What is it about?
Polychlorinated biphenyls (PCBs) are persistent environmental pollutants that can severely disrupt the endocrine system. In the present study, early-weanedmale ratswere administered a single dose of 2,3,6-20,50-pentachlorinated biphenyl (PCB 95; 32 mg/kg per day, by i.p. injection) for two consecutive days (postnatal days (PNDs) 15 and 16) and killed 24 and 48 h after the administration of the last dose. Compared with the control group, administration of PCB 95 induced a reduction (P!0.01) in serum concentrations of thyroxine, triiodothyronine, and GH and an increase (P!0.01) in the serum concentration of TSH at PNDs 17 and 18. These conspicuous perturbations led to some histopathological deterioration in the thyroid gland characterized by follicular degeneration, edema, fibrosis, hemorrhage, luminal obliteration, and hypertrophy with reduced colloidal contents at PND 18. The dyshormonogenesis and thyroid dysgenesismay be attributed to the elevation ofDNAfragmentationatPNDs 17 and 18. Furthermore, this hypothyroid state revealed higher (P!0.01) serum concentrations of leptin, adiponectin, and tumor necrosis factor and lower (P!0.01) serum concentrations of IGF1 and insulin at both PNDs compared with the control group. Interestingly, the body weight of the neonates in the PCB 95 group exhibited severe decreases throughout the experimental period in relation to that of the control group. These results imply that PCB 95 may act as a disruptor of the developmental hypothalamic–pituitary–thyroid axis. Hypothyroidism caused by PCB 95 may impair the adipokine axis, fat metabolism, and in general postnatal development. Thus, further studies need to be carried out to understand this concept.
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Why is it important?
Five conclusions can be drawn from these data. The first is that the developmental exposure to PCB 95 in the early weaning period seems to alter TH synthesis and secretion, either by acting directly on the thyroid gland or by acting on the pituitary or hypothalamic control of TSH or GH/IGF1 secretion. The second is that the administration appears to induce hypothyroidism via thyroid dysgenesis and dyshormonogenesis. These drastic effects may play a significant role in thyroid diseases. The third is that PCB 95 seems to play the role of a stress-responsive factor in the neonatal endocrine system (HPTA). The fourth is that hypothyroidism caused by PCB 95 seems to alter the development of the adipokine axis, fat metabolism, and in general postnatal development. The final conclusion is that the administration of PCB 95 seems to lead to thyroid adipokine dysfunction. These changes may be either directly or indirectly related to TH action. More interestingly, the toxicity of PCBs is dependent on compound congeners, dose, exposure duration, developmental period, and the species involved. From this, it can be concluded that the endocrine-disrupting compounds can exert complex, mosaic effects during an animal’s life cycle (Zoeller et al. 2012). Further investigations are required to elucidate the potential associations with human health.
Perspectives
– Studies focusing on the direct relationship between HPTA and fat tissue are needed to clarify the developmental interactions between thyroid function status and adipokines. Future research should also determine the dose of PCBs received by developing rats from placental and lactation exposure, as well as the hepatic catabolic responses of developing neonates to PCBs, to explain the lack of effects of PCBs at later postnatal ages. – Longitudinal studies of the developmental neuroendocrine system in newborns/infants should be carried out in fish-eating populations because fish is a major source of PCBs. Any degree of thyroid disruption that affects the concentrations of THs on a population basis should be considered a biomarker of adverse outcomes, which may have important societal effects (Miller et al. 2009). – Future studies also need to elucidate important interactions among contaminants, hormones, protein expression, and other phenotypic or physiological measures to gain understanding of what factors – or groups of factors – are driving phenotypic changes in animals living in affected environments.
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: Early weaning PCB 95 exposure alters the neonatal endocrine system: thyroid adipokine dysfunction, Journal of Endocrinology, December 2013, Bioscientifica,
DOI: 10.1530/joe-13-0302.
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