CAJ | 학술논문

目的探讨长期低硒、低蛋白质和低维生素E(VE)膳食对大鼠甲状腺组织及其激素代谢的影响.方法 Wistar大鼠40只,按体质量随机分为4组:低硒低蛋白低VE组、低硒低蛋白常VE组、常硒常蛋白低VE组、常硒常蛋白常VE组.饲养至第26周处死,测定大鼠全血谷胱甘肽过氧化物酶(GSH-Px)和肝脏Ⅰ型5'-脱碘酶(ID Ⅰ)活性,血清活性氧(ROS)、丙二醛(MDA)、三碘甲状腺原氨酸(T3)、四碘甲状腺原氨酸(T4)和促甲状腺激素(TSH)水平;光镜下观察甲状腺组织病理学改变.结果 ①硒+蛋白质和vE对大鼠全血GSH-Px和肝脏ID Ⅰ活性的影响均无交互作用(F值分别为0.003、0.871,P＞0.05),但对血清MDA和ROS水平的影响均存在交互作用(F值分别为13.057、6.706,P＜0.05或＜0.01).②硒+蛋白质和VE对血清T3、T4水平均有影响(F值分别为431.977、28.271、6.570、41.419,P＜0.05).但均无交互作用(F值分别为0.871、0.136,P＞0.05).无论在低硒低蛋白还是常硒常蛋白条件下,常VE组T4水平[(79.095±12.199)、(64.392±6.261)μg/L]均高于低VE组[(61.068±6.648)、(44.176±7.090)μg/L],差异有统计学意义(t值分别为3.670、6.045,P＜0.01);在低VE条件下,常硒常蛋白组T3、T4水平[(0.718±0.079)、(44.176±7.090)μg/L]均低于低硒低蛋白组[(0.966±0.156)、(61.068±6.648)μg/L],差异有统计学意义(t值分别为4.568、4.916,P＜0.01);在常VE条件下,常硒常蛋白组Td水平[(64.392±6.261)μg/L]低于低硒低蛋白组[(79.095±12.199)μg/L],差异有统计学意义(t=3.033,P＜0.01).③低硒低蛋白低VE膳食大鼠甲状腺滤泡上皮细胞出现变性坏死,而补充VE可减轻这种损伤:常硒常蛋白低VE膳食大鼠偶见滤泡腔内胶质稀疏.结论长期低硒、低蛋白、低VE膳食可导致大鼠体内含硒酶活性降低,从而引起机体氧化代谢产物堆积,甲状腺组织出现病理性损伤,其激素代谢紊乱,而在低硒、低蛋白膳食中补充适量VE可部分降低这种损伤现象. 目的探討長期低硒、低蛋白質和低維生素E(VE)膳食對大鼠甲狀腺組織及其激素代謝的影響.方法 Wistar大鼠40隻,按體質量隨機分為4組:低硒低蛋白低VE組、低硒低蛋白常VE組、常硒常蛋白低VE組、常硒常蛋白常VE組.飼養至第26週處死,測定大鼠全血穀胱甘肽過氧化物酶(GSH-Px)和肝髒Ⅰ型5'-脫碘酶(ID Ⅰ)活性,血清活性氧(ROS)、丙二醛(MDA)、三碘甲狀腺原氨痠(T3)、四碘甲狀腺原氨痠(T4)和促甲狀腺激素(TSH)水平;光鏡下觀察甲狀腺組織病理學改變.結果 ①硒+蛋白質和vE對大鼠全血GSH-Px和肝髒ID Ⅰ活性的影響均無交互作用(F值分彆為0.003、0.871,P＞0.05),但對血清MDA和ROS水平的影響均存在交互作用(F值分彆為13.057、6.706,P＜0.05或＜0.01).②硒+蛋白質和VE對血清T3、T4水平均有影響(F值分彆為431.977、28.271、6.570、41.419,P＜0.05).但均無交互作用(F值分彆為0.871、0.136,P＞0.05).無論在低硒低蛋白還是常硒常蛋白條件下,常VE組T4水平[(79.095±12.199)、(64.392±6.261)μg/L]均高于低VE組[(61.068±6.648)、(44.176±7.090)μg/L],差異有統計學意義(t值分彆為3.670、6.045,P＜0.01);在低VE條件下,常硒常蛋白組T3、T4水平[(0.718±0.079)、(44.176±7.090)μg/L]均低于低硒低蛋白組[(0.966±0.156)、(61.068±6.648)μg/L],差異有統計學意義(t值分彆為4.568、4.916,P＜0.01);在常VE條件下,常硒常蛋白組Td水平[(64.392±6.261)μg/L]低于低硒低蛋白組[(79.095±12.199)μg/L],差異有統計學意義(t=3.033,P＜0.01).③低硒低蛋白低VE膳食大鼠甲狀腺濾泡上皮細胞齣現變性壞死,而補充VE可減輕這種損傷:常硒常蛋白低VE膳食大鼠偶見濾泡腔內膠質稀疏.結論長期低硒、低蛋白、低VE膳食可導緻大鼠體內含硒酶活性降低,從而引起機體氧化代謝產物堆積,甲狀腺組織齣現病理性損傷,其激素代謝紊亂,而在低硒、低蛋白膳食中補充適量VE可部分降低這種損傷現象.
목적 탐토장기저서、저단백질화저유생소E(VE)선식대대서갑상선조직급기격소대사적영향.방법 Wistar대서40지,안체질량수궤분위4조:저서저단백저VE조、저서저단백상VE조、상서상단백저VE조、상서상단백상VE조.사양지제26주처사,측정대서전혈곡광감태과양화물매(GSH-Px)화간장Ⅰ형5'-탈전매(ID Ⅰ)활성,혈청활성양(ROS)、병이철(MDA)、삼전갑상선원안산(T3)、사전갑상선원안산(T4)화촉갑상선격소(TSH)수평;광경하관찰갑상선조직병이학개변.결과 ①서+단백질화vE대대서전혈GSH-Px화간장ID Ⅰ활성적영향균무교호작용(F치분별위0.003、0.871,P＞0.05),단대혈청MDA화ROS수평적영향균존재교호작용(F치분별위13.057、6.706,P＜0.05혹＜0.01).②서+단백질화VE대혈청T3、T4수평균유영향(F치분별위431.977、28.271、6.570、41.419,P＜0.05).단균무교호작용(F치분별위0.871、0.136,P＞0.05).무론재저서저단백환시상서상단백조건하,상VE조T4수평[(79.095±12.199)、(64.392±6.261)μg/L]균고우저VE조[(61.068±6.648)、(44.176±7.090)μg/L],차이유통계학의의(t치분별위3.670、6.045,P＜0.01);재저VE조건하,상서상단백조T3、T4수평[(0.718±0.079)、(44.176±7.090)μg/L]균저우저서저단백조[(0.966±0.156)、(61.068±6.648)μg/L],차이유통계학의의(t치분별위4.568、4.916,P＜0.01);재상VE조건하,상서상단백조Td수평[(64.392±6.261)μg/L]저우저서저단백조[(79.095±12.199)μg/L],차이유통계학의의(t=3.033,P＜0.01).③저서저단백저VE선식대서갑상선려포상피세포출현변성배사,이보충VE가감경저충손상:상서상단백저VE선식대서우견려포강내효질희소.결론 장기저서、저단백、저VE선식가도치대서체내함서매활성강저,종이인기궤체양화대사산물퇴적,갑상선조직출현병이성손상,기격소대사문란,이재저서、저단백선식중보충괄량VE가부분강저저충손상현상.
Objective To explore the effect of associated deficiency of selenium,protein and vitamin E(VE)on the thyroid iniury and thyroid hormone metabolism of the rats in a long-term.Methods The Wistar rats were randomly divided into four groups:Group A with selenium deficiency and low protein and VE;Group B with selenium deficiency,low protein but adequate VE;Group C,adequate selenium and protein but low VE;Group D,adequate selenium.protein and VE.The rats were killed at the end of 26th week.Glutathione peroxidase(GSH-Px)activity in the rat blood and type I 5'-deiodinase activity of the rat liver were determined.The content of triiodothyronine(T3),tetraiodothyronine(T4),thyrotropic-stimulating hormone(TSH),activated oxygen(ROS)and malonaldehyde(MDA)were detected in serum. The changes of thyroid histopathology were observed under light microscope.Results ①The interactive effect of selenium+protein and VE was not significant on GSH-Px and ID I activity(F=0.003,0.871,P＞0.05),but it was significant on MDA and ROS content(F=13.057,6.706,P＜0.05 or＜0.01). ②Selenium+protein and VE could influence T3 and T4 content(F=431.977,28.271,6.570,41.419,P＜0.05).The interactive effect of selenium±protein and VE was not significant on T3 and T4 content(F=0.871,0.136,P＞0.05).Whether in the condition of low selenium and protein or supplementary,T4 contents of supplementary VE group[(79.095±12.199),(64.392±6.261)μg/L]were respectively higher than the low VE group[(61.068±6.648),(44.176±7.090)μg/L],the difference being statistically significant(t = 3.670,6.045, P ＜ 0.01). In the condition of low VE, T3[(0.718 ± 0.079)μg/L] and T4[(44.176 ±7.090)μg/L] content of supplementary selenium and protein group was lower than that in the low selenium and protein group[ (0.966 ± 0.156), (61.068 ± 6.648)μg/L], the difference being statistically significant (t = 4.568,4.916, P ＜0.01 ). With supplementary VE, T4 content of supplementary selenium and protein group[ (64.392 ± 6.261 )μg/L] was lower than that in the low selenium and protein group [(79.095 ± 12.199)μg/L], the difference being statistically significant (t = 3.033, P ＜ 0.01 ). ③Degeneration and necrosis of follicular epithelial cell were induced by diet of low selenium, protein and VE, which could be relieved by supplymentary VE. The sparseness of intracavitary glue was observed occationally in the supplementary selenium and protein but low VE group. Conclusions Long-term deficiency of selenium, protein and VE results in the decrease of the selenoenzymes of rats, which causes accumulation of the oxidative products, as well as thyroid pathological injury and thyroid hormone metabolism disorder, but supplement of adequate VE can reduce the oxidative damage in rats having low selenium and protein diet.