Dariyerli Nuran, Toplan Selmin, Akyolcu Mehmet Can, Hatemi Husrev, Yigit Gunnur
Department of Physiology, Istanbul University, Cerrahpasa Medical Faculty, Istanbul, Turkey.
Endocrine. 2004 Oct;25(1):1-5. doi: 10.1385/ENDO:25:1:01.
The present study was planned to explain the relation between erythrocyte osmotic fragility and oxidative stress and antioxidant statue in primary hypothyroid-induced experimental rats. Twenty-four Spraque Dawley type female rats were divided into two, as control (n = 12) and experimental (n = 12), groups weighing between 160 and 200 g. The experimental group animals have received tap water methimazole added standard fodder to block the iodine pumps for 30 d (75 mg/100 g). Control group animals were fed tap water and only standard fodder for the same period. At the end of 30 d blood samples were drawn from the abdominal aorta of the rats under ether anesthesia. T3, T4, and TSH levels were measured and the animals that had relatively lower T3, T4, and higher TSH levels were accepted as hypothyroid group. Hormone levels of the control group were at euthyroid conditions. Osmotic fragility, as a lipid peroxidation indicator malondialdehyde (MDA), antioxidant defense system indicators superoxide dismutase (SOD) and glutathione (GSH) levels were measured in the blood samples. Osmotic fragility test results: There was no statistically significant difference found between maximum osmotic hemolysis limit values of both group. Minimum osmotic hemolysis limit value of hypothyroid group was found to be higher than that of control group values (p < 0.02). The standard hemolysis and hemolytic increment curve of the hypothyroid group drawn according to osmotic fragility test results was found to be shifted to the right when compared to control group's curve. This situation and hemolytic increment value, which shows maximum hemolysis ratio, is the proof of increased osmotic fragility of the erythrocytes in hypothyroidism. There is no statistically significant difference found between hypothyroid and control groups in the lipid peroxidation indicator MDA and antioxidant indicators SOD and GSH levels. As a result of our study it may be concluded that hypothyroidism may lead to an increase in osmotic fragility of erythrocytes. But the increase in erythrocyte osmotic fragility does not originate from lipid peroxidation.
本研究旨在解释原发性甲状腺功能减退诱导的实验大鼠红细胞渗透脆性与氧化应激及抗氧化状态之间的关系。将24只Spraque Dawley品系雌性大鼠分为两组，即对照组（n = 12）和实验组（n = 12），体重在160至200克之间。实验组动物饮用添加了甲巯咪唑的自来水，并给予标准饲料，以阻断碘泵30天（75毫克/100克）。对照组动物在同一时期仅饮用自来水和标准饲料。30天结束时，在乙醚麻醉下从大鼠腹主动脉采集血样。测量T3、T4和TSH水平，将T3、T4水平相对较低且TSH水平较高的动物作为甲状腺功能减退组。对照组的激素水平处于甲状腺功能正常状态。在血样中测量作为脂质过氧化指标的丙二醛（MDA）、抗氧化防御系统指标超氧化物歧化酶（SOD）和谷胱甘肽（GSH）水平。渗透脆性测试结果：两组的最大渗透溶血极限值之间未发现统计学显著差异。甲状腺功能减退组的最小渗透溶血极限值高于对照组（p < 0.02）。根据渗透脆性测试结果绘制的甲状腺功能减退组的标准溶血和溶血增量曲线与对照组曲线相比向右移动。这种情况以及显示最大溶血率的溶血增量值证明了甲状腺功能减退时红细胞渗透脆性增加。甲状腺功能减退组与对照组在脂质过氧化指标MDA以及抗氧化指标SOD和GSH水平上未发现统计学显著差异。我们的研究结果可能得出结论，甲状腺功能减退可能导致红细胞渗透脆性增加。但红细胞渗透脆性的增加并非源于脂质过氧化。
