Neonatal Bisphenol A Exposure Alters Thyroid-Axis and Prooxidant-Antioxidant Balance in Brain of Rat (Published)
The aim of this study was to investigate the possible effects of neonatal bisphenol A (BPA) exposure on the neuroendocrine system (thyroid-brain axis). 20 or 40 µg/kg of BPA was orally administered to neonatal male albino rats (Rattus norvigicus) from postnatal days (PNDs) 15 to 30. Both administrations gave rise to a lower serum thyroxine (T4) and triiodothyronine (T3) levels, and higher thyrotropin (TSH) level than control group at PND 30. Also, a marked reduction in serum of neonatal growth hormone (GH) was observed in both treated groups. In neonatal cerebellum and cerebrum, the elevations of oxidative markers [lipid peroxidation (LPO), nitric oxide (NO), and hydrogen peroxide (H2O2)] due to both administrations were observed at PND 30, along with decreased activities of antioxidants markers [total ascorbic acid (TAA), total thiol (t-SH), glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST), and catalase (CAT)] with respect to control group. Thus, hypothyroidism in BPA might disturb the neonatal thyroid-brain axis via production of free radicals, and this, might destruct the plasma membrane and cellular components delaying cerebrum and cerebellum development.
LACTATING PTU EXPOSURE: II- ALTERS THYROID-AXIS AND PROOXIDANT-ANTIOXIDANT BALANCE IN NEONATAL CEREBELLUM (Published)
The aim of the present study was to evaluate the effect of lactating 6-propyl-2-thiouracil (PTU) on the interactions between the thyroid-axis and prooxidant/antioxidant markers in neonates. PTU was administered to female rats in drinking water (0.1% w/v) from birth to lactation day (LD) 30. The administration gave rise to a highly significant decrease in serum thyroxine (T4) and triiodothyronine (T3) levels and increase in serum thyrotropin (TSH) level in both dams and their offspring at LDs 20 and 30 relative to control group. Also, in PTU group, a marked depression was observed in serum of neonatal growth hormone (GH). In this hypothyroid state, obvious elevation of oxidative markers (protein carbonyls, lipid peroxidation, NO and H2O2) was observed at postnatal days (PNDs) 20 and 30, along with decreased activities of antioxidants markers (total thiol, glutathione, glutathione peroxidase, superoxide dismutase and catalase) in neonatal cerebellum with respect to control group. Also, the administration caused some histopathological changes in neonatal cerebellar cortex, such as oedema, vacuoles, reduction of the Purkinje cells, and cellular fragmentations at PND 30. Thus, hypothyroidism in lactating PTU impairs the neonatal neuroendocrine system via production of free radicals, and this, may cause damage of proteins and lipids at the plasma membrane and cellular components delaying cerebellum development
The purpose of this study was to determine the effects of lactating propylthiouracil (PTU) on the thyroid-neural development in newborns. PTU was administered to female rats in drinking water (0.1% w/v) from birth to lactation day (LD) 30. A hypothyroid state was recorded at LDs 20 and 30 in both dams and their offspring where a marked depression (P<0.01) was observed in serum thyroxine (T4) and triiodothyronine (T3) levels, while a reverse pattern was noticed in serum thyrotropin (TSH) level as compared to a control group. Also, the maternal administration caused a highly significant decrease in the level of neonatal growth hormone (GH) at postnatal days (PNDs) 20 and 30. This hypothyroid condition produced inhibitory effects on 5′-monodeiodinase (5′-DI), and on cholinergic enzymes [butyrylcholinesterase (BuchE) and acetylcholinesterase (AchE)] in the neonatal cerebellum at the studied PNDs. This may also delay partially the development of the cerebellar Purkinje cells (PCs) via altering the dendritic morphology at both examined PNDs. All tested parameters in the control group followed a synchronized course of development, and their progress may depend, largely on thyroid state. Thus, PTU may act as a developmental thyroid-neural disruptor, causing dyshormonogenesis and cerebellum dysgenesis