In utero exposure of high-dose di-n-butyl phthalate resulted in opposite effects on testicular cell apoptosis in late embryonic and pubertal male rat offspring

2017 ◽  
Vol 36 (12) ◽  
pp. 1236-1247 ◽  
Author(s):  
H Shen ◽  
K Liao ◽  
H-F Wu ◽  
H-C Lu ◽  
Y Li ◽  
...  
Keyword(s):  
Western Blot ◽  
Cell Apoptosis ◽  
In Utero ◽  
Male Rat ◽  
In Utero Exposure ◽  
High Dose ◽  
Testicular Cell ◽  
Rat Testis ◽  
Rat Offspring ◽  
Butyl Phthalate

Objective: To investigate the effects of in utero exposure to high-dose di- n-butyl phthalate (DBP) on testicular cell apoptosis in late embryonic and pubertal male rat offspring. Methods: Twenty pregnant Sprague-Dawley (SD) rats were divided into two groups. During gestation day (GD) 12 to GD 19, control group was given 1 ml day−1 of olive oil and experimental group was given DBP 500 mg kg−1 day−1 by gavage. On GD 19.5 and postnatal day (PND) 45, the testes were removed. Morphological analysis of the testes was observed by transmission electron microscopy and hematoxylin and eosin (H&E) staining. Testicular cell apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). The expression of Bcl-2, Bax, and p53 was presented by immunohistochemistry (IHC) and western blot. Data of the two groups was compared using independent samples t-test and Mann–Whitney test by SPSS 20.0. Results: H&E staining showed that spermatogenetic cells were significantly decreased in DBP exposed pubertal rat testis. The apoptosis index of testes in DBP-treated group was significantly lower on GD 19.5 but higher on PND 45 than that of the controls ( p < 0.01). IHC and western blot revealed significantly increased expression of Bcl-2 in GD 19.5 rat testis and Bax and p53 in PND 45 rat testis after DBP exposure, compared with the control ( p < 0.05). Conclusion: In utero exposure of high-dose DBP resulted in opposite effects on testicular cell apoptosis in late embryonic and pubertal rat offspring. The overexpression of Bcl-2, Bax, and p53 might be related to the occurrence of abnormal apoptosis and finally produce male infertility.

scholarly journals In utero exposure to transient ischemia-hypoxemia promotes long-term neurodevelopmental abnormalities in male rat offspring

JCI Insight ◽  
2020 ◽  
Vol 5 (10) ◽  
Author(s):  
Arvind Palanisamy ◽  
Tusar Giri ◽  
Jia Jiang ◽  
Annie Bice ◽  
James D. Quirk ◽  
...  
Keyword(s):  
In Utero ◽  
Male Rat ◽  
In Utero Exposure ◽  
Transient Ischemia ◽  
Rat Offspring ◽  
Neurodevelopmental Abnormalities

Effect of In-Utero Exposure to High Dose Diethylstilbestrol on Intervertebral Disk in Adult Male and Female Progeny

2012 ◽  
Vol 2 (1_suppl) ◽  
pp. s-0032-1319931-s-0032-1319931
Author(s):  
S. Al Rowas ◽  
R. Gawri ◽  
R. Haddad ◽  
A. Almaawi ◽  
L. E. Chalifour ◽  
...  
Keyword(s):  
Adult Male ◽  
In Utero ◽  
Intervertebral Disk ◽  
In Utero Exposure ◽  
High Dose ◽  
Female Progeny ◽  
Male And Female

scholarly journals In Utero Exposure to Di(n)butyl Phthalate Reduces Testicular Testosterone and Testes Size in a Dose-Dependent Manner in Harlan Sprague Dawley Fetal Rats.

2009 ◽  
Vol 81 (Suppl_1) ◽  
pp. 636-636
Author(s):  
Kembra L. Howdeshell ◽  
Johnathan Furr ◽  
Christy R. Lambright ◽  
Vickie Wilson ◽  
L. Earl Gray
Keyword(s):  
In Utero ◽  
In Utero Exposure ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
Fetal Rats ◽  
Testes Size ◽  
Butyl Phthalate ◽  
Dose Dependent

scholarly journals In utero and lactational exposure to triclocarban: Age-associated changes in reproductive parameters of male rat offspring

2020 ◽  
Vol 401 ◽  
pp. 115077
Author(s):  
Nathália Orlandini Costa ◽  
Simone Forcato ◽  
Andreza Manzato Cavichioli ◽  
Marina Rangel Ferro Pereira ◽  
Daniela Cristina Ceccatto Gerardin
Keyword(s):  
In Utero ◽  
Male Rat ◽  
Reproductive Parameters ◽  
Lactational Exposure ◽  
Rat Offspring

scholarly journals Vinclozolin Exposure in Utero Induces Postpubertal Prostatitis and Reduces Sperm Production via a Reversible Hormone-Regulated Mechanism

Endocrinology ◽  
2010 ◽  
Vol 151 (2) ◽  
pp. 783-792 ◽  
Author(s):  
Prue A. Cowin ◽  
Elspeth Gold ◽  
Jasna Aleksova ◽  
Moira K. O'Bryan ◽  
Paul M. D. Foster ◽  
...  
Keyword(s):  
Germ Cell ◽  
Cell Apoptosis ◽  
Reproductive Tract ◽  
Nuclear Factor Κb ◽  
In Utero ◽  
High Dose ◽  
Nuclear Factor ◽  
Testicular Germ Cell ◽  
Male Reproductive Tract ◽  
Germ Cell Apoptosis

Vinclozolin is an endocrine-disrupting chemical (EDC) that binds with high affinity to the androgen receptor (AR) and blocks the action of gonadal hormones on male reproductive organs. An alternative mechanism of action of Vinclozolin involves transgenerational effects on the male reproductive tract. We previously reported in utero Vinclozolin exposure-induced prostatitis (prostate inflammation) in postpubertal rats concurrent with down-regulation of AR and increased nuclear factor-κB activation. We postulated the male reproductive abnormalities induced by in utero Vinclozolin exposure could be reversed by testosterone supplementation, in contrast to the permanent modifications involving DNA methyltransferases (Dnmts) described by others. To test this hypothesis, we administered high-dose testosterone at puberty to Vinclozolin-treated rats and determined the effect on anogenital distance (AGD); testicular germ cell apoptosis, concentration of elongated spermatids, and the onset of prostatitis. Concurrently we examined Dnmt1, −3A, −3B, and −3L mRNA expression. Consistent with previous reports, in utero exposure to Vinclozolin significantly reduced AGD, increased testicular germ cell apoptosis 3-fold, reduced elongated spermatid number by 40%, and induced postpubertal prostatitis in 100% of exposed males. Administration of high-dose testosterone (25 mg/kg) at puberty normalized AGD, reduced germ cell apoptosis, and restored elongated spermatid number. Testosterone restored AR and nuclear factor-κB expression in the prostate and abolished Vinclozolin-induced prostatitis. Altered Dnmt expression was evident with in utero Vinclozolin exposure and was not normalized after testosterone treatment. These data demonstrate in utero Vinclozolin-induced male reproductive tract abnormalities are AR mediated and reversible and involve a mechanism independent of Dnmt expression.

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