SUPEROXIDE ANION-RADICAL PRODUCTION AS A CADMIUM-MEDIATED MECHANISM OF TOXICITY IN AVIAN THYROID - AN ELECTRON SPIN RESONANCE STUDY BY SPIN-TRAPPING

Citation
P. Prakash et al., SUPEROXIDE ANION-RADICAL PRODUCTION AS A CADMIUM-MEDIATED MECHANISM OF TOXICITY IN AVIAN THYROID - AN ELECTRON SPIN RESONANCE STUDY BY SPIN-TRAPPING, Comparative biochemistry and physiology. Part C, Pharmacology toxicology & endocrinology, 118(1), 1997, pp. 89-95
Citations number
68
Categorie Soggetti
Biology,"Pharmacology & Pharmacy",Toxicology
ISSN journal
13678280
Volume
118
Issue
1
Year of publication
1997
Pages
89 - 95
Database
ISI
SICI code
1367-8280(1997)118:1<89:SAPAAC>2.0.ZU;2-B
Abstract
Cadmium (Cd) induced superoxide anion radical (O-2(-)) generation in v ivo has been demonstrated in the thyroid gland of Columba livia interm edia 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 treatme nt. After the 7th and 10th day of Cd intoxication, the thyroid gland r esumes normal reducing atmosphere characterized by a very low LPO leve l, total decay of O-2(-) and an adaptive recovery of depleted GSH to t hat of control. A high level of SOD activity over the experimental per iod and return of GSH content to that of control by the 7th day of tre atment till the 10th day suggest their role as a very effective oxyrad ical scavenging sink during Cd-mediated oxidative assault. A low plasm a triiodothyronine (T-3) level, decreased plasma T-3/T-4 ratio over mo st 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 un der acute Cd-exposure is due to impaired thyroid hormonogenesis under an oxidative stress and a direct Cd-inhibition of peripheral monodeiod ination of T-4 to T-3. (C) 1997 Elsevier Science Inc.