Effects of the peroxisome proliferator di(2-ethylhexyl)phthalate on cell turnover and peroxisome proliferation in primary chick embryo hepatocytes

2012 ◽  
Vol 31 (12) ◽  
pp. 2856-2860 ◽  
Author(s):  
Elio Arias
Keyword(s):  
Chick Embryo ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferation ◽  
Cell Turnover ◽  
Ethylhexyl Phthalate

Ultrastructural Study of Peroxisome Proliferation in Hepatocytes by Quick-Freezing and Deep-Etching Method

1988 ◽  
Vol 46 ◽  
pp. 258-259
Author(s):  
S. Ohno
Keyword(s):  
Electron Microscopy ◽  
Liquid Nitrogen ◽  
Ultrastructural Study ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferation ◽  
Solution Ph ◽  
Deep Etching ◽  
Quick Freezing ◽  
Ethylhexyl Phthalate ◽  
Conventional Electron Microscopy

It had been emphasized that luminar continuities between sER and peroxisomes were detected by conventional electron microscopy. However, recent studies ruled out the luminar continuities between sER and peroxisomes. Lazarow et al. reported that peroxisomal proteins were synthesized on free ribosomes and postulated the existence of “peroxisomal reticulum” distinct from the ER. The object of this study is to clarify the proliteration mechanism of peroxisomes after administration of a peroxisome proliferator, DEHP (di-2- ethylhexyl phthalate).Mice treated with 2% DEHP for 1, 3, 5 and 7 days and normal mice were perfused with 2% paraformaldehyde in 0.1M phosphate buffered solution, pH 7.4, (PB) for 5 min. The livers were cut into small pieces, washed in PB to remove cytoplasmic soluble proteins and were fixed again with 2% paraformaldehyde-0.25% glutaraldehyde for 30 min. They were quickly frozen in isopentane-propane mixture (around -190 C) and fractured in liquid nitrogen to remove the damaged surface tissues. They were deeply etched in Eiko FD-3S machine (-95°C, 2-6xl0-7 Torr) and rotary shadowed with platinum.

scholarly journals Specific changes in the protein composition of rat liver in response to the peroxisome proliferators ciprofibrate, Wy-14,643 and di-(2-ethylhexyl)phthalate

1985 ◽  
Vol 227 (3) ◽  
pp. 767-775 ◽  
Author(s):  
T Watanabe ◽  
N D Lalwani ◽  
J K Reddy
Keyword(s):  
Gel Electrophoresis ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferation ◽  
Peroxisome Proliferators ◽  
Two Dimensional ◽  
Two Dimensional Gel Electrophoresis ◽  
Basic Proteins ◽  
Acidic Proteins ◽  
Liver Homogenates ◽  
Ethylhexyl Phthalate

The hypolipidaemic agents ciprofibrate and Wy-14,643 ([4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio]acetic acid) and the phthalate-ester plasticizer di-(2-ethylhexyl)-phthalate (DEHP), like other peroxisome proliferators, produce a significant hepatomegaly and induce the peroxisomal fatty acid beta-oxidation enzyme system together with profound proliferation of peroxisomes in hepatic parenchymal cells. Changes in the profile of liver proteins in rats following induction of peroxisome proliferation by ciprofibrate, Wy-14,643 and DEHP have been analysed by high-resolution two-dimensional gel electrophoresis. The proteins of whole liver homogenates from normal and peroxisome-proliferator-treated rats were separated by two-dimensional gel electrophoresis using isoelectric focusing for acidic proteins and nonequilibrium pH gradient electrophoresis for basic proteins. In the whole liver homogenates, the quantities of six proteins in acidic gels and six proteins in the basic gels increased following induction of peroxisome proliferation. Peroxisome proliferator administration caused a repression of three acidic proteins in the liver homogenates. By the immunoblot method using polyspecific antiserum against soluble peroxisomal proteins and monospecific antiserum against peroxisome proliferation associated Mr 80000 polypeptide (polypeptide PPA-80), the majority of basic proteins induced by these peroxisome proliferators appeared to be peroxisomal proteins. Polypeptide PPA-80 becomes the most abundant protein in the total liver homogenates of peroxisome-proliferator-treated rats. These results indicate that ciprofibrate, DEHP and Wy-14,643 induce marked changes in the profile of specific hepatic proteins and that some of these changes should serve as a baseline to identify a set of gene products that may assist in defining the specific ‘peroxisome proliferator domain’.

Possible Mechanisms in Hepatocarcinogensis by the Peroxisome Proliferator Di(2-Ethylhexyl)Phthalate

1989 ◽  
Vol 21 (1) ◽  
pp. 65-102 ◽  
Author(s):  
James G. Conway ◽  
Russell C. Cattley ◽  
James A. Popp ◽  
Byron E. Butterworth
Keyword(s):  
Peroxisome Proliferator ◽  
Ethylhexyl Phthalate

scholarly journals Embryonic exposures to mono-2-ethylhexyl phthalate induce larval steatosis in zebrafish independent of Nrf2a signaling

2020 ◽  
pp. 1-9
Author(s):  
Karilyn E. Sant ◽  
Hadley M. Moreau ◽  
Larissa M. Williams ◽  
Haydee M. Jacobs ◽  
Anna M. Bowsher ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatic Steatosis ◽  
Antioxidant Response ◽  
Abnormal Development ◽  
Fish Length ◽  
Peroxisome Proliferator ◽  
Primary Metabolite ◽  
Peroxisome Proliferator Activated Receptor ◽  
Expression Of Genes ◽  
Ethylhexyl Phthalate

Abstract Mono-2-ethylhexyl phthalate (MEHP) is the primary metabolite of the ubiquitous plasticizer and toxicant, di-2-ethylhexyl phthalate. MEHP exposure has been linked to abnormal development, increased oxidative stress, and metabolic syndrome in vertebrates. Nuclear factor, Erythroid 2 Like 2 (Nrf2), is a transcription factor that regulates gene expression in response to oxidative stress. We investigated the role of Nrf2a in larval steatosis following embryonic exposure to MEHP. Wild-type and nrf2a mutant (m) zebrafish embryos were exposed to 0 or 200 μg/l MEHP from 6 to either 96 (histology) or 120 hours post fertilization (hpf). At 120 hpf, exposures were ceased and fish were maintained in clean conditions until 15 days post fertilization (dpf). At 15 dpf, fish lengths and lipid content were examined, and the expression of genes involved in the antioxidant response and lipid processing was quantified. At 96 hpf, a subset of animals treated with MEHP had vacuolization in the liver. At 15 dpf, deficient Nrf2a signaling attenuated fish length by 7.7%. MEHP exposure increased hepatic steatosis and increased expression of peroxisome proliferator-activated receptor alpha target fabp1a1. Cumulatively, these data indicate that developmental exposure alone to MEHP may increase risk for hepatic steatosis and that Nrf2a does not play a major role in this phenotype.

scholarly journals The Role of Peroxisome Proliferator–Activated Receptor Gamma (PPARγ) in Mono(2-ethylhexyl) Phthalate (MEHP)-Mediated Cytotrophoblast Differentiation

2019 ◽  
Vol 127 (2) ◽  
pp. 027003 ◽  
Author(s):  
Hussein Shoaito ◽  
Julia Petit ◽  
Audrey Chissey ◽  
Nicolas Auzeil ◽  
Jean Guibourdenche ◽  
...  
Keyword(s):  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ethylhexyl Phthalate

In Vitro Evaluation of Plasticizer Activity on the Growth and Metabolism of Chick Embryo Fibroblasts and on the Development of Chick Embryo Lungs

1992 ◽  
Vol 20 (6) ◽  
pp. 475-482 ◽  
Author(s):  
G Stabellini ◽  
O Fiocchi ◽  
A Pellati ◽  
A Caruso
Keyword(s):  
Cell Proliferation ◽  
Protein Synthesis ◽  
Chick Embryo ◽  
Primary Cultures ◽  
Embryonic Cells ◽  
Cytostatic Effect ◽  
Dna And Protein Synthesis ◽  
Embryo Fibroblasts ◽  
Ethylhexyl Phthalate

Administration of di(2-ethylhexyl) phthalate (DEHP) to primary cultures of chick embryo fibroblasts brought about a decrease in cell proliferation rate after 48 h and an inhibition of both DNA and protein synthesis measured by [3H]thymidine and [3H]leucine, respectively, after 48h. The growth of chick embryo lung rudiments in vitro was also depressed by DEHP treatment. Lung rudiment were smaller in DEHP-treated embryos after 6 days' treatment. These results indicate that DEHP has a cytostatic effect on embryonic cells and tissues. L'administration de di(2-éthylhexyl) phthalate (DEHP) à des cultures primaires de fibroblastes d'embryon de poulet a provoqué une diminution du taux de prolifération cellulaire après 48 heures et une inhibition de la synthèse à la fois d'ADN et de protéines mesurée, respectivement, par [3H]thymidine et [3H]leucine après 48 h. La croissance des ébauches pulmonaires de l'embryon de poulet in vitro a également été abaissée par le traitement DEHP. Les ébauches pulmonaires étaient plus petites dans les embryons traités au DEHP après un traitement de 6 jours. Ces résultats indiquent que le DEHP a un effet cytostatique sur les cellules et tissus embryonnaires.

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