Postnatal exposure to low-dose decabromodiphenyl ether adversely affects mouse testes by increasing thyrosine phosphorylation level of cortactin

Miyaso, Hidenobu; Nakamura, Noriko; Matsuno, Yoshiharu; Kawashiro, Yukiko; Komiyama, Masatoshi; Mori, Chisato

doi:10.2131/jts.37.987

Cited by 17 publications

(24 citation statements)

References 46 publications

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“…Based on the results of a previous in vitro study (Sebkova et al 2012), it can be assumed that with an elevated in vivo estrogen exposure, capacitation may start in the epididymal spermatozoa. On the other hand, it has been reported that estrogens trigger multiple phosphorylation pathways in the testicular tissue or can change their cell sensitivity (Miyaso et al 2012). For this reason it is possible to consider that potential molecular changes in testicular sperm, and individual sperm developmental stages can lead to a higher number of capacitated sperm observed in the epididymis.…”

Section: Discussionmentioning

confidence: 99%

In vivo exposure to 17β-estradiol triggers premature sperm capacitation in cauda epididymis

Děd¹,

Šebková²,

Černá³

et al. 2013

Reproduction

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Estrogens play a crucial role in spermatogenesis and estrogen receptor a knock-out male mice are infertile. It has been demonstrated that estrogens significantly increase the speed of capacitation in vitro; however this may lead to the reduction of reproductive potential due to the decreased ability of these sperm to undergo the acrosome reaction. To date the in vivo effect of estrogens on the ability of sperm to capacitate has not been investigated. Therefore, in this study, we exposed mice (nZ24) to 17b-estradiol (E 2 ) at the concentration of 20 ng/ml either during puberty from the fourth to seventh week of age (nZ8), or continuously from birth for a period of 12 weeks (nZ8) at which age the animals from both groups were killed. The capacitation status of epididymal and testicular sperm was analysed by tyrosine phosphorylation (TyrP) antibody (immunofluorescence and western blot) and chlortetracycline (CTC) assay. According to our results, in vivo exposure to increased E 2 concentrations caused premature sperm capacitation in the epididymis. The effect of E 2 , however, seems reversible because after the termination of the exposure premature epididymal sperm capacitation is decreased in animals treated during puberty. Furthermore the changes in epididymal sperm capacitation status detected by TyrP and CTC positively correlate with plasma levels of E 2 and the expression of the estrogen-dependent trefoil factor 1 (Tff1) gene in testicular tissue. Therefore, our data implicate that in vivo exposure to E 2 under specific conditions leads to the premature capacitation of mouse sperm in epididymis with a potential negative impact on the sperm reproductive fitness in the female reproductive tract.

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Section: Discussionmentioning

confidence: 99%

In vivo exposure to 17β-estradiol triggers premature sperm capacitation in cauda epididymis

Děd¹,

Šebková²,

Černá³

et al. 2013

Reproduction

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“…Our group reported that although the mean body and epididymal weights were not affected in mice exposed to 0.025 mg/kg BDE-209, the mean testicular weight and sperm counts were significantly lower in the exposed group (Miyaso et al, 2012). Levels of serum testosterone and transcripts encoding the androgen receptor (Ar), thyroid hormone receptor alpha (Thra), and its variant, Thra1 in the Sertoli cells declined significantly in mice exposed to 0.025 mg/kg BDE-209 in our previous study (Miyaso et al, 2014).…”

Section: Introductionmentioning

confidence: 72%

“…Ultrapure water was purified using a RFD280NC system (ADVAN-TEC, Dublin, CA, USA). BDE-209 and all other reagents were obtained from Sigma-Aldrich (St. Louis, MO, USA), as described previously (Miyaso et al, 2012(Miyaso et al, , 2014.…”

Section: Reagentsmentioning

confidence: 99%

“…In the exposed group, mice (n = 8) were administered BDE-209 at doses of 0.025 mg/kg/day by subcutaneous injection on postnatal days 1 to 5, as previously described (Miyaso et al, 2012;Miyaso et al, 2014). Control group mice (n = 8) were administered corn oil by subcutaneous injection.…”

Section: Animals and Administration Of Bde-209mentioning

confidence: 99%

“…Control group mice (n = 8) were administered corn oil by subcutaneous injection. Mice were sacrificed at 12 weeks of age (postnatal days 84) by CO 2 euthanasia, followed by the collection of whole blood and testes (Miyaso et al, 2012(Miyaso et al, , 2014.…”

Section: Animals and Administration Of Bde-209mentioning

confidence: 99%

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The effects of early postnatal exposure to a low dose of decabromodiphenyl ether (BDE-209) on serum metabolites in male mice

2016

Self Cite

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-The toxicity of decabromodiphenyl ether (BDE-209) has been reported in several studies. However, there is not much known about the toxicological biomarkers that characterize BDE-209 exposure. In this study, we subcutaneously exposed mice to 0.025 mg/kg/day BDE-209 on postnatal days 1-5 and sacrificed the animals at 12 weeks of age (day 84). Flow injection analysis and hydrophilic interaction chromatography-triple quadrupole mass spectrometry were used to determine the serum metabolomes of these mice in order to characterize the effects of BDE-209 exposure. Data analysis showed a good separation between control and exposed mice (R 2 = 0.953, Q 2 = 0.728, and ANOVA of the crossvalidated residuals (CV-ANOVA): P-value = 0.0317) and 54 metabolites were identified as altered in the exposed animals. These were selected using variable importance (VIP) and loadings scaled by a correlation coefficient criteria and orthogonal partial least squares discriminant analysis (OPLS-DA). BDE-209-exposed mice showed lower levels of long-chain acylcarnitines and citrate cycle-related metabolites, and higher levels of some amino acids, long-chain phospholipids, and short-chain acylcarnitines. The disruption of fatty acid, carbohydrate, and amino acid metabolism observed in the serum metabolome might be related to the previously observed impaired spermatogenesis in mice with early postnatal exposure to a low dose of BDE-209.

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Microenvironment for spermatogenesis and sperm maturation

Miyaso

Ogawa

Itoh

2022

Histochem Cell Biol

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Postnatal exposure to low-dose decabromodiphenyl ether adversely affects mouse testes by increasing thyrosine phosphorylation level of cortactin

Cited by 17 publications

References 46 publications

In vivo exposure to 17β-estradiol triggers premature sperm capacitation in cauda epididymis

In vivo exposure to 17β-estradiol triggers premature sperm capacitation in cauda epididymis

The effects of early postnatal exposure to a low dose of decabromodiphenyl ether (BDE-209) on serum metabolites in male mice

Microenvironment for spermatogenesis and sperm maturation

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