Effects of a single dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin, given at post-puberty, in senescent mice

Esser, Charlotte; Steinwachs, Swantje; Herder, Christian; Majora, Marc; Lai, Zhi-Wei

doi:10.1016/j.toxlet.2005.01.007

Cited by 8 publications

(6 citation statements)

References 50 publications

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“…The activated AhR induces the expression of various genes with xenobiotic response elements in their enhancer regions, such as the gene for cytochrome P450 1A1 (CYP1A1). Esser et al (2005) found that TCDD interfered with the physiological signaling of the AhR, led to cell-specific changes in gene transcription and cell differentiation, and thereby producing toxic effects. TCDD combined with AhR, and thereby induced a change in the expression of monoamine oxidase related to CYP450 enzymes activated by AhR (Poland and Kimbrough, 1984).…”

Section: Discussionmentioning

confidence: 99%

Effects of vitamin E on reproductive hormones and testis structure in chronic dioxin-treated mice

Yin

Zhou

et al. 2011

Toxicol Ind Health

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The purpose of this study was to investigate the effects of vitamin E on reproductive hormones and testis structure in mice treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Five experimental groups of a combination of TCDD and vitamin E were designed as follows: 0 ng/kg/d and 0 mg/kg/d (control group), 100 ng/kg/d and 0 mg/kg/d (Group I), 100 ng/kg/d and 20 mg/kg/d (Group II), 100 ng/kg/d and 100 mg/kg/d (Group III), and 100 ng/kg/d and 500 mg/kg/d (Group IV) respectively. Vitamin E and TCDD were given by oral gavage for 7 weeks. The results demonstrated that TCDD decreased the levels of brain gonadotropin releasing hormone (GnRH), testis luteinizing hormone (LH) and follicle stimulating hormone (FSH), serum testosterone and testis spermatozoa number, and damaged testis structure. Vitamin E at 20 mg/kg alleviated the decrease of GnRH; vitamin E at 20, 100, and 500 mg/kg antagonized the decline of LH and FSH; vitamin E at 20 and 100 mg/kg reversed the decrease of testosterone and spermatozoa number; and vitamin E at 100 mg/kg decreased the damage of the testis structure caused by TCDD. The results indicate that vitamin E antagonizes the reproductive endocrine toxicity and alleviates the changes in testicular structure caused by TCDD.

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Section: Discussionmentioning

confidence: 99%

Effects of vitamin E on reproductive hormones and testis structure in chronic dioxin-treated mice

Yin

Zhou

et al. 2011

Toxicol Ind Health

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“…(8) Our previous study showed TCDD increased serum I L-1 level and the percentage of spleen CD8 + T lymphocyte, and declined serum IL-2 level and the percentage of spleen CD4 + T lymphocyte in mice. (16) But Esser et al (23) showed that no differences in the frequencies of B-cells, T-cells, or NK-cells were detectable after a single dose of TCDD given to young mice. The reason of various results above could be relative to the different sensitivity of immune index to TCDD, the used TCDD dosage, and individual difference in animals.…”

Section: The Effects Of Tcdd Treatment On Nk Cell Activity and Lymphomentioning

confidence: 99%

“…TCDD interfered with physiological signaling of the AhR, leading to cell-specific changes in gene transcription and cell differentiation, and thereby produced toxic effects. (23) The expression of genes in the AhR-dependent pathway, including AhR, aryl-hydrocarbon receptor nuclear translocator (ARNT), CYP1A1, and CYP1B1 transcripts, and the CYP1A1-associated 7-ethoxyresorufin-O-deethylase (EROD) activity was measured in lymphocytes. (29) But Dong et al (30) showed that TCDD did not increase the AhR expression, while enhanced the expression of CYP1A6 mRNA, CYP1A7 mRNA and CYP1A protein in Xenopus laevis.…”

Section: The Effects Of Tcdd Treatment On Nk Cell Activity and Lymphomentioning

confidence: 99%

The effects of vitamin E on NK cell activity and lymphocyte proliferation in treated mice by 2,3,7,8-tetrachlorodibenzo-p-dioxin

Wang

Zhou

et al. 2009

Immunopharmacology and Immunotoxicology

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The study was conducted to investigate the effects of vitamin E on NK cell activity and lymphocyte proliferation in tr eated female mice by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). In chronic TCDD trial, 45 mice were divided into 5 groups, and the levels of TCDD and vitamin E were 0 and 0, 100 and 0, 100 and 20, 100 and 100, and 100 ng/kg/d and 500 mg/kg/d, respectively. In acute TCDD trial, 24 mice were divided into three groups, and the levels of TCDD and vitamin E were 0 and 0, 30 and 0, and 30 microg/kg and 100 mg/kg, respectively. The results showed chronic TCDD-treatment caused decrease tendencies of spleen NK cell activity and lymphocyte proliferation, and vitamin E 100mg/kg alleviated the decreases tendencies caused by chronic TCDD-treatment, and the lymphocyte proliferation in the group given vitamin E 100mg/kg was significantly higher than that of the chronic TCDD-treated group. Acute TCDD-treatment suppressed the NK cell activity and lymphocyte proliferation, and vitamin E 100mg/kg significantly alleviated the decrease caused by acute TCDD-treatment. These results suggested that TCDD resulted in immunotoxicity, and the toxicity of acute TCDD-treatment was severe compared with chronic TCDD, while vitamin E alleviated the immunotoxicity from TCDD.

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“…6 TCDD binds to aryl hydrocarbon receptor (AHR), which binds to AHR nuclear translocator in the cytosol and then translocates to the nucleus to induce the expression of aryl hydrocarbon hydroxylases (cytochrome P450 s). 7 Esser et al 8 reported that TCDD produces toxic effects by interfering with the physiological signaling of AHR. In utero exposure to TCDD results in reduction of sperm count with an increase in morphological abnormal sperm in their adulthood.…”

Section: Introductionmentioning

confidence: 99%

Maternal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin suppresses male reproductive functions in their adulthood

et al. 2020

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2,3,7,8-Tetrachlorodibenzo- p-dioxin (TCDD) is a ubiquitous environmental contaminant in the environment. The developmental period is more sensitive to TCDD and there is a possibility that maternal exposure to TCDD may affect in adulthood. Adult female Wistar rats were exposed to 0.5, 1.0, and 2.0 µg/kg TCDD during the critical stage of organogenesis, that is, on GD15. The results revealed a significant decrease in indices of reproductive organ weight in adult male rats exposed to prenatal TCDD, and dose-dependent reduction in epididymal sperm reserves, percent motile, and viable sperm with an increase in percent morphological abnormal sperm. Polymerase chain reaction analysis revealed downregulated expression levels of steroidogenic markers such as steroidogenic acute regulatory, cholesterol side-chain cleavage, and 3β- and 17β-hydroxysteroid dehydrogenase (HSDs) in experimental rats. Immunofluorescence sections portrayed reduced distribution of 3β- and 17β-HSD proteins in testes of experimental rats. Furthermore, spermatogenic markers (acid phosphatase, alkaline phosphatase, lactate dehydrogenase, and sorbitol dehydrogenase) were significantly altered in the testes. Serum levels of testosterone, follicle stimulating hormones, and luteinizing hormone were significantly decreased. Testicular levels of hydrogen peroxide and lipid peroxidation were significantly elevated with a decline in superoxide dismutase, catalase, glutathione peroxidase activities, and total thiol levels. Moreover, histological and morphometric examination of testicular cross-sections depicted degenerative changes. Male fertility assessment in adult rats revealed a significant decrease in mating index, fertility index, and mean number of pre- and postimplantations with an increase in pre- and postimplantation losses in rats cohabited with in utero TCDD-exposed adult males. In conclusion, the findings of this study provided clear evidence that maternal exposure to TCDD during the critical stage of development results in suppressed reproductive health in adulthood.

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Effects of a single dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin, given at post-puberty, in senescent mice

Cited by 8 publications

References 50 publications

Effects of vitamin E on reproductive hormones and testis structure in chronic dioxin-treated mice

Effects of vitamin E on reproductive hormones and testis structure in chronic dioxin-treated mice

The effects of vitamin E on NK cell activity and lymphocyte proliferation in treated mice by 2,3,7,8-tetrachlorodibenzo-p-dioxin

Maternal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin suppresses male reproductive functions in their adulthood

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