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.
Ahmed R. G. | Ahmed R. G. | 2259