Neonatal exposure to bisphenol A alters the hypothalamic-pituitary-thyroid axis in female rats

2018 ◽  
Vol 285 ◽  
pp. 81-86 ◽  
Author(s):  
Marina O. Fernandez ◽  
Nadia S. Bourguignon ◽  
Paula Arocena ◽  
Matías Rosa ◽  
Carlos Libertun ◽  
...  
2003 ◽  
Vol 144 ◽  
pp. s175-s176
Author(s):  
K. Kobayashi ◽  
M. Miyagawa ◽  
R.S. Wang ◽  
M. Suda ◽  
S. Sekiguchi ◽  
...  

1983 ◽  
Vol 102 (3) ◽  
pp. 386-391 ◽  
Author(s):  
Rubén Boado ◽  
Edgardo Ulloa ◽  
Angel A. Zaninovich

Abstract. In the present work the effects of oestradiol benzoate (EB) on pituitary and plasma concentrations of TSH, plasma T4 and T3, and thyroidal activity of male and female rats have been studied. Wistar rats weighing between 150 to 200 g were injected sc with varying doses of EB in corn oil for 9 or 30 days. The animals were exsanguinated by cardiac puncture and the hypophyses removed and individually homogenized at 4°C in 200 μl PBS buffer. Pituitary and plasma TSH were measured by radioimmunoassay. Thyroidal activity was evaluated by a 4 h 131I uptake and by 48 h thyroidal release plasma slopes derived form the ratio PB[125I] (from thyroidal secretion) to PB[131I] (from exogenous [131I]T4). In both male and female rats the 10 and 25 μg doses of EB produced a significant decrease in pituitary TSH content; this effect was more pronounced when the 25 μg dose was given over 30 days. Plasma T4 decreased significantly; plasma T3 was moderately elevated in all groups (NS) and significantly increased in female rats treated with 25 μg EB (P < 0.01). It is concluded that EB induced a marked depression of intrapituitary TSH, probably due to a decrease in synthesis, without affecting the release of TSH into the circulation. Moreover, EB accelerated peripheral T4 kinetics and thyroid gland activity, albeit to a moderate degree.


1983 ◽  
Vol 104 (2) ◽  
pp. 201-205 ◽  
Author(s):  
Yoshiaki Kawai ◽  
Mizuo Azukizawa ◽  
Nobuyuki Ashida ◽  
Yuichi Kumahara ◽  
Kiyoshi Miyai

Abstract. TRH (10 and 1000 μg/kg body weight) was administered ip daily to neonatal rats from day 0 to 9 after birth (Neo-TRH rats) and their pituitary-thyroid axis was examined on days 4, 10, 21 and 90. The pituitary TSH content in Neo-TRH rats was significantly smaller than in controls on days 4 and 10. The serum TSH levels in Neo-TRH rats were significantly lower than those in controls on days 4 (male group only), 10 and 21 (only 10 μg/kg group). The serum T4 levels in Neo-TRH rats were lower than in controls on day 10. The reduced pituitary TSH content and serum TSH and T4 were restored to control levels on day 90. However, the response of serum TSH to exogenous TRH (10 μg/kg/ip) was blunted in Neo-TRH rats on days 10, 21 and 90. It is concluded that repetitive administration of TRH during the neonatal period suppresses the pituitary-thyroid axis in neonatal life, even after the basal hormone level has been restored to normal.


1996 ◽  
Vol 150 (2) ◽  
pp. 169-178 ◽  
Author(s):  
G A C van Haasteren ◽  
E Linkels ◽  
H van Toor ◽  
W Klootwijk ◽  
E Kaptein ◽  
...  

Abstract The reduced thyroid activity during short-term starvation is associated with a lowered hypothalamic synthesis and secretion of TRH. However, little is known about the cause of the reduced thyroid function during prolonged malnutrition. We have therefore studied the effects of food reduction to one-third of normal (FR33) on the hypothalamus-pituitary-thyroid axis of male and female Wistar rats. After 3 weeks body weights of FR33 rats were almost 50% lower than those of controls. In both sexes, FR33 caused marked increases in serum corticosterone, and decreases in serum TSH, thyroxine (T4), free T4, tri-iodothyronine (T3) and free T3. While the free T3 fraction (FFT3) in serum decreased, the free T4 fraction (FFT4) tended to increase. Electrophoretic analysis indicated that decreased FFT3 was correlated with an increased thyroxine-binding globulin, while the increase in FFT4 seemed due to a decreased thyroxine-binding prealbumin binding capacity. Total RNA and proTRH mRNA in the hypothalamus were not affected by FR33. Median eminence and posterior pituitary TRH content tended to increase in FR33 rats, suggesting that hypothalamic TRH release is reduced in FR33 rats. Anterior pituitary TSH content was decreased by FR33 in both sexes, but pituitary TSHβ mRNA and TRH receptor status were not affected except for increased pituitary TSHβ mRNA in female FR33 rats. Although FR33 had no effect on pituitary weight, pituitary RNA and membrane protein content in FR33 rats were 50–70% lower than values in controls. In conclusion, prolonged food reduction suppresses the pituitary-thyroid axis in rats. In contrast to short-term food deprivation, the mechanism whereby serum TSH is suppressed does not appear to involve decreases in proTRH gene expression, but may include effects on pituitary mRNA translation. Our results further support the hypothesis that TSH release may be lowered by increased corticosterone secretion, although the mechanism of this effect may differ between acute starvation and prolonged food reduction. Journal of Endocrinology (1996) 150, 169–178


2020 ◽  
Vol 87 (4) ◽  
pp. 503-511
Author(s):  
Jing Qiu ◽  
Yanyan Sun ◽  
Wen Sun ◽  
Yonghong Wang ◽  
Teng Fan ◽  
...  

Author(s):  
David López-Rodríguez ◽  
Delphine Franssen ◽  
Elena Sevrin ◽  
Arlette Gérard ◽  
Cédric Balsat ◽  
...  

Abstract Exposure to Bisphenol A (BPA), a ubiquitous endocrine disrupting chemical (EDC) is known to produce variable effects on female puberty and ovulation. This variability of effects is possibly due to differences in dose and period of exposure. Little is known about the effects of adult exposure to environmentally relevant doses of this EDC and the differences in effect after neonatal exposure. This study aims at comparing the effects of neonatal versus adult exposure to a very low or a high dose of BPA for two weeks on ovulation and folliculogenesis and exploring the hypothalamic mechanisms involved in such disruption by BPA. One day-old and 90 day-old female rats received daily subcutaneous injections of corn oil (vehicle) or BPA (25 ng/kg/d or 5 mg/kg/d) for 15 days. Neonatal exposure to both BPA doses significantly disrupted the estrous cycle and induced a decrease in primordial follicles. Effects on estrous cyclicity and folliculogenesis persisted into adulthood, consistent with a disruption of organizational mechanisms. During adult exposure, both doses caused a reversible decrease in antral follicles and corpora lutea. A reversible disruption of the estrous cycle associated with a delay and a decrease in the amplitude of the LH surge was also observed. Alterations of the hypothalamic expression of the clock gene Per1 and the novel reproductive peptide Phoenixin indicated a disruption of the hypothalamic control of the preovulatory LH surge by BPA.


1985 ◽  
Vol 109 (2) ◽  
pp. 237-242 ◽  
Author(s):  
R. Iglesias ◽  
M. Llobera ◽  
E. Montoya

Abstract. The effect of chronic oral thyrotrophin-releasing hormone (TRH) administration on thyrotrophin (TSH), l-triiodothyronine (T3) and l-thyroxine (T4) serum levels, pituitary TSH concentration and serum response to acute TRH injection, has been studied in female rats under different thyroidal conditions: shamoperated control animals, and thyroidectomized animals receiving 25 μg l-T4/100 g body weight/day. After 30 days, these groups were divided into two subgroups (6–10 animals per group), one receiving the aforementioned treatment and the other the same plus 2 mg TRH/10 ml distilled water (DW), as drinking water. TRH-treated sham-operated animals showed significantly reduced serum and pituitary TSH levels and inceased serum T3 levels at most of the times studied (1, 6, 10, 18 and 34 days of oral TRH or DW administration), and a transient elevation in serum T4 between day 1 and 6. Thyroidectomized-l-T4-treated animals showed increased serum and pituitary TSH levels throughout the treatment and reduced T3 and T4 serum levels at the beginning, as compared to thyroidectomized-l-T4-treated animals. TSH response to iv TRH administration on the 10th day of oral TRH administration was reduced in controls chronically treated with oral TRH as compared to nontreated controls, and was increased in thyroidectomizedl-T4-treated animals on chronic TRH vs the same group on oral DW. These results suggest that chronic TRH administration can stimulate TRH synthesis in vivo, bypassing the inhibitory effects of thyroid hormones, the increased pituitary TSH reserve being responsible for the partial restoration of a response to acute TRH injection in the thyroidectomized-l-T4-treated animals.


2007 ◽  
Vol 194 (1) ◽  
pp. 201-212 ◽  
Author(s):  
Lucas Monje ◽  
Jorgelina Varayoud ◽  
Enrique H Luque ◽  
Jorge G Ramos

The xenoestrogen bisphenol A (BPA) is commonly ingested by humans. We examined the effects of neonatal exposure to low versus high doses of BPA over the control of estrogen receptor α (ERα) expression in the preoptic area (POA) of prepubertal female rats. Pups received s.c. injections every 48 h of BPA (high dose, 20 mg/kg and low dose, 0.05 mg/kg) or diethylstilbestrol (DES, 0.02 mg/kg) from postnatal day (PND) 1 to PND7 and were killed at PND8 or PND21. Relative expression of ERα transcripts containing alternative 5′-untranslated regions OS, ON, O, OT, and E1 in POA were evaluated by RT-PCR. Methylation status of ERα promoters was determined by bisulfited DNA restriction analysis and ERα protein by immunohistochemistry. In PND8, the high dose of BPA and DES diminished total ERα mRNA levels, mediated by the decreased expression of ERα-O and ERα-OT variants. In contrast, the low dose of BPA augmented total ERα mRNA by increasing the expression of the ERα-E1 variant. In PND21, both BPA doses increased total ERα mRNA by means of the augmented expression of ERα-O and ERα-OT variants. In PND21, the methylation status of the ERα promoters and the circulating levels of estradiol were similar in all experimental groups. At PND8 and PND21, DES and the high dose of BPA decreased, while the low dose of BPA increased ERα protein in the POA. These findings show that neonatal BPA exposure alters the abundance of hypothalamic ERα transcript variants and protein in a dose-dependent manner.


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