甲状腺激素缺乏对不同发育时期大鼠脑组织氧化应激指标的影响

目的：研究甲状腺激素缺乏对不同发育时期大鼠脑组织丙二醛（MDA）、总抗氧化力（TAC）及超氧化物歧化酶（SOD）的影响，探讨甲状腺激素缺乏影响鼠脑发育的机制。方法：实验组以丙基硫氧嘧啶溶液灌胃孕鼠制造大鼠围产期甲状腺激素缺乏模型，收集出生后7、14和21 d的仔鼠血清和脑组织，测定血清游离三碘甲状原氨酸及甲状腺素（FT3 、FT4）水平，脑组织匀浆后检测MDA、TAC及SOD的水平。正常孕鼠所产的年龄匹配仔鼠作为对照组，同样测定上述指标。结果：21 d实验组仔鼠脑组织MDA水平高于正常对照组［(14.63±3.44) μmol/g vs (10.52±2.32) μmol/g，P<0.05］；TAC水平高于正常对照组［(0.051±0.006) mmol/g- vs (0.042±0.003) mmol/g，P<0.05］；SOD活性高于正常对照组［(79.63±10.10) μmol?min-1/g vs （63.51±8.35） μmol/min/g，P<0.05］。实验组与对照组7 d和14 d的标本MDA水平、TAC水平及SOD活性比较差异无显著性［7 d MDA:(11.20±2.39) μmol/g vs (12.29±1.79) μmol/g,P>0.05;14 d MDA: (13.07±3.16) μmol/g vs (12.98±2.93) μmol/g,P>0.05;7 d TAC:(0.046±0.006) mmol/g- vs (0.047±0.004) mmol/g,P>0.05;14 d TAC:(0.042±0.007) mmol/g vs (0.046±0.007) mmol/g,P>0.05;7 d SOD:(66.34±11.20) μmol/min/g vs (65.49±7.52) μmol/min/g,P>0.05;14 d SOD:(67.53±12.01) μmol/min/g vs (64.57±8.28) μmol/min/g,P>0.05］。结论：大鼠脑发育期甲状腺激素缺乏可引起脑组织MDA水平、TAC水平及SOD活性的改变，这可能参与了甲状腺功能减退性脑损伤的发生。

Effect of thyroid hormone deficiency on oxidative stress parameters in different developing stages of rat brain

Objective To study the effect of thyroid hormone deficiency on malonaldehyde (MDA)and total antioxidative capacity(TAC)and superoxide dismutase(SOD)levels in different developing stages of rat brain and further explore the mechanism of impaired brain development caused by thyroid hormone deficiency. Methods Perinatal hypothyroidism was induced by administering propylthiouracil(PTU)solution to the dams by gavage(2 % PTU 1.5mL·d-1)beginning on embryonic day 15.The blood samples of pups in different developing stages(7,14,21d)were collected to measure serum FT3and FT4levels.And the braintissues were collected to measure MDA,TAC and SOD levels in brain homogenate.Age matched controls were pups from normal dams without administering propylthiouracil(PTU)solution.Results Compared with age matched controls,the MDA and TAC and SOD levels were increased in hypothyroid group of 21dpups (MDA:14.63μmol·g-1±3.44 μmol· g-1 g vs 10.52 μmol· g-1 ±2.32 μmol· g-1,P <0.05;TAC:0.051mmol·g-1±0.006 mmol·g-1 vs 0.042 mmol·g-1 ±0.003 mmol·g-1,P <0.05;SOD:79.63μmol·min-1·g-1±10.10μmol·min-1·g-1 vs 63.51μmol·min-1·g-1±8.35μmol·min-1·g-1,P<0.05),but for the 7dand 14dpups,there were no differences between two groups (7d MDA:11.20μmol·g-1±2.39μmol·g-1 vs 12.29μmol·g-1±1.79μmol·g-1,P>0.05;14dMDA:13.07μmol·g-1± 3.16μmol·g-1 vs 12.98μmol·g-1 ±2.93μmol·g-1,P>0.05;7d TAC:0.046 mmol·g-1 ± 0.006mmol·g-1 vs 0.047 mmol·g-1±0.004 mmol·g-1,P>0.05;14dTAC:0.042 mmol·g-1± 0.007mmol·g-1 vs 0.046mmol·g-1±0.007mmol·g-1,P>0.05;7dSOD:66.34μmol·min-1·g-1± 11.20μmol·min-1·g-1 vs 65.49μmol·min-1·g-1±7.52μmol·min-1·g-1,P>0.05;14dSOD:67.53μmol·min-1 · g-1 ± 12.01 μmol · min-1 · g-1 vs 64.57 μmol · min-1 · g-1 ± 8.28μmol·min-1·g-1,P>0.05).Conclusion Thyroid hormone deficiency during rat brain development may cause the changes of MDA,TAC and SOD levels and this may be related to brain damage caused by thyroid hormone deficiency.