Vitamin E protects against thyroxine-induced acceleration of lipid peroxidation in cardiac and skeletal muscles in rats.

Abstract

SummaryTo determine whether vitamin E protects against thyroxine induced oxidative stress in heart and soleus (slow oxidative) muscles, lipid peroxide (thiobarbituric acid-reactive substances) and antioxidant enzymes were measured in those tissues of hyperthyroid rats supplemented with vitamin E. The rats were rendered hyperthyroid by the administration of L-thyroxine in their drinking water. In experiment (EXPT) I, 30mg/kg/dose of alpha-tocopheryl acetate was administered to the vitamin E-treated group. In EXPT II, the rats were fed a diet containing either <1IU/kg (deficient diet), 20IU/kg (control E diet), or 500IU/kg (high E diet) of vitamin E and hyperthyroidism was induced. In EXPT I, hyperthyroidism induced an increase in oxidative enzymes, mitochondrial superoxide dismutase and lipid peroxide level, and a decrease in cytosolic superoxide dismutase, glutathione peroxidase and catalase in both tissues. Vitamin E treatment inhibited the increase in lipid peroxide level totally in the heart and partially in the soleus, with minimal changes in the other biochemical indices studied. In EXPT II, the lipid peroxide level was markedly increased in both tissues of the vitamin E-deficient group, and decreased in those of the group fed high E diet. There were some adaptive changes in the levels of cytosolic superoxide dismutase, glutathione peroxidase, and catalase in response to vitamin E deficiency, whereas neither oxidative enzymes nor mitochondrial superoxide dismutase were altered. These results suggest that vitamin E protects against lipid peroxidation in hyperthyroid heart and skeletal muscle independently of the changes in oxidative enzymes and antioxidant enzymes.

The role of thyroid hormone calorigenesis in the redox regulation of gene expression

“…The latter changes and the increase in the hepatic activity of NOS and MnSOD induced by T 3 are abrogated by the administration of α-tocopherol prior to T 3 (Fernández et al, 2005a;2005b). This is in agreement with the normalization or diminution of oxidative stress-related parameters induced by hyperthyroid state in response to α-tocopherol (Asayama et al, 1989;Fernández et al, 2002), NAC (Fernández et al, 2002), or ascorbic acid (Seven et al, 1998), as well as antithyroid therapy alone (Videla et al, 1988;Adali et al, 1999) or combined with α-tocopherol (Adali et al, 1999). Suppression of T 3 -induced gene expression by α-tocopherol and NAC, antioxidants having different mechanisms of action, strengthens the contention that the underlying mechanisms are oxidant dependent (Macdonald et al, 2003).…”

Role of Lipid Peroxidation in the Epidemiology and Prevention of Breast Cancer

“…There is supporting evidence that lipid peroxidation may play a role in the potential anticarcinogenic effect of other breast cancer factors, including soy (28,(181)(182)(183)(184)(185)(186)(187), marine n-3 fatty acids (46), thyroid diseases (188)(189)(190)(191)(192)(193)(194)(195)(196)(197)(198)(199)(200)(201)(202), green tea (203)(204)(205)(206)(207), vitamin D (208), calcium (209)(210)(211)(212), folate (213), and isothiocyanates (214)(215)(216)(217).…”

Oxidative Stress in Graves’ Disease

“…Increased myocardial [11] and aortic wall [12] oxidative stress have also been observed in thyorotoxic rats. Vitamin E was also found to protect against a thyroxine-induced increase of lipid peroxidation in cardiac and skeletal muscles in rats [13]. …”