Effects of developmental exposure to indole-3-carbinol or2,3,7,8-tetrachlorodibenzo-p-dioxin on reproductive potential of male rat offspring

Wilker, Clynn E.; Johnson, Larry; Safe, Stephen

doi:10.1016/s0041-008x(96)80010-x

Cited by 67 publications

(9 citation statements)

References 48 publications

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“…In the present study, testicular weight was maintained during adulthood, which corroborates the results of a previous study using the same dose of TCDD and duration of exposure (Wilker et al 1996). The results regarding testicular weight can be correlated with those regarding testosterone concentrations, which were similar among the experimental groups.…”

Section: Discussionsupporting

confidence: 91%

“…In contrast with these results, in the present study there were no changes in DSP and number of mature spermatids in male offspring Sprague-Dawley rats exposed to either TCDD or resveratrol. Wilker et al (1996) reported similar results using 0.5, 1.0 and 2.0 mg kg À1 TCDD at GD15. This can be explained by the findings of Simanainen et al (2004), who reported that sperm parameters differed based on resistance to AhR alleles, which varies in different rat strains.…”

Section: Discussionsupporting

confidence: 61%

“…Moreover, Bjerke and Peterson (1994) reported decreased bodyweight on PND1 for rats treated with TCDD (1 mg kg À1 on GD15), whereas no weight loss was observed at PND133. Wilker et al (1996) showed that male rat offspring exposed to TCDD (1 mg kg À1 on GD15) had decreased bodyweight on PND1 compared with the control group. Therefore, we can suggest that TCDD affects fetal programming of adult life, and its effect may be persistent.…”

Section: Discussionmentioning

confidence: 99%

“…Pregnant rats in the TCDD and TþR groups were treated with 1 mg kg À1 TCDD diluted in dimethylsulfoxide (DMSO) by gavage on GD15. Wilker et al (1996) demonstrated that 1.0 mg kg À1 TCDD is the lowest dose that effectively induces reproductive disorders. The oral LD 50 for TCDD in male Sprague-Dawley rats is 43 mg kg À1 (Agency for Toxic Substances and Disease Registry (ATSDR) 1998).…”

Section: Experimental Design and Treatmentmentioning

confidence: 99%

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Can resveratrol attenuate testicular damage in neonatal and adult rats exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin during gestation?

Erthal

Siervo

Silveira

et al. 2018

Reprod. Fertil. Dev.

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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is considered one of the most toxic dioxins. The effects of TCDD are exerted via binding to the aryl hydrocarbon receptor (AhR). The aim of the present study was to evaluate the possible protective effects of resveratrol, an AhR antagonist, against testicular damage caused by TCDD exposure during pregnancy. Pregnant female Sprague-Dawley rats were divided into four groups: a control group; a group treated with 1µgkg-1, p.o., TCDD on Gestational Day (GD) 15; a group treated with 20µgkg-1, p.o., resveratrol on GD10-21; and a group treated with both TCDD and resveratrol. Rats were weighed and killed, and neonatal testes were collected for histopathological analysis on Postnatal Day (PND) 1. At PND90, adult male rats were killed and the testes collected for histopathological analysis and determination of sperm count. Resveratrol had a protective effect against the effects of TCDD on Sertoli cell number in adult and neonate testes, as well as against the effects of TCDD on abnormal seminiferous tubules in adults. Combined administration of TCDD and resveratrol altered the kinetics of spermatogenesis and the proportion of neonatal testicular compartments compared with the control group In addition, combined TCDD and resveratrol treatment decreased seminiferous tubule diameter in adult male rats compared with the control group. In conclusion, resveratrol may protect against some TCDD-induced testicular damage, but, based on the parameters assessed, the administration of resveratrol and TCDD in combination may result in more severe toxicity than administration of either drug alone.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 61%

Section: Discussionmentioning

confidence: 99%

Section: Experimental Design and Treatmentmentioning

confidence: 99%

See 2 more Smart Citations

Can resveratrol attenuate testicular damage in neonatal and adult rats exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin during gestation?

Erthal

Siervo

Silveira

et al. 2018

Reprod. Fertil. Dev.

View full text Add to dashboard Cite

show abstract

“…Nowadays, it is well-known that testis function is a primary target of a large number of pollutants. Delayed establishment of spermatogenesis (295), impaired differentiation of internal and external male genital structures (296), reduced sperm production and disruption of the hypothalamic–pituitary–gonadal axis (297), decreased anogenital distance and decreased prostate and seminal vesicle weights (298, 299), among others, represent just some of the multiple observations performed.…”

Section: Pharmacological Agents and Xenobiotics May Affect Sertoli Cementioning

confidence: 99%

Molecular Mechanisms and Signaling Pathways Involved in Sertoli Cell Proliferation

et al. 2019

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Sertoli cells are somatic cells present in seminiferous tubules which have essential roles in regulating spermatogenesis. Considering that each Sertoli cell is able to support a limited number of germ cells, the final number of Sertoli cells reached during the proliferative period determines sperm production capacity. Only immature Sertoli cells, which have not established the blood-testis barrier, proliferate. A number of hormonal cues regulate Sertoli cell proliferation. Among them, FSH, the insulin family of growth factors, activin, and cytokines action must be highlighted. It has been demonstrated that cAMP/PKA, ERK1/2, PI3K/Akt, and mTORC1/p70SK6 pathways are the main signal transduction pathways involved in Sertoli cell proliferation. Additionally, c-Myc and hypoxia inducible factor are transcription factors which participate in the induction by FSH of various genes of relevance in cell cycle progression. Cessation of proliferation is a pre-requisite to Sertoli cell maturation accompanied by the establishment of the blood-testis barrier. With respect to this barrier, the participation of androgens, estrogens, thyroid hormones, retinoic acid and opioids has been reported. Additionally, two central enzymes that are involved in sensing cell energy status have been associated with the suppression of Sertoli cell proliferation, namely AMPK and Sirtuin 1 (SIRT1). Among the molecular mechanisms involved in the cessation of proliferation and in the maturation of Sertoli cells, it is worth mentioning the up-regulation of the cell cycle inhibitors p21Cip1, p27Kip, and p19INK4, and of the gap junction protein connexin 43. A decrease in Sertoli cell proliferation due to administration of certain therapeutic drugs and exposure to xenobiotic agents before puberty has been experimentally demonstrated. This review focuses on the hormones, locally produced factors, signal transduction pathways, and molecular mechanisms controlling Sertoli cell proliferation and maturation. The comprehension of how the final number of Sertoli cells in adulthood is established constitutes a pre-requisite to understand the underlying causes responsible for the progressive decrease in sperm production that has been observed during the last 50 years in humans.

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Expression of the aryl hydrocarbon receptor (AhR) and the aryl hydrocarbon receptor nuclear translocator (ARNT) in fetal, benign hyperplastic, and malignant prostate

et al. 1998

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Effects of developmental exposure to indole-3-carbinol or2,3,7,8-tetrachlorodibenzo-p-dioxin on reproductive potential of male rat offspring

Cited by 67 publications

References 48 publications

Can resveratrol attenuate testicular damage in neonatal and adult rats exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin during gestation?

Can resveratrol attenuate testicular damage in neonatal and adult rats exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin during gestation?

Molecular Mechanisms and Signaling Pathways Involved in Sertoli Cell Proliferation

Expression of the aryl hydrocarbon receptor (AhR) and the aryl hydrocarbon receptor nuclear translocator (ARNT) in fetal, benign hyperplastic, and malignant prostate

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