What is it about?

This study tested whether maternal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) may disrupt the development of neuroendocrine system of their offspring during the perinatal period. TCDD (0.2 or 0.4 lg/kg body weight) was orally administered to pregnant rats from gestation day (GD) 1 to lactation day (LD) 30. Potential effects on neuroendocrine function were evaluated by measuring serum thyroid hormone levels in pregnant rats and their offspring and measuring some biochemical parameters in cerebellum of these offspring on GD 16 and 19, and LD 10, 20, and 30. In both treated groups, a decrease in serum thyroxine (T4), triiodothyronine (T3) and increase in thyrotropin (TSH) levels were noticed during the tested days in dams and offspring, as well as GH levels were decreased in offspring with respect to control group. In cerebellum of control offspring, the levels of monoamines, c-aminobutyric acid (GABA) and acetylcholinesterase (AchE) were found to be increased from GD 16 to LD 30. The hypothyroid conditions due to both maternal administrations of TCDD produced inhibitory effects on monoamines and AchE, and stimulatory actions on GABA in cerebellum of offspring. These alterations were dose and age dependent. Overall, these results suggest that TCDD may act as neuroendocrine disruptor.

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Why is it important?

In conclusion, both maternal administrations of TCDD may impair the development of cerebellum of their offspring via THs and this may, in general, delay the growth and differentiation of the neuroendocrine system (Fig. 1). Thus, TCDD may act as endocrine- and neural-disrupting actions on the development of THs-cerebellum axis during perinatal period. However, it remains to be clarified whether the reported effects of TCDD on development of neuroendocrine system in animal models might be relevant to human health.

Perspectives

There are still many uncertainties on the effect of endocrine disrupting chemicals on thyroid hormones-dependent brain development. Thus, it is critical that neuroendocrinologists and neurotoxicologists work together to fully characterize the multiple neuro-molecular mechanisms of TCDD, particularly the aryl hydrocarbon receptors. Also, more information is needed to determine the role of growth factors and some antioxidant compounds against the neurotoxic effect of persistent organic pollutants, particularly TCDD during the development.

Full Professor Ahmed R. G.
Division of Anatomy and Embryology, Zoology department, Faculty of Science, Beni-Suef University, Egypt.

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This page is a summary of: Perinatal TCDD exposure alters developmental neuroendocrine system, Food and Chemical Toxicology, June 2011, Elsevier,
DOI: 10.1016/j.fct.2011.03.008.
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