Home > Journals > Minerva Endocrinologica > Past Issues > Minerva Endocrinologica 2017 March;42(1) > Minerva Endocrinologica 2017 March;42(1):8-14

CURRENT ISSUE
 

JOURNAL TOOLS

eTOC
To subscribe
Submit an article
Recommend to your librarian
 

ARTICLE TOOLS

Publication history
Reprints
Permissions
Cite this article as

 

ORIGINAL ARTICLE   

Minerva Endocrinologica 2017 March;42(1):8-14

DOI: 10.23736/S0391-1977.16.02359-2

Copyright © 2015 EDIZIONI MINERVA MEDICA

language: English

A new insight on the role of zinc in the regulation of altered thyroid functions during lithium treatment

Xuemei LI 1, Fuyuan LI 2, Chen F. LI 3

1 Department of Endocrinology, Rizhao Hospital of Traditional Chinese Medicine, Rizhao, China; 2 Yishui Central Hospital, Linyi, China; 3 Department of Endocrinology, Juxian People’s Hospital, Rizhao, China


PDF


BACKGROUND: Lithium salts are widely used for the treatment of mental disorders but cause thyroid dysfunctions while zinc is an essential trace element and is required for a broad range of biological activities. The present study was designed to explore the potential of zinc in regulating 131I biokinetics and thyroid functions following lithium therapy.
METHODS: To carry out the investigations, 40 female sprague dawley rats weighing 110-140g were segregated into four groups viz. Group I animals served as untreated controls, group II animals were given lithium (Li2CO31.1 g/kg diet), group III animals were supplemented with zinc (227 mg ZnSO4/L drinking water) and animals in group IV were given a combined treatment of lithium and zinc. The treatments were given for durations of 1, 2 and 4 months.
RESULTS: Following intraperitoneal administration of 0.37 MBq carrier- free-131I, a significant depression in the thyroidal 131I uptake both at 2 and 24 hrs was observed following lithium treatment for all the durations which however was brought to within normal levels following zinc supplementation. Lithium treatment caused a significant elevation in the thyroidal biological half lives of 131I which was appreciably attenuated following 2 and 4 months of zinc supplementation. Lithium administration for 2 and 4 months significantly decreased serum T3 and T4 levels which however were increased following zinc supplementation. Lithium treatment for 4 months caused a significant decrease in the thyroidal activities of Na+ K+ ATPase and monoamine oxidase which were brought to near normal levels by zinc. Further, lithium treatment for 4 months raised thyroidal levels of lipid peroxidation and catalase which however were normalized by zinc supplementation. On the contrary, thyroidal levels of reduced glutathione and glutathione S transferase decreased significantly following 2 and 4 months of lithium treatment but were significantly increased following zinc treatment.
CONCLUSIONS: The present study concludes that zinc supplementation is helpful in attenuating the adverse effects caused by lithium on thyroid functions and can effectively regulate the biokinetics of 131I.


KEY WORDS: Lithium - Zinc - Thyroid gland

top of page