Animal Ecophysiology Laboratory, Faculty of Sciences, Badji Mokhtar University, BP 12 Sidi Amar, Annaba, Algeria.
Environ Toxicol Pharmacol. 2011 Jan;31(1):33-41. doi: 10.1016/j.etap.2010.09.003. Epub 2010 Sep 15.
The aim of this study was to determine whether the effects of thyroid dysfunction induce oxidative stress in the blood and heart of male Wistar rats. Rats were randomly divided into three groups: group I served as control rats. Group II was treated daily with 0.05% benzythiouracile (BTU) administered in drinking water. Rats of group III have received l-thyroxine sodium salt (0.0012%), in drinking water. The results showed that thyroid dysfunction rats had poor growth performance. On the other hand, in hyperthyroid rats, a marked decrease compared with control occurred of some hematological parameters such red blood cell number (RBC), haemoglobin (Hb) concentration and haematocrit (Ht). There was also a significant increase in erythrocyte numbers and heart TBARS concentrations in hypothyroid rats compared with control. These results were associated with a fall in the total antioxidant status (TAS) in the serum of the hyperthyroid rats. Alteration of the antioxidant system in the hypo-/hyperthyroidism-induced rats was confirmed by the significant increase of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities and a decline in glutathione (GSH) content in both tissues were detected in hyperthyroid group compared to controls. On the other hand, serum transaminase activities (aspartate transaminase (AST); alanine transaminase (ALT)) were elevated indicating hepatic cellular damage after treatment with exogenous L-thyroxine. Moreover, serum lactate dehydrogenase (LDH), gamma-glutamyl transferase (GGT) and creatine phosphokinase (CPK) activities were increased in the hyperthyroidism rats. These results indicated that excessive thyroxin (long term) ingestion had an adverse effect on animal health and performance. We conclude that thyroid dysfunction induces oxidative stress and modifies some biochemical parameters of erythrocytes, heart and liver disease; our results show the occurrence of a state of oxidizing stress in relation to hyperthyroidism.
本研究旨在确定甲状腺功能障碍是否会导致雄性 Wistar 大鼠血液和心脏产生氧化应激。大鼠被随机分为三组：I 组作为对照组。II 组大鼠每天饮用含 0.05%苯硫脲嘧啶（BTU）的水。III 组大鼠给予左旋甲状腺素钠（0.0012%），溶于饮用水中。结果显示，甲状腺功能障碍大鼠生长性能较差。另一方面，在甲状腺功能亢进大鼠中，与对照组相比，一些血液学参数如红细胞数（RBC）、血红蛋白（Hb）浓度和血细胞比容（Ht）显著降低。甲状腺功能减退大鼠的红细胞数量和心脏 TBARS 浓度也明显高于对照组。这些结果与甲状腺功能亢进大鼠血清总抗氧化状态（TAS）下降有关。甲状腺功能减退/亢进诱导大鼠抗氧化系统的改变通过超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GPx）活性显著增加和两种组织中谷胱甘肽（GSH）含量下降得到证实与对照组相比，在甲状腺功能亢进组中检测到。另一方面，血清转氨酶活性（天冬氨酸转氨酶（AST）；丙氨酸转氨酶（ALT））升高表明在用外源性 L-甲状腺素治疗后肝脏细胞受损。此外，甲状腺功能亢进大鼠血清乳酸脱氢酶（LDH）、γ-谷氨酰转移酶（GGT）和肌酸磷酸激酶（CPK）活性增加。这些结果表明，过量甲状腺素（长期）摄入对动物健康和性能有不良影响。我们得出结论，甲状腺功能障碍会导致氧化应激，并改变红细胞、心脏和肝脏疾病的一些生化参数；我们的结果表明，与甲状腺功能亢进有关，会发生氧化应激状态。
