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Published on: November 20, 2015
Perinatal hypothyroidism modulates antioxidant defence status in the developing rat liver and heart
Hongmei Zhang1,1, Yan Dong1,1, Qing Su1,1
1Department of Endocrinology, Xin Hua Hospital affiliated with Shanghai Jiaotong University School of Medicine, Shanghai 200092, People's Republic of China.
Insights
Perinatal hypothyroidism alters oxidative stress markers in rat liver and heart, affecting antioxidant defenses like catalase and glutathione. Thyroxine replacement therapy did not fully restore these parameters.
Area of Science:
- Biochemistry
- Endocrinology
- Toxicology
Background:
- Perinatal hypothyroidism can impact organ development and function.
- Oxidative stress plays a role in various physiological and pathological processes.
Purpose of the Study:
- To investigate oxidative stress parameters and antioxidant defense status in the liver and heart of perinatal hypothyroid rats.
- To assess the effects of hypothyroidism on specific oxidative stress markers and antioxidant enzymes.
Main Methods:
- Comparison of oxidative stress markers (protein carbonyl, hydroxyl radical) and antioxidant enzyme activities (SOD, CAT, GPx) in liver and heart tissues.
- Measurement of vitamin E, glutathione (GSH) levels, and total antioxidant capacity.
- Evaluation of the impact of thyroxine replacement therapy.
Main Results:
- Hypothyroidism significantly decreased hydroxyl radical levels in the heart but not liver.
- Catalase activity increased in the liver, while glutathione peroxidase activity increased in the heart.
- Vitamin E levels decreased in the liver, and glutathione levels elevated in both organs.
- Total antioxidant capacity was higher in the hypothyroid liver.
Conclusions:
- Perinatal hypothyroidism significantly modulates oxidative stress and antioxidant status in the developing rat liver and heart.
- Thyroxine replacement therapy was insufficient to normalize all observed alterations.
Abstract:
In the present study, we investigated oxidative stress parameters and antioxidant defence status in perinatal hypothyroid rat liver and heart. We found that the proteincarbonyl content did not differ significantly between the three groups both in the pup liver and in the heart. The OH˙ level was significantly decreased in the hypothyroid heart but not in the liver compared with controls. A slight but not significant decrease in SOD activity was observed in both perinatal hypothyroid liver and heart. A significantly increased activity of CAT was observed in the liver but not in the heart of hypothyroid pups. The GPx activity was considerably increased compared with controls in the perinatal hypothyroid heart and was unaltered in the liver of hypothyroid pups. We also found that vitamin E levels in the liver decreased significantly in hypothyroidism and were unaltered in the heart of perinatal hypothyroid rats. The GSH content was elevated significantly in both hypothyroid liver and heart. The total antioxidant capacity was higher in the liver of the hypothyroid group but not in the hypothyroid heart. Thyroxine replacement could not repair the above changes to normal. In conclusion, perinatal hypothyroidism modulates the oxidative stress status of the perinatal liver and heart.
