The effects of thyroid dysfunction on DNA damage and apoptosis in liver and heart tissues of rats

Author:

Guler Gulnur1,Dasdelen Dervis1,Baltaci Saltuk Bugra1,Sivrikaya Abdullah2,Baltaci Abdulkerim Kasim1,Mogulkoc Rasim1

Affiliation:

1. Deparment of Physiology , Medical School, Selcuk University , Konya , Turkey

2. Deparment of Biochemistry , Medical School, Selcuk University , Konya , Turkey

Abstract

Abstract Objectives Thyroid hormones affect many enzymes, organs, and systems. They also play a role in complex biological events including development and growth. The main objective of this study was to analyze the effects of thyroid dysfunction on DNA damage and apoptosis in liver and heart tissues as well as the treatment of these disorders. Methods Thirty-eight Wistar-albino male rats were randomly divided into five groups: 1. Control group (n=6): The rats were sacrificed without any application and liver and heart samples were collected. 2. Hypothyroidism group (n=8): Prophyltiouracil (PTU)-10 mg/kg/day was applied to induce hypothyroidism by intraperitoneal route for two weeks. 3. Hypothyroidism + Thyroxine group (n=8): After one week of PTU application (10 mg/kg/day), a high dose of l-thyroxine (1.5 mg/kg/day) was applied by intraperitoneal route for one week. 4. Hyperthyroidism group (n=8): l-thyroxine (0.3 mg/kg/day) was applied intraperitoneally to induce hyperthyroidism for two weeks. 5. Hyperthyroidism + PTU group (n=8): After one week of high dose l-thyroxine application, PTU (10 mg/kg/day) was applied for one week. Results Liver and heart tissues were collected to evaluate 8-hydroxy-2 deoxyguanosine (8-OHdG), caspase-8 and caspase-9 levels. Hypothyroidism caused DNA damage in the liver, while hyperthyroidism caused DNA damage in the heart tissue. Hyperthyroidism also led to a significant increase in levels of caspase-8 and caspase-9 in liver tissue. Conclusions The results of the study show that DNA damage and caspase levels in the heart and liver are affected differently in experimental hypothyroidism and hyperthyroidism.

Publisher

Walter de Gruyter GmbH

Subject

Endocrinology,Molecular Biology,General Medicine,Endocrinology, Diabetes and Metabolism

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