects of ammonium molybdate on lipid peroxidation, antioxidant, biochemical and semen parameters in male Wistar rats. Group I served as control while group II, III and IV received 50, 100 and 150 mg kgG for 60 days and thereafter left for recovery study for 60 days. The present study examined the effects of ammonium molybdate on serum testosterone, Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH) along with sperm parameters. Estimations were also made for marker biochemical and antioxidant parameters in testis. Ammonium molybdate treatment resulted in a dose dependent reduction in serum testosterone, FSH, LH, sperm count, motility and viability. The concentration of total protein and sialic acid as well as activities of acid phosphatase (ACP) and alkaline phosphatase (ALP) were decreased in a dose dependent manner while there was a significant increase in the glycogen and cholesterol level in testis. The level of Thiobarbituric Acid Reactive substance (TBARs) was increased while the activities of superoxide dismutase and concentration of glutathione and ascorboic acid was decreased significantly in testis of rats treated with ammonium molybdate. All the parameters showed significant improvement after 60 days of treatment withdrawal in highest dose group. The findings suggested that ammonium molybdate exerts a deleterious effect on testicular function by altering biochemical and antioxidant status of the testes.

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“…Although both sexes are affected, males exhibit the highest degree and number of detrimental effects. Specific male defects caused by environmental estrogen exposures in vertebrates include: intersex (25,29), diminished sperm count (27,(35)(36)(37), genital tract alterations (38), increased germ cell apoptosis (30,33), and male induced embryonic mortality (31,39).…”

mentioning

confidence: 99%

“…Although most rodent model studies show decreased sperm production and/or increased apoptosis of germ cells after exposure (27,30,33,35), others have failed to confirm these findings (40). Additionally, recent in vitro exposures of human spermatozoa to catechol estrogens (e.g., quercetin, diethylstilbestrol and pyrocatechol) indicate an impact on sperm DNA integrity through altered redox cycling, but estrogen (17␤-estradiol) and other estrogen analogues (nonylphenol and BPA) do not show this effect (41).…”

mentioning

confidence: 99%

Aneuploid sperm formation in rainbow trout exposed to the environmental estrogen 17α-ethynylestradiol

Brown

Schultz

Cloud

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Environmental contaminants that mimic native estrogens (i.e., environmental estrogens) are known to significantly impact a wide range of vertebrate species and have been implicated as a source for increasing human male reproductive deficiencies and diseases. Despite the widespread occurrence of environmental estrogens and recognized detrimental effects on male vertebrate reproduction, no specific mechanism has been determined indicating how reduced fertility and/or fecundity is achieved. Previous studies show that male rainbow trout, Oncorhynchus mykiss, exposed to the environmental estrogen 17␣-ethynylestradiol (EE2) before gamete formation and fertilization produce progeny with significantly reduced embryonic survival. To determine whether this observed decrease results from sperm chromosome alterations during spermatogenesis, male rainbow trout were exposed to 10 ng of EE2/l for 50 days. After exposure, semen was collected and sperm aneuploidy levels analyzed with two chromosome markers by fluorescent in situ hybridization. In vitro fertilizations were also conducted by using control and exposed sperm crossed to eggs from an unexposed female for offspring analysis. Evaluations for nucleolar organizer region number and karyotype were performed on developing embryos to determine whether sperm aneuploidy translated into embryonic aneuploidy. Results conclusively show increased aneuploid sperm formation due to EE2 exposure. Additionally, embryonic cells from propagated progeny of individuals possessing elevated sperm aneuploidy display high levels of embryonic aneuploidy. This study concludes that EE2 exposure in sexually developing male rainbow trout increases levels of aneuploid sperm, providing a mechanism for decreased embryonic survival and ultimately diminished reproductive success in EE2 exposed males.aneuploidy ͉ EE2 ͉ xenoestrogens

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Epididymal sperm motion as a parameter of male reproductive toxicity: sperm motion, fertility, and histopathology in ethinylestradiol-treated rats

Cited by 42 publications

References 25 publications

Assessment of quantitative dual-parameter flow cytometric analysis for the evaluation of testicular toxicity using cyclophosphamide- and ethinylestradiol-treated rats.

Assessment of quantitative dual-parameter flow cytometric analysis for the evaluation of testicular toxicity using cyclophosphamide- and ethinylestradiol-treated rats.

Assessment of Molybdenum Induced Alteration in Oxidative Indices, Biochemical Parameters and Sperm Quality in Testis of Wistar Male Rats

Aneuploid sperm formation in rainbow trout exposed to the environmental estrogen 17α-ethynylestradiol

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