Role of ascorbic acid in cadmium-induced thyroid dysfunction and lipid peroxidation

J Appl Toxicol. Sep-Oct 1998;18(5):317-20. doi: 10.1002/(sici)1099-1263(1998090)18:5<317::aid-jat514>3.0.co;2-u.

Abstract

A study on the effects of ascorbic acid (AA) on heavy metal (cadmium)-induced thyroid dysfunction and lipid peroxidation (LPO) was carried out in Swiss male mice. The animals were administered with either cadmium (1.0 mg kg(-1) body wt.) alone or in combination with AA (1 mM) every day for 15 days. While cadmium treatment led to a decrease in the serum concentrations of thyroid hormones and hepatic type I iodothyronine 5'-monodeiodinase (5'D-I) activity, an increase in the level of lipid peroxidation was observed. The metal-induced decrease in hepatic 5'D-I activity and serum triiodothyronine (T3) concentration was restored by treatment with AA. However, AA could not restore the serum thyroxine (T4) concentration. The increased level of LPO was also ameliorated by AA. It appears that the protective effect of AA against cadmium-induced thyroid dysfunction is mediated through its antioxidative action.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Ascorbic Acid / pharmacology*
  • Cadmium / toxicity*
  • Lipid Peroxidation / drug effects*
  • Male
  • Mice
  • Radioimmunoassay
  • Thyroid Diseases / chemically induced*
  • Thyroxine / blood
  • Triiodothyronine / blood

Substances

  • Cadmium
  • Triiodothyronine
  • Ascorbic Acid
  • Thyroxine