scholarly journals Tissue Distribution and Associated Toxicological Effects of Decabrominated Diphenyl Ether in Subchronically Exposed Male Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Fuxin Wang ◽  
Jianshe Wang ◽  
Guocheng Hu ◽  
Xiaojun Luo ◽  
Bixian Mai ◽  
...  

Concerns about decabrominated diphenyl ether (BDE-209) have arisen recently due to its increasing concentrations in the environment. We investigated the tissue concentration, distribution, and the debromination of BDE-209 after oral exposure, using rats as a model. Three groups of male rats were administrated by oral gavage with corn oil containing 0, 10, or 50 mg/kg bw/day of BDE-209 over 90 days. After exposure, BDE-209 and its metabolites levels in the liver, kidney, and adipose of the rats were measured. The mRNA expression levels of cytochrome P450 (CYP) enzymes in liver, serum thyroid hormone levels, and open-field tests were also measured. BDE-209 and several octa- and nona-BDE congeners were detected in the tissues of the dosed rats, indicating that BDE-209 was bioavailable and biotransformative in male rats. BDE-209 and its debrominated congeners had no mRNA level effect on selective genes from the CYP family in the liver or on the spontaneous behavior of adult male rats. Conversely, the level of thyroid hormone, total triiodothyronine (T3) in rats from the dosed treatments increased significantly compared to the control group.

2020 ◽  
Vol 32 (10) ◽  
pp. 914
Author(s):  
M. S. Garcia ◽  
W. A. Orcini ◽  
R. L. Peruquetti ◽  
J. E. Perobelli

This study investigated the reproductive toxicity of methylmercury (MeHg) and Aroclor (Sigma-Aldrich), alone or in combination, following exposure of prepubertal male rats considering the chromatoid body (CB) as a potential target. The CB is an important molecular regulator of mammalian spermatogenesis, primarily during spermatid cytodifferentiation. Male Wistar rats were exposed to MeHg and/or Aroclor , according the following experimental design: control group, which was administered in corn oil (vehicle) only; MeHg-treated group, which was administered 0.5mg kg−1 day−1 MeHg; Aroclor-treated group, which was administered 1mg kg−1 day−1 Aroclor; Mix-LD, group which was administered a low-dose mixture of MeHg (0.05mg kg−1 day−1) and Aroclor (0.1mg kg−1 day−1); and Mix-HD group, which was administered a high-dose mixture of MeHg (0.5mg kg−1 day−1) and Aroclor (1.0mg kg−1 day−1). MeHg was diluted in distilled water and Aroclor was made up in corn oil (volume 1mL kg−1). Rats were administered the different treatments from PND23 to PND53 by gavage, . The morphophysiology of CBs was analysed, together with aspects of steroid hormones status and regulation, just after the last treatment on PND53. In addition, the long-term effects on sperm parameters were assessed in adult animals. MeHg exposure increased mouse VASA homologue (MVH) protein levels in seminiferous tubules, possibly affecting the epigenetic status of germ cells. Aroclor produced morphological changes to CB assembly, which may explain the observed morphological defects to the sperm flagellum and the consequent decrease in sperm motility. There were no clear additive or synergistic effects between MeHg and Aroclor when administered in combination. In conclusion, this study demonstrates that MeHg and Aroclor have independent deleterious effects on the developing testis, causing molecular and morphological changes in CBs. To the best of our knowledge, this is the first study to show that CBs are targets for toxic agents.


1994 ◽  
Vol 142 (1) ◽  
pp. 77-84 ◽  
Author(s):  
R Vranckx ◽  
M Rouaze-Romet ◽  
L Savu ◽  
P Mechighel ◽  
M Maya ◽  
...  

Abstract We have investigated the role of the thyroid compared with the hypophysis in the regulation of the two saturable thyroid hormone carriers of rat serum, thyroxine-binding globulin (TBG) and transthyretin (TTR). We examined, at serum and hepatic mRNA level, the responses of TBG and TTR to thyroidectomy (Tx), hypophysectomy (Hx) and replacement treatments with tri-iodothyronine (T3) or/and GH, both hormones which are depleted when the thyroid or hypophysis are removed. The studies were performed on male rats at the age of 8 weeks, when the developmentally regulated TBG becomes undetectable after its transient postnatal rise, while the non-developmentally regulated TTR presents its normal, age-independent level of expression. Tx-induced TBG re-expression was completely reversed by T3 replacement and unresponsive to GH replacement. TTR in the serum, on the other hand, was not affected by Tx or T3 replacement, moderately reduced by Tx in terms of the amount of mRNA, and markedly reduced by GH replacement. GH treatment, moreover, inhibited the expression of TTR in euthyroid controls. Hx, like Tx, induced TBG re-expression, an effect efficiently antagonized by T3 replacement. However, TBG synthesis was higher in Hx than in Tx rats and less effectively antagonized by T3 replacement. Most unexpectedly, GH induced a dramatic further increase in TBG synthesis, and the TBG synthesized in the GH-replaced Hx rats was entirely resistant to down-regulation by T3 replacement. TTR was markedly decreased at both serum and hepatic levels by Hx, unaffected by T3 and further decreased by GH replacement. Our evidence is consistent with two distinct regulatory pathways for TBG, one under direct negative control by the thyroid hormones, without GH mediation, and the other independent of the thyroid, but involving GH, possibly for its role in the control of carbohydrate metabolism. We have shown that TTR depends little on the thyroid and is regulated by pituitary factors in a complex way, since it is inhibited by Hx but also by treatment with GH. The divergent regulatory pathways of TBG and TTR may be important in the homeostasis of thyroid hormone bioavailability. Journal of Endocrinology (1994) 142, 77–84


Chemosphere ◽  
2017 ◽  
Vol 186 ◽  
pp. 749-756 ◽  
Author(s):  
Xiu-Bo Mi ◽  
Lian-Jun Bao ◽  
Chen-Chou Wu ◽  
Charles S. Wong ◽  
Eddy Y. Zeng

2021 ◽  
Vol 9 (3) ◽  
pp. 253-257
Author(s):  
Volkan Gelen ◽  
Emin Şengül ◽  
Dursun Ali Çınar

5‐fluorouracil (5-FU), a pyrimidine analogue anticarcinogenic agent, is widely used in the solid tumors treatment. Use of the 5-FU causes cardiotoxicity. Our aim in this study investigations effects of Quercetin and Rutin on ECG parameters in the 5-FU-induced cardiotoxicity in rats. In the present study used male rats. Rats were divided randomly to eight group. The control group was given intragastric corn oil for 14 days. The 5-FU group rats were given ig corn oil for 14 days and injected intraperitoneal the single dose of 5-FU(50 mg/kg) on the eleventh day. The Q50+5-FU and Q100+5-FU groups were given ig 50 mg/kg and 100 mg/kg Q for 14 days, respectively and these groups were injected single dose of 5-FU(50 mg/kg) on the 11th days of Q application. The group Q100 was Q(100 mg/kg-ig) for 14 days. The Rutin50+5-FU and Rutin100+5-FU groups were injected ig 50 mg/kg and 100 mg/kg of the Rutin for 14 days, respectively. These groups were injected single dose of 5-FU(50 mg/kg) in the 11th days of Rutin application. The Rutin 100 group was given Rutin(100 mg/kg-ig) for 14 days. In the end of experimental application recorded to ECGs of the rats. 5-FU administration rats were observed that it was caused sinus tachycardia and ST elevation. Also, in the 5-FU group QRS segment was shorter and the duration and amplitude of the P was different from other groups. In both doses of Q and Rutin were prevented these changes and our findings were seen the consistent with the literature.


2013 ◽  
Vol 33 (3) ◽  
pp. 230-239 ◽  
Author(s):  
M A Ahbab ◽  
Ü Ündeğer ◽  
N Barlas ◽  
N Başaran

Phthalates are diester derivatives of phthalic acid widely used in many commercial applications. The aim of this study is therefore to evaluate possible genotoxicity of di- n-hexyl phthalate (DHP) and dicyclohexyl phthalate (DCHP) at different concentrations using single-cell gel electrophoresis (comet) and terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end-labeling (TUNEL) assays in testes samples of male rat pups. DCHP and DHP in corn oil were administered to the pregnant rats by gavage at the doses of 0 (vehicle), 20, 100, and 500 mg kg−1 day−1 from gestational day 6 (GD6) to GD19. After delivery, male rats were allowed to grow until prepubertal, pubertal, and adulthood. At necropsy, the blood samples were collected from heart and were excised immediately. The apoptotic cells of prepubertal, pubertal, and adult testis were detected using TUNEL assay. The comet assay was performed on blood lymphocytes and testes samples of adult male rats. The comet assay results showed that tail length, tail intensity, olive tail moment (OTM), and percentage of DNA present in tail were higher when DHP content was increased. Judging from the values of OTM and percentage of DNA, DHP could significantly induce DNA breakage at doses of 100 and 500 mg kg−1 day−1 compared with the control group. An increase in TUNEL-positive cells of prepubertal, pubertal, and adult testicular cells was observed in the treated groups. In conclusion, prenatal exposure to DHP and DCHP may possess genotoxic risk to testicular cells of rats at all stages of development, even at adulthood.


1976 ◽  
Vol 231 (2) ◽  
pp. 366-369 ◽  
Author(s):  
FX Pi-Sunyer ◽  
JM Conway ◽  
M Lavau ◽  
G Campbell ◽  
AB Eisenstein

Forty-eight male rats were fed a nutritionally complete diet containing 30% of dietary energy as fat. For 24 animals (control) the fat source was corn oil, for the remaining 24 rats (experimental) the fat source was a triundecanoin-corn oil mixture (7:3, wt/wt). After 6 wk, groups of control and experimental rats were killed after 0, 24, and 48 h of fasting. In the experimental group, adipose tissue fatty acids contained, on average, 280 mmol undecanoate/mol fatty acid. In the control group, no odd-numbered fatty acids were present. During fasting, the experimental groups had higher plasma glucose and alanine levels, higher plasma insulin-to-glucagon ration, and lower liver phosphenol pyruvate caboxykinase. The results suggest that the terminal propionate residues generated when odd carbon fatty acids are oxidized become gluconeogenic precursors and cause a reduced need for gluconeogenesis from protein.


PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7039
Author(s):  
Lin Wang ◽  
Jie Xu ◽  
Feng Zeng ◽  
Xiangjun Fu ◽  
Weihong Xu ◽  
...  

Objective Environmental endocrine disruptors (EEDs) with a weak ability to mimic estrogen have been associated with thyroid dysfunction. However, little is known about the effect of nonylphenol (NP), a well-known EED, on thyroid structure. The present study evaluates whether gestational and lactational exposure to NP impacts growth and thyroid structure in F1 male rats. Methods A total of 60 rats were gavaged with NP (25, 50, and 100 mg/kg), estradiol (E2, 30 μg/kg/day), and corn oil alone (vehicle control) from gestational day 6 to postnatal day (PND) 21. Serum thyroid hormones free triiodothyronine (FT3), free thyroxine (FT4) and thyroid stimulating hormone levels were detected by automated chemiluminescence immunoassay analyzer. The NP level in the thyroid was measured using high-performance liquid chromatography. The ultrastructure of follicular epithelial cells was examined using transmission electron microscopy. Histopathology was conducted using hematoxylin and eosin staining. Results On PND 0, exposure to 50 and 100 mg/kg/day NP led to a significant decrease in the average litter size, litter weight and number of live pups per litter compared to the control group (P < 0.05). Dams exposed to NP during perinatal period demonstrated decreased serum levels of FT3 and FT4 in F1 male rats, when compared to the control group (P < 0.05). The NP level in the control group was 3.39 ± 0.08 ng/mg, while NP levels in the low, middle, and high dose groups ranged from 5.20 to 11.00 ng/mg. Exposure caused a dose-related increase in NP level in the thyroid of male pups (P < 0.01). The thicknesses of the thyroid follicular epithelium were 2.06 ± 0.37 μm in the control group and 3.97 ± 1.61 μm in the high-dose group. The thickness of the thyroid follicular epithelium increased with an increase in treatment dose in a dose-dependent manner (P < 0.05). The sizes of the thyroid follicles were 1,405.53 ± 866.62 μm2 in the control group and 317.49 ± 231.15 μm2 in the high-dose group. With increasing NP dosages, animals showed a decreased size of the thyroid follicle (P < 0.01). Thyroid follicular cells of NP-treated rats showed mildly swollen mitochondria and dilated rough endoplasmic reticulum in the cytoplasm. Conclusion Nonylphenol can cross the placental barrier and accumulate in the thyroid of F1 male rats. Gestational and lactational exposure to NP in dams impacted both development and growth of pups and damaged the ultrastructure of their thyroid tissue, which may further negatively influence normal thyroid function.


2019 ◽  
Vol 11 (3) ◽  
pp. 20-31
Author(s):  
Carla de Oliveira Carletti ◽  
Rodrigo Correia Santos ◽  
Luis Fernando Sierra de Araújo ◽  
Murilo Américo de Paiva Santos ◽  
Mariana Matera Veras ◽  
...  

The purpose of thestudy was to evaluate the behavioral changes of male and female adultrats exposed to fine and ultrafine particulate matter (PM≤2,5) suspended in air pollution during development. Wistar rats aged 7 postnataldayswere exposed to the chamber of an atmospheric particle concentrator. Open field tests and sucrose preference tests were performed to assess the presence of anxiety and depression behaviors. Male rats from the pollution group showed reduced locomotor activity and length of stay in the open field center when compared to the control group. The sucrose preference test showed statistical significance between the pollution and control groups(male+female), and among the males of the pollution and control group.The study concluded thatexposure to PM≤2.5 causes behavioral changes characteristic of depression and anxietyin adult male rats exposed during the developmental period.


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