Horm Metab Res 2006; 38(10): 639-649
DOI: 10.1055/s-2006-954592
Original Basic

© Georg Thieme Verlag KG Stuttgart · New York

Ultrastructural Effects of Low Dosage Endocrine Disrupter Chemicals on Neural Cells of the Chicken Embryo Model

E. Pretorius 1 , M. S. Bornman 2 , J. Marx 1 , E. Smit 1 , C. F. van der Merwe 3
  • 1Department of Anatomy, School of Health Sciences, Faculty of Health Sciences, University of Pretoria, South Africa
  • 2Departments of Urology, School of Medicine, Faculty of Health Sciences, University of Pretoria, South Africa
  • 3Laboratory for Microscopy and Microanalysis, University of Pretoria, South Africa
Further Information

Publication History

Received 2 March 2006

Accepted after revision 10 May 2006

Publication Date:
30 October 2006 (online)

Abstract

Previous research suggests that endocrine disrupters (EDCs) like nonylphenol cause apoptosis (both via the intrinsic and extrinsic pathway) and that ROS generation and Ca2+ play a fundamental role in the process. We have investigated morphological changes induced by 17β-estradiol, nonylphenol, 17α-ethynylestradiol and diethylstilbestrol on the in ovo neural chick embryo model by using transmission and scanning electron microscopy (TEM and SEM). We found that estrogenic substances such as nonylphenol, diethylstilbestrol (DES) and 17α-ethynylestradiol, as well as 17β-estradiol cause ultrastructural changes to developing neurons, resulting in damage to the plasma, mitochondrial as well as nuclear membranes. Furthermore, both apoptotic blebbing and necrotic (or oncotic) budding was seen in TEM and SEM micrographs. SEM shows that nonylphenol-exposed neurons have irregular cell surfaces with pseudopodia, cell shrinkage and breakages in the plasma membrane - typical of apoptosis. TEM indicated that plasma membranes and double nuclear membranes have structural changes, with apoptotic bodies (blebbing) and disrupted mitochondrial membranes. In 17α-ethynylestradiol-exposed neurons, disruption of the plasma membrane with cell swelling and vacuolization was present. No apoptotic bodies or budding were noted here. 17β-Estradiol induced openings in the plasma membrane, while DES-exposed neurons did not show any morphological changes. Therefore we conclude that EDC damage is morphologically visible and the damage is recognized as apoptosis and oncosis. Estrogenic substances may hence modify hormonal actions thereby leaving the developing nervous system more susceptible to damaging events.

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Correspondence

E. Pretorius

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South Africa

Phone: +27/12/319 25 33

Fax: +27/12/319 22 40

Email: resia.pretorius@up.ac.za

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