Effects of maternal exposure to di- n -butyl phthalate during pregnancy and breastfeeding on ovarian development and function of F1 female rats

2016 ◽  
Vol 43 ◽  
pp. 38-43 ◽  
Author(s):  
Zuoliang Xie ◽  
Jianping Wang ◽  
Fen Dai ◽  
Xubing Jin ◽  
Kele Wu ◽  
...  
2010 ◽  
Vol 29 (1) ◽  
pp. 99-105 ◽  
Author(s):  
Marina T. Guerra ◽  
Wellerson R. Scarano ◽  
Fabíola C. de Toledo ◽  
Janete A.A. Franci ◽  
Wilma De G. Kempinas

1999 ◽  
Vol 161 (1) ◽  
pp. 69-75 ◽  
Author(s):  
VK Srivastava ◽  
JK Hiney ◽  
V Rettori ◽  
WL Dees

Nitric oxide (NO) has been shown to contribute to ovarian development and function. In non-ovarian tissues NO can be altered by ethanol (ETOH), a drug considered to be a gonadal toxin in men as well as male and female rats. The present study was undertaken to determine if some of the detrimental effects of chronic ETOH exposure on prepubertal ovarian function could be due to ETOH-induced alterations in the intraovarian NO system. Rats were implanted with intragastric cannulae on day 24 and began receiving control or ETOH diets on day 29. All rats were killed on day 34, determined to be in the late juvenile stage of development, and their ovaries and blood were collected. We analyzed the expression of the two constitutive forms of nitric oxide synthase (NOS), i.e. neuronal (n) NOS and endothelial (e) NOS, as well as the inducible (i) form of NOS protein in the ovaries of control and ETOH-treated rats by Western immunoblotting. Results demonstrate that eNOS protein increased markedly (P<0.02; 140 kDa) in ETOH-treated rats compared with controls. ETOH treatment did not alter the protein expression of nNOS (155 kDa) and only slightly increased that of iNOS (130 kDa). We also assessed NOS activity as determined by nitrite accumulation and by the conversion of L-[14C]arginine to L-[14C]citrulline. In this regard, the ETOH-treated animals showed an increase in ovarian nitrite generation (P<0.05), as well as an increase in ovarian citrulline formation (P<0.0001), when compared with control animals. Along with the above described ETOH-induced increases in ovarian eNOS and NO activity, the serum levels of estradiol were concomitantly suppressed (P<0.001) in the ETOH-treated rats. These results demonstrate for the first time the ETOH-induced changes in the prepubertal ovarian NO/NOS system, and suggest that these alterations contribute to the detrimental actions of the drug on prepubertal ovarian development and function.


2018 ◽  
Vol 34 (11) ◽  
pp. 744-752 ◽  
Author(s):  
Maha M Rashad ◽  
Mona K Galal ◽  
Adel M EL-Behairy ◽  
Eman M Gouda ◽  
Said Z Moussa

The aim of this study was to investigate the effects of maternal exposure to di-( n-butyl) phthalate (DBP) on testicular development and function in pre-pubertal and post-pubertal male rat offspring. Fourteen pregnant female rats were equally divided into two groups: a control group and a DBP-treated group. During gestation day (GD) 12 to postnatal day (PND) 14, the control group was administered 1 ml/day corn oil, and the DBP-treated group was administered DBP 500 mg/kg/day by oral gavage. On PND 25 (pre-puberty) and PND 60 (post-puberty), blood for serum and the testes were collected from five male offspring of each group. To determine the relationship between the methylation state of the c-Myc promoter and the expression of the c-Myc gene, some apoptotic-related genes, such as p53 and Bax, the anti-apoptotic Bcl-2 gene, and some growth arrest-related genes, such as BRD7 and GAS1, were examined. Compared with the control ( p < 0.05), at pre-puberty, DBP induces c-Myc hyper-methylation with significant downregulation for c-Myc, p53, Bax genes, and significant upregulation for Bcl-2, BRD7, and GAS1, while at post puberty, the methylation state and expression of c-Myc and apoptosis-related genes returned to control levels in the same sequence with the fold change in the expression of BRD7 and GAS1 genes. These findings suggest that DBP induced a transient pre-pubertal increase in c-Myc promoter methylation that may be associated with disruption of both apoptotic and growth mechanisms in the testes.


2014 ◽  
Author(s):  
Raffaella Rossetti ◽  
Irene Negri ◽  
Chiara Castronovo ◽  
Palma Finelli ◽  
Luca Persani

2002 ◽  
Vol 7 (1-3) ◽  
pp. d2006 ◽  
Author(s):  
Barbara Vanderhyden

Author(s):  
Weinberg-Shukron A ◽  
Rachmiel M ◽  
Renbaum P ◽  
Gulsuner S ◽  
Walsh T ◽  
...  

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Viridiana Navarrrete ◽  
Marcos Ayala ◽  
Antonio Rodriguez ◽  
Francisco Villarreal ◽  
Israel Ramirez-Sanchez

1954 ◽  
Vol 10 (3) ◽  
pp. 266-NP ◽  
Author(s):  
I. CHESTER JONES ◽  
A. WRIGHT

SUMMARY The adrenal of male and female rats with persistent diabetes insipidus showed a prominent zona fasciculata and zona reticularis. The zona glomerulosa was narrow or absent. The results from this and the preceding three papers are here reviewed together. It is concluded that control of salt-electrolyte metabolism cannot be ascribed to the zona glomerulosa. It is probable that the zona fasciculata is reponsible for most of the adrenocortical secretions. The zona glomerulosa is a vegetative back-water of cells, which is able to produce minimal amounts of adrenocortical secretions without stimulation by pituitary hormones, but is only of significance when the latter are absent. Rising amounts of circulating adrenocorticotrophic hormone (ACTH) can transform the zona glomerulosa into actively secreting cells of the zona fasciculata type. After cessation of such activity the zona glomerulosa re-forms, as the amount of ACTH will maintain only a certain volume of zona fasciculata (and zona reticularis) against the rigid limiting inner circumference formed by the medulla; some of the cells derived from the chief area of cell division in the outer part of the zona fasciculata do not mature to cells of the zona fasciculata type, but form zona glomerulosa cells. It is thought that cell migration occurs from the cells of the outer region of the zona fasciculata to the zona reticularis and that this is, normally, a slow process.


Sign in / Sign up

Export Citation Format

Share Document