Abstract

Cadmium (Cd) induced superoxide anion radical (O ·− 2) generation in vivo has been demonstrated in the thyroid gland of Columba livia intermedia by electron spin resonance (ESR) spin trapping. A single dose of Cd caused generation of O ·− 2, elevated lipid peroxidation (LPO) and superoxide dismutase (SOD) activity and depletion of glutathione (GSH) content in the thyroid gland on the 1st and 3rd day after the treatment. After the 7th and 10th day of Cd intoxication, the thyroid gland resumes normal reducing atmosphere characterized by a very low LPO level, total decay of O ·− 2 and an adaptive recovery of depleted GSH to that of control. A high level of SOD activity over the experimental period and return of GSH content to that of control by the 7th day of treatment till the 10th day suggest their role as a very effective oxyradical scavenging sink during Cd-mediated oxidative assault. A low plasma triiodothyronine (T 3) level, decreased plasma T 3/T 4 ratio over most of the study period and a transient drop in plasma thyroxine (T 4) level during early phase of acute poisoning indicate that pigeons are in the hypothyroid state. We propose that avian thyroid dysfunction under acute Cd-exposure is due to impaired thyroid hormonogenesis under an oxidative stress and a direct Cd-inhibition of peripheral monodeiodination of T 4 to T 3.

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