不同剂量X射线对生长发育期仔鼠肺组织抗氧化酶活性、组织结构及相关特异蛋白表达的影响
|
摘要
目的:
通过对不同剂量X射线辐射后,生长发育期仔鼠肺组织抗氧化酶活性、组织结构和相关特异蛋白表达情况等动态变化的研究,探讨X射线对生长发育期动物肺组织的综合影响,为发育生物学研究和临床电离辐射疾病治疗及空间辐射防护提供实验依据。
方法:
选5–7日龄昆明小鼠,随机分为6组,每组32只。每日分别接受吸收剂量为0.0、0.5、2.0、3.5、5.0、6.5 Gy的X射线全身辐射一次,连续辐射三日。在辐射后1、5、10、20 d分别断头处死各组仔鼠8只,取出肺组织,研磨稀释离心后,取上清液检测SOD、GSH-PX活力及MDA、GSH含量的变化。另取各组仔鼠肺组织,采用组织学方法观察组织结构的动态变化,并测量肺泡直径和肺泡隔厚度的动态变化情况;采用免疫组织化学方法观察肺组织中Bax、KGF蛋白表达的动态变化情况,并利用图像分析软件及体视学测量方法对Bax、KGF蛋白表达强度进行定量分析。
结果:
1.X射线辐射影响生长发育期仔鼠肺组织SOD的活性。经0.5Gy和2.0Gy X射线辐射后仔鼠肺组织SOD活性均高于对照组,差异显著或极显著(P<0.05或P<0.01)。初期逐渐升高,后期降低且接近正常水平。经3.5Gy、5.0Gy和6.5Gy X射线辐射后仔鼠肺组织SOD活性先降低后升高,且均低于对照组,差异显著或极显著(P<0.05或P<0.01)。
2.X射线辐射影响生长发育期仔鼠肺组织MDA的含量。经0.5Gy和2.0Gy X射线辐射后仔鼠肺组织MDA含量均低于对照组,差异显著或极显著(P<0.05或P<0.01)。初期逐渐降低,后期升高且接近正常水平。经3.5Gy、5.0Gy和6.5Gy X射线辐射后仔鼠肺组织MDA含量先升高后降低,且均高于对照组,差异显著或极显著(P<0.05或P<0.01)。
3.X射线辐射影响生长发育期仔鼠肺组织GSH-Px的活性。经0.5Gy X射线辐射后仔鼠肺组织GSH-Px活性均高于对照组,差异显著或极显著(P<0.05或P<0.01),且随着时间呈下降趋势。经2.0Gy、3.5Gy、5.0Gy和6.5Gy X射线辐射后仔鼠肺组织GSH-PX活性均低于对照组,差异显著或极显著(P<0.05或P<0.01),且均呈先下降后逐渐恢复的趋势。
4.X射线辐射影响生长发育期的仔鼠肺脏中GSH的含量。经0.5Gy X射线辐射后初期,仔鼠肺组织GSH含量均高于对照组,差异极显著(P<0.01);后期,仔鼠肺组织GSH含量降低且接近对照组,差异不显著或显著(P>0.05或P<0.05)。经2.0Gy、3.5Gy、5.0Gy和6.5Gy X射线辐射后仔鼠肺组织GSH含量降低但均低于对照组,差异显著或极显著(P<0.05或P<0.01)。
5.X射线辐射影响生长发育期仔鼠肺的组织结构。经不同剂量X射线辐射后仔鼠肺泡直径和肺泡隔厚度均有不同程度的变化。经0.5Gy、2.0Gy X射线辐射后仔鼠肺间质细胞致密,肺泡直径及肺泡隔厚度与对照组相比均有不同程度的减少。经3.5Gy、5.0Gy和6.5Gy X射线辐射后肺泡直径和肺泡隔厚度与对照组相比均有不同程度的增加。
6.X射线辐射影响生长发育期仔鼠肺组织中Bax蛋白的表达。Bax蛋白在各不同剂量辐射组仔鼠肺组织中均有不同程度的表达,其表达强度随辐射剂量的增大而增强,随着时间逐渐恢复至接近正常水平。
7.X射线辐射影响生长发育期仔鼠肺组织中KGF蛋白的表达。KGF蛋白在各不同剂量辐射组仔鼠肺组织中均有不同程度的表达。其表达强度随辐射剂量的增大而增强,随着时间呈下降趋势且最终接近正常水平。结论:
1.X射线辐射对生长发育期仔鼠的抗氧化酶活性有明显影响。小剂量X射线辐射后仔鼠肺组织中超氧化物歧化酶活性初期升高后期降低、丙二醛含量初期降低后期升高,大剂量X射线辐射后则恰好相反。小剂量X射线辐射后初期谷胱甘肽过氧化物酶活性及还原型谷胱甘肽含量均高于对照组,而后期均低于对照组,且均随着时间呈下降趋势。
2.X射线辐射影响生长发育期仔鼠肺的组织结构。经不同剂量的X射线辐射后仔鼠肺泡直径和肺泡隔厚度均有不同程度的变化。小剂量X射线辐射后仔鼠肺间质细胞致密,肺泡直径及肺泡隔厚度与对照组相比均有不同程度的减少。大剂量X射线辐射后肺泡直径和肺泡隔厚度与对照组相比均有不同程度的增加。
3.X射线辐射影响生长发育期仔鼠肺组织中Bax及KGF蛋白的表达。Bax及KGF蛋白在仔鼠肺组织中均有不同程度的表达,其表达强度随辐射剂量的增大而增强,对细胞损伤与修复的诱导亦增强。具体表现为:辐射初期在肺组织细胞中均有较强的阳性分布,随后Bax蛋白的表达逐渐减弱,最终恢复至接近正常水平;而KGF蛋白的表达呈下降趋势且最终接近正常水平。
高剂量电离辐射可引起机体内产生大量超氧阴离子自由基(O2-.),从而造成机体组织中细胞的过氧化损伤,而低剂量的电离辐射又可诱导生物体的免疫兴奋。电离辐射还可以使机体各种免疫细胞的功能被激活,特别是T细胞的激活和分化,导致有氧代谢旺盛,产生超氧阴离子自由基高于静止状态。所以低剂量辐射后仔鼠的肺组织抗氧化酶活性升高,脂质化水平降低。而大剂量电离辐射产生的自由基由于无法及时清除而攻击细胞,致使组织损伤,抗氧化酶活性降低,Bax、KGF蛋白高度表达。而在辐射后一段时间内各组仔鼠各检测指标及组织结构均有不同程度恢复正常的趋势。表明X射线辐射影响生长发育期仔鼠肺组织抗氧化酶活性、组织结构及相关特异蛋白的表达。大剂量电离辐射对生长发育期仔鼠具有损伤作用,但机体具有一定的抗辐射机能。
OBJECTIVE:
To study the effects of different dosages of X-ray on lung of developing filial mice, antioxide enzymes activity , the structure and inter related polypeptides after irradiation were determined, which is to explore the synthetical effect on lung of developing filial mice,provide a basis for developmental biology,clinical cure of irradiation damnification and prevention of irradiation.
METHODS:
Age of 5-7 days filial mice were choosed and divided into six groups(32 per group).The six groups irradiated by different dosages(0.0,0.5,2.0,3.5,5.0,6.5 Gy) X-rays respective every day and persisted three days. Eight filial mice of every group were killed (1、5、10、20 d) after irradiation, and effect on the activities of Superoxide dismutase(SOD),Glutathione Peroxidase (GSH-Px),and the contents of Maleic dialdehyde (MDA) , Reduced Glutathione Hormone (GSH) in lung were determined after this tissue be skived from this filial mice and confect to liquid supernatant. Changes of histological structure were observed by histological methods and thickness of Alveolar Septa and diameter of Alveolous were measured. Expressions of Bax and KGF in lung of filial mice were observed by immunohistochemistry method. The expression intensity of them was measuring by Stereological method and image analysis.
RESULT:
1. X-ray affects the SOD activity in lung of filial mice at their growing periods. After the radiation of 0.5Gy and 2.0Gy X-ray, SOD activity in lung of filial mice is higher than the control group with apparent or extremely apparent differences (P<0.05 or P<0.01). Early stages it increases gradually, later decreasing and then increasing and all of which are lower than the control groups with apparent or extremely apparent difference(P<0.05 or P<0.01).
2. X-ray affects the MDA content in lung of filial mice in their growing periods. After the radiation of 0.5Gy and 2.0Gy X-ray, content of MDA in lung of filial mice is lower than the control group with apparent or extremely apparent differences (P<0.05 or P<0.01). Those were being radiated by 0.5Gy and 2.0Gy X-ray, MDA content in their lungs decreases and approximately equal to the normal level in early stages, later increases and even reach the normal level later. After the radiation of 3.5Gy, 5.0Gy and 6.5Gy, MDA content in the lung tissue of filial mice increases at first and then decreases later after that, and all of which are above that of the control groups with apparent or extremely apparent differences(P<0.05 or P<0.01).
3. X-ray affects GSH-Px activity in lung of the filial mice during their growing periods. After 1-20d by 0.5Gy X-ray radiation, GSH-Px activity in the lung of filial mice is higher than the control group with extremely apparent or apparent differences(P<0.01or P<0.05), and the activity decreases as the time passing by. With the X-ray radiation of 2.0、3.5、5.0 and 6.5Gy, GSH-Px activity in lung of filial mice is lower than that of the control group with apparent or extremely apparent differences (P<0.05 or P<0.01) and has the tendency of decreasing-to-increasing.
4. X-ray affects the GSH content in lung of filial mice during their growing periods. After the radiation of 0.5Gy X-ray after early stages, GSH content in lung of filial mice is higher than the control group with extremely apparent differences(P<0.01). Later, GSH content in lung of filial mice decreases even reaches to that of the control group with unapparent or apparent differences(P>0.05 or P<0.05). With the X-ray radiation of 2.0、3.5、5.0 and 6.5Gy, GSH content in the lung of filial mice is lower than the control group with apparent and extremely apparent differences (P<0.05 or P<0.01).
5. X-ray affects the histological structure in lung of filial mice. X-ray radiation affects the diameter of Alveolar and the thickness of Alveolar Septa for different degrees in filial mice. After being radiated by 0.5 Gy and 2.0 Gy X-ray radiation, the interstitial cells in the lung of filial mice are in high density, the diameter of Alveolar and the thickness of Alveolar Septa decrease by different degrees. The diameter of Alveolar and the thickness Alveolar Septa of the 3.5Gy, 5.0Gy and 6.5Gy groups increase with various degrees compared with that of the control group.
6. X-ray affects the expression of Bax protein in lung of filial mice. There Bax protein immunoreaction appeared in lung of filial mice, and the intensity of the immunoreaction was increased with augmentation of dosages, but decreased gradually, and recovered to nearly normal levels over time.
7. X-ray affects the expression of KGF in lung of filial mice. There KGF immunoreaction appeared in lung of filial mice, and the intensity of the immunoreaction was increased with augmentation of dosages. It increased in the beginning and then decreased, but increased later, and come back to normal level finally.
CONCULSION:
1. X-ray affects the activity of antioxidase in lung of filial mice remarkably.
After the radiation of low doses, SOD activity in lung of filial mice increases gradually in early stages, later decreasing. MDA content in lung of filial mice decreases gradually in early stages, later increasing. After the radiation of high doses, it is contradictory. After the radiation of low doses, GSH-Px activity and GSH content in lung of filial mice is higher than the control group in early stages and that is lower than the control group later, all that decreases gradually over time. 2. X-ray affects the histological structure in lung of filial mice. X-ray radiation affects the diameter of Alveolar and the thickness of Alveolar Septa for different degrees in filial mice. After the radiation of low doses, the interstitial cells in the lung of filial mice are in high density, the diameter of Alveolar and the thickness of Alveolar Septa decrease by different degrees. The diameter of Alveolar and the thickness Alveolar Septa of the high doses groups increase with various degrees compared with that of the control group.
3. X-ray affects the expression of Bax and KGF protein in lung of filial mice. The intensity of the immunoreaction was increased with augmentation of dosages, its induction of injury and repair of cell has increased. Specifically as follows: after radiation in the early stages, the expression of Bax and KGF protein had strong positive distribution in lung of filial mice, but the expression of Bax decreased gradually, and recovered to nearly normal levels over time. And the expression of KGF increased in the early stages and decreased gradually, but later recovered to nearly normal levels over time.
High-doses of ionizing radiation can produce a large number of superoxide anion radicals in the organic body, resulting in oxidative damages in cells of the body tissue. While low -doses of ionizing radiation can induce immune excitation. Radiation can also activate the functions of various immune cells of the body, especially for the activation and differentiation of T-cell, which resulting in aerobic metabolism prosperity and the production of superoxide anion radicals even higher than the static state. So the activities of antioxidant-enzyme in tissue of the filial mice increased and content of lipid decreased after the low dosage X-ray. Free radical which produce by large dosage X-ray and could not be eliminate timely will assault cell and cause damage to tissue and activities of antioxidant-enzyme decreased. Histological structure of lung of the filial mice obviously changed after large dosage irradiation. Radiation can increase expression of Bax and KGF in lung of filial mice. There was a trend that the activity of target enzyme, expression of Bax and KGF and histological structure recovered slowly to the normal level after irradiation. The irradiation of X-rays affects the activity of target enzyme, expression of Bax and KGF and histological structure of developing filial mice significantly. In short, large dosages of irradiation would cause disadvantageous effect on developing filial mice,but the organism also have enginery to resist the radiation.
通过对不同剂量X射线辐射后,生长发育期仔鼠肺组织抗氧化酶活性、组织结构和相关特异蛋白表达情况等动态变化的研究,探讨X射线对生长发育期动物肺组织的综合影响,为发育生物学研究和临床电离辐射疾病治疗及空间辐射防护提供实验依据。
方法:
选5–7日龄昆明小鼠,随机分为6组,每组32只。每日分别接受吸收剂量为0.0、0.5、2.0、3.5、5.0、6.5 Gy的X射线全身辐射一次,连续辐射三日。在辐射后1、5、10、20 d分别断头处死各组仔鼠8只,取出肺组织,研磨稀释离心后,取上清液检测SOD、GSH-PX活力及MDA、GSH含量的变化。另取各组仔鼠肺组织,采用组织学方法观察组织结构的动态变化,并测量肺泡直径和肺泡隔厚度的动态变化情况;采用免疫组织化学方法观察肺组织中Bax、KGF蛋白表达的动态变化情况,并利用图像分析软件及体视学测量方法对Bax、KGF蛋白表达强度进行定量分析。
结果:
1.X射线辐射影响生长发育期仔鼠肺组织SOD的活性。经0.5Gy和2.0Gy X射线辐射后仔鼠肺组织SOD活性均高于对照组,差异显著或极显著(P<0.05或P<0.01)。初期逐渐升高,后期降低且接近正常水平。经3.5Gy、5.0Gy和6.5Gy X射线辐射后仔鼠肺组织SOD活性先降低后升高,且均低于对照组,差异显著或极显著(P<0.05或P<0.01)。
2.X射线辐射影响生长发育期仔鼠肺组织MDA的含量。经0.5Gy和2.0Gy X射线辐射后仔鼠肺组织MDA含量均低于对照组,差异显著或极显著(P<0.05或P<0.01)。初期逐渐降低,后期升高且接近正常水平。经3.5Gy、5.0Gy和6.5Gy X射线辐射后仔鼠肺组织MDA含量先升高后降低,且均高于对照组,差异显著或极显著(P<0.05或P<0.01)。
3.X射线辐射影响生长发育期仔鼠肺组织GSH-Px的活性。经0.5Gy X射线辐射后仔鼠肺组织GSH-Px活性均高于对照组,差异显著或极显著(P<0.05或P<0.01),且随着时间呈下降趋势。经2.0Gy、3.5Gy、5.0Gy和6.5Gy X射线辐射后仔鼠肺组织GSH-PX活性均低于对照组,差异显著或极显著(P<0.05或P<0.01),且均呈先下降后逐渐恢复的趋势。
4.X射线辐射影响生长发育期的仔鼠肺脏中GSH的含量。经0.5Gy X射线辐射后初期,仔鼠肺组织GSH含量均高于对照组,差异极显著(P<0.01);后期,仔鼠肺组织GSH含量降低且接近对照组,差异不显著或显著(P>0.05或P<0.05)。经2.0Gy、3.5Gy、5.0Gy和6.5Gy X射线辐射后仔鼠肺组织GSH含量降低但均低于对照组,差异显著或极显著(P<0.05或P<0.01)。
5.X射线辐射影响生长发育期仔鼠肺的组织结构。经不同剂量X射线辐射后仔鼠肺泡直径和肺泡隔厚度均有不同程度的变化。经0.5Gy、2.0Gy X射线辐射后仔鼠肺间质细胞致密,肺泡直径及肺泡隔厚度与对照组相比均有不同程度的减少。经3.5Gy、5.0Gy和6.5Gy X射线辐射后肺泡直径和肺泡隔厚度与对照组相比均有不同程度的增加。
6.X射线辐射影响生长发育期仔鼠肺组织中Bax蛋白的表达。Bax蛋白在各不同剂量辐射组仔鼠肺组织中均有不同程度的表达,其表达强度随辐射剂量的增大而增强,随着时间逐渐恢复至接近正常水平。
7.X射线辐射影响生长发育期仔鼠肺组织中KGF蛋白的表达。KGF蛋白在各不同剂量辐射组仔鼠肺组织中均有不同程度的表达。其表达强度随辐射剂量的增大而增强,随着时间呈下降趋势且最终接近正常水平。结论:
1.X射线辐射对生长发育期仔鼠的抗氧化酶活性有明显影响。小剂量X射线辐射后仔鼠肺组织中超氧化物歧化酶活性初期升高后期降低、丙二醛含量初期降低后期升高,大剂量X射线辐射后则恰好相反。小剂量X射线辐射后初期谷胱甘肽过氧化物酶活性及还原型谷胱甘肽含量均高于对照组,而后期均低于对照组,且均随着时间呈下降趋势。
2.X射线辐射影响生长发育期仔鼠肺的组织结构。经不同剂量的X射线辐射后仔鼠肺泡直径和肺泡隔厚度均有不同程度的变化。小剂量X射线辐射后仔鼠肺间质细胞致密,肺泡直径及肺泡隔厚度与对照组相比均有不同程度的减少。大剂量X射线辐射后肺泡直径和肺泡隔厚度与对照组相比均有不同程度的增加。
3.X射线辐射影响生长发育期仔鼠肺组织中Bax及KGF蛋白的表达。Bax及KGF蛋白在仔鼠肺组织中均有不同程度的表达,其表达强度随辐射剂量的增大而增强,对细胞损伤与修复的诱导亦增强。具体表现为:辐射初期在肺组织细胞中均有较强的阳性分布,随后Bax蛋白的表达逐渐减弱,最终恢复至接近正常水平;而KGF蛋白的表达呈下降趋势且最终接近正常水平。
高剂量电离辐射可引起机体内产生大量超氧阴离子自由基(O2-.),从而造成机体组织中细胞的过氧化损伤,而低剂量的电离辐射又可诱导生物体的免疫兴奋。电离辐射还可以使机体各种免疫细胞的功能被激活,特别是T细胞的激活和分化,导致有氧代谢旺盛,产生超氧阴离子自由基高于静止状态。所以低剂量辐射后仔鼠的肺组织抗氧化酶活性升高,脂质化水平降低。而大剂量电离辐射产生的自由基由于无法及时清除而攻击细胞,致使组织损伤,抗氧化酶活性降低,Bax、KGF蛋白高度表达。而在辐射后一段时间内各组仔鼠各检测指标及组织结构均有不同程度恢复正常的趋势。表明X射线辐射影响生长发育期仔鼠肺组织抗氧化酶活性、组织结构及相关特异蛋白的表达。大剂量电离辐射对生长发育期仔鼠具有损伤作用,但机体具有一定的抗辐射机能。
OBJECTIVE:
To study the effects of different dosages of X-ray on lung of developing filial mice, antioxide enzymes activity , the structure and inter related polypeptides after irradiation were determined, which is to explore the synthetical effect on lung of developing filial mice,provide a basis for developmental biology,clinical cure of irradiation damnification and prevention of irradiation.
METHODS:
Age of 5-7 days filial mice were choosed and divided into six groups(32 per group).The six groups irradiated by different dosages(0.0,0.5,2.0,3.5,5.0,6.5 Gy) X-rays respective every day and persisted three days. Eight filial mice of every group were killed (1、5、10、20 d) after irradiation, and effect on the activities of Superoxide dismutase(SOD),Glutathione Peroxidase (GSH-Px),and the contents of Maleic dialdehyde (MDA) , Reduced Glutathione Hormone (GSH) in lung were determined after this tissue be skived from this filial mice and confect to liquid supernatant. Changes of histological structure were observed by histological methods and thickness of Alveolar Septa and diameter of Alveolous were measured. Expressions of Bax and KGF in lung of filial mice were observed by immunohistochemistry method. The expression intensity of them was measuring by Stereological method and image analysis.
RESULT:
1. X-ray affects the SOD activity in lung of filial mice at their growing periods. After the radiation of 0.5Gy and 2.0Gy X-ray, SOD activity in lung of filial mice is higher than the control group with apparent or extremely apparent differences (P<0.05 or P<0.01). Early stages it increases gradually, later decreasing and then increasing and all of which are lower than the control groups with apparent or extremely apparent difference(P<0.05 or P<0.01).
2. X-ray affects the MDA content in lung of filial mice in their growing periods. After the radiation of 0.5Gy and 2.0Gy X-ray, content of MDA in lung of filial mice is lower than the control group with apparent or extremely apparent differences (P<0.05 or P<0.01). Those were being radiated by 0.5Gy and 2.0Gy X-ray, MDA content in their lungs decreases and approximately equal to the normal level in early stages, later increases and even reach the normal level later. After the radiation of 3.5Gy, 5.0Gy and 6.5Gy, MDA content in the lung tissue of filial mice increases at first and then decreases later after that, and all of which are above that of the control groups with apparent or extremely apparent differences(P<0.05 or P<0.01).
3. X-ray affects GSH-Px activity in lung of the filial mice during their growing periods. After 1-20d by 0.5Gy X-ray radiation, GSH-Px activity in the lung of filial mice is higher than the control group with extremely apparent or apparent differences(P<0.01or P<0.05), and the activity decreases as the time passing by. With the X-ray radiation of 2.0、3.5、5.0 and 6.5Gy, GSH-Px activity in lung of filial mice is lower than that of the control group with apparent or extremely apparent differences (P<0.05 or P<0.01) and has the tendency of decreasing-to-increasing.
4. X-ray affects the GSH content in lung of filial mice during their growing periods. After the radiation of 0.5Gy X-ray after early stages, GSH content in lung of filial mice is higher than the control group with extremely apparent differences(P<0.01). Later, GSH content in lung of filial mice decreases even reaches to that of the control group with unapparent or apparent differences(P>0.05 or P<0.05). With the X-ray radiation of 2.0、3.5、5.0 and 6.5Gy, GSH content in the lung of filial mice is lower than the control group with apparent and extremely apparent differences (P<0.05 or P<0.01).
5. X-ray affects the histological structure in lung of filial mice. X-ray radiation affects the diameter of Alveolar and the thickness of Alveolar Septa for different degrees in filial mice. After being radiated by 0.5 Gy and 2.0 Gy X-ray radiation, the interstitial cells in the lung of filial mice are in high density, the diameter of Alveolar and the thickness of Alveolar Septa decrease by different degrees. The diameter of Alveolar and the thickness Alveolar Septa of the 3.5Gy, 5.0Gy and 6.5Gy groups increase with various degrees compared with that of the control group.
6. X-ray affects the expression of Bax protein in lung of filial mice. There Bax protein immunoreaction appeared in lung of filial mice, and the intensity of the immunoreaction was increased with augmentation of dosages, but decreased gradually, and recovered to nearly normal levels over time.
7. X-ray affects the expression of KGF in lung of filial mice. There KGF immunoreaction appeared in lung of filial mice, and the intensity of the immunoreaction was increased with augmentation of dosages. It increased in the beginning and then decreased, but increased later, and come back to normal level finally.
CONCULSION:
1. X-ray affects the activity of antioxidase in lung of filial mice remarkably.
After the radiation of low doses, SOD activity in lung of filial mice increases gradually in early stages, later decreasing. MDA content in lung of filial mice decreases gradually in early stages, later increasing. After the radiation of high doses, it is contradictory. After the radiation of low doses, GSH-Px activity and GSH content in lung of filial mice is higher than the control group in early stages and that is lower than the control group later, all that decreases gradually over time. 2. X-ray affects the histological structure in lung of filial mice. X-ray radiation affects the diameter of Alveolar and the thickness of Alveolar Septa for different degrees in filial mice. After the radiation of low doses, the interstitial cells in the lung of filial mice are in high density, the diameter of Alveolar and the thickness of Alveolar Septa decrease by different degrees. The diameter of Alveolar and the thickness Alveolar Septa of the high doses groups increase with various degrees compared with that of the control group.
3. X-ray affects the expression of Bax and KGF protein in lung of filial mice. The intensity of the immunoreaction was increased with augmentation of dosages, its induction of injury and repair of cell has increased. Specifically as follows: after radiation in the early stages, the expression of Bax and KGF protein had strong positive distribution in lung of filial mice, but the expression of Bax decreased gradually, and recovered to nearly normal levels over time. And the expression of KGF increased in the early stages and decreased gradually, but later recovered to nearly normal levels over time.
High-doses of ionizing radiation can produce a large number of superoxide anion radicals in the organic body, resulting in oxidative damages in cells of the body tissue. While low -doses of ionizing radiation can induce immune excitation. Radiation can also activate the functions of various immune cells of the body, especially for the activation and differentiation of T-cell, which resulting in aerobic metabolism prosperity and the production of superoxide anion radicals even higher than the static state. So the activities of antioxidant-enzyme in tissue of the filial mice increased and content of lipid decreased after the low dosage X-ray. Free radical which produce by large dosage X-ray and could not be eliminate timely will assault cell and cause damage to tissue and activities of antioxidant-enzyme decreased. Histological structure of lung of the filial mice obviously changed after large dosage irradiation. Radiation can increase expression of Bax and KGF in lung of filial mice. There was a trend that the activity of target enzyme, expression of Bax and KGF and histological structure recovered slowly to the normal level after irradiation. The irradiation of X-rays affects the activity of target enzyme, expression of Bax and KGF and histological structure of developing filial mice significantly. In short, large dosages of irradiation would cause disadvantageous effect on developing filial mice,but the organism also have enginery to resist the radiation.
引文
白巨利,孟紫强.SO2吸入对大鼠肺P53、bax、bcl-2mRNA和蛋白表达的影响[J].环境与职业学,2006,23(2):100-104.
崔玉芳,丁彦青,徐菡等.大剂量γ线照射对小鼠免疫功能近期、远期的影响[J].细胞与分子免疫学杂志,2004,20(6):675-677.
崔玉芳,丁彦青,杜雪梅.细胞凋亡与辐射免疫损伤研究进展[J].国外医学·放射医学核医学分册,2002,26(6):271-274.
陈玉琴,俞诗源,张虎林等.红腹锦鸡肾的组织结构及EGFR,TGF-β,AQP-2在肾中的表达[J].动物学报,2008,54(2):332～341.
邓海平,俞诗源,陈玉琴等.X射线辐射对仔鼠体重、皮毛生长及肝、肾脏组织SOD、CAT活力及MDA含量的影响[J].动物学报,2008,54(6):1029-1037.
丁克祥.SOD应用研究集[M].原子能出版社,1991,181-207.
邓文,李毓琦.低剂量γ射线照射后骨髓细胞抗自由基损伤的兴奋效应[J].中国公共卫生学报,1997,16(1):56-58.
丁续红,吴小军,李清泉等.肺癌组织中bcl-2和Bax的表达[J].肿瘤研究与临床,1999,11(6):374-376.
封丽,邓大平.低剂量辐射对大鼠免疫功能影响的研究[J].中国辐射卫生,2007,16(1):26–27.
何淑杰,叶飞,刘树铮.X射线诱导转录因子活化与凋亡的关系[J]..中华放射医学与防护杂志,2002,22(1):4-6.
何中乾,蒋健,陆一鸣.氧自由基在大鼠肠缺血再灌流致肺损伤中的作用[J].同济大学学报(医学版),2002, 23(5):368-370.
金顺子,刘树铮,2002.X射线全身照射对免疫细胞共刺激分子表达的影响[J].中华放射医学与防护杂志,22(4):256-259.
李彩霞,卢晓晔,黄中新等.人胎肺发育过程中P53和Bax的表达及意义[J].中国组织化学与细胞化学杂志,2006,15(5):487-490.
刘婷婷.电磁辐射与电磁污染[J].现代物理知识,2006.18(1):30-31.
刘树铮.医学放射生物学[M].北京:原子能出版社,1998,256-270.
刘树铮.辐射免疫学研究的回顾与展望[J].中华放射医学与防护杂志,2005,25(2):193-200.
刘颖,刘永彪,高超等.超氧化物歧化酶对小鼠肝脏和免疫细胞的辐射防护作用[J].徐州医学院学报,2002,22(2):146-148.
刘亚宁.电磁辐射生物效应的机理研究述评[J].基础医学与临床,2000,20(1):20-23.
彭庆远,钟辉秀,尹朝伦.硒、GSH-PX、SOD、MDA测定在探测肝脏疾病过氧化脂质损伤中的临床应用[J].国外医学临床生物化学与检验学分册,2001,22(6):324.
庞轶兵,丁桂荣.2450 MHz微波辐照对小鼠脑组织SOD活性及GSH、MDA含量的影响[J].中华放射医学与防护杂志,2003,23(3):186-187.
孙存着.生物医学ESR研究论文集(I).北京:1989,67-70.
邵寒娟,陈亮,林涛.角质细胞生长因子研究进展[J].生命科学,2004,16(1):27-30.
王樯,黄中新,夏潮涌.小鼠肺发育中细胞增殖与凋亡及相关调控基因的表达[J].解剖学报,2000,31(4):372-375.
王小华,余争平,程天民.角质细胞生长因子.国外医学临床生物化学与检测学分册[J],2000,21(4):213-214.
王晓君,魏登邦,魏莲等.高原鼢鼠和高原鼠兔肺细叶的结构特征[J].动物学报,2008,54(3):531-539.
薛丽香,金顺子,刘建香等.电离辐射对小鼠免疫器官SOD基因转录以及蛋白活性的影响[J].中华放射医学与防护杂志,2002,12(5):347-349. 夏冰芝.X射线对花背蟾蜍胚胎发育的影响及肺蛋白的差异表达.西北师范大学硕士学位论文,2007:10-11.
夏寿萱.放射生物学[M].北京:军事医学科学出版社,1998,35-43.
谢漪,张红,党秉荣等. X射线低剂量多次辐射对小鼠外周血淋巴细胞的影响.辐射研究与辐射工艺学报,2007,25(6):368-370.
余鸿,刘敦玉,吴雨岭等.c-Fos和巢蛋白在鼠胚肺内的表达及缺氧对其影响[J].中国现代医学杂志,2006,16(16):2457-2460.
杨明建,孔福全,展永等.各种自由基清除剂在γ射线辐照DNA损伤中的作用[J].核技术, 2007,30(4):255-258.
张变英.60Co-γ射线对白腐真菌和黑曲霉的诱变效应以及对木质素降解的研究[J].广西大学硕士学位论文,2003:15-17.
邹国林,裘名宜,朱彤.超氧化物歧化酶研究的历史、现状及应用前景[J].氨基酸杂志,1991,3:28-32.
张欢乐,吴伟,吴兴中,2008.维生素A缺乏对大鼠肺脏发育的影响[J].中国实验动物学报,16(3):220-223.
赵卫平,张红,邱嵘等.碳离子全身辐照对小鼠血清及肝脏中超氧化物歧化酶活性、丙二醛含量和脑组织中还原性谷胱甘肽浓度的影响[J].辐射研究与辐射工艺学报,2007,25(2):33-36.
张弋,许松青,江慧琳等.纳洛酮对犬缺血再灌注损伤肺组织的MDA、SOD、NO的影响[J].广州医学院学报,2003,31(3):48-50.
赵琢道,1990.氧自由基与肺损伤[J].临床荟萃,5(4):31-32.
余鸿,刘敦玉,吴雨岭等.c-Fos和巢蛋白在鼠胚肺内的表达及缺氧对其影响[J].中国现代医学杂志,2006,16(16):2457-2460.
王彦良.电离辐射对人体健康的影响[J].科学之友,2008,23:103-105.
Anderson RE.Ionizing radiation and the immune response.Adv.Immunol.1976,4:215-235.
Alarid ET,Rubin JS,YoungP,etal.Keratinocyte growth factor function sinepithelial induction during seminal vesicle development[J]. Proc Natl Acad Sci,1994,91(3):1074~1078.
Bai C and Jones DP. GSH transport and GSH-dependent detoxication in small intestine of rats exposed in vivo to hypoxia[J]. Am J Physiol,1996,271(4): 701-706.
Bernecker OY,Huq F,Heist EK,et al.Apoptosis in heart failure and the senescent heart[J]. Cardiovasc Toxicol,2003,3(3):183-190.
Borok Z,Danto S I,Dimen L,et al.Na+-K+-ATPase expression in alveolar epithelial cells:upregulation of active ion transport by c-Fos[J]. Am J Physiol,1998,274:149-158.
Ciriolo MR,Palamara AT,Incerpi S,et al. Loss of GSH, oxidative stress, and decrease of intracellular PH as sequential steps in viral infection[J]. J Biol Chem,1997,272(5): 2700-2708.
Edwards MJ,Shiota K,Smith MS,et al. Hyperthermia and birth defects[J]. Reprod Toxicol,1995,9:411-425.
Freed BM,Rapoport R,Leempert N.Inhibition of early events in the human T-lymphocyte response to mitogens and alloantigens by hydrogen peroxide.Arch Surg,1987,122 (1):99–104.
Flanders KC, 2002. Mice lacking Smad3 are protected against cutaneous injury induced by ionizing radiation.AM.J.Pathol,160:1057-1068.
Goll DE,Thompson VF,Li HQ,et al. The calpain system[J]. Physiol Rev,2003,83(3): 731-801.
Harrington NP, Chambers KA, Rose WM, 1997. Radiation damage and immune suppression in splenic mononuclear cell populations.Clin.Exp.Immunol.107:417-424.
Hwang C,Sinskey AJ,Lodish HF. Oxidized redox state of glutathione in the endoplasmic reticulum[J]. Science,1992,257(5076): 1496-1502.
John J E,Kunal K.The ex vivo differential expression of apoptosis signaling cofactors in the developing perinatal lung:essential role of oxygenation during the transition from placental to pulmonary-based respiration[J].Biochemical and Biophysical Research Communications,2001,281 (2): 311-316.
Liu SZ,Qi J,Zhang YC.Signal transduction in lymphocytes after low-dose radiation[J].Int. J Occup Med Toxicol,1994,3:185-191.
Rubin JS,Osada H,Finch PW,et al. Purification and characterization of a newly identified growth factor specific for epithelial cells[J]. PNAS,1989,86(3):802-806.
Stark G. Biochimica Biophysica Acta, 1991, 1071(2):103-122.
Shibata M,Murray M,Tessler A,et al. Single injections of a DNA plasmid that contains the human bcl-2 gene prevent loss and atrophy of distinct neuronal populations after apinal cord injury in adult rats[J]. Neuroehabil Neural Repair,2000,14(4): 319-330.
Seaman WE,Gindhart TD,Blackman MA.Suppression of natural killing in vitro by monocyte and polymorph nuclear leukocytes : requirement for reactive metabolites for oxygen[J]. Clin. Invest,1982,69 (4):876–888.
Ulich T R,Yi E S,Longmuir K,et al. Keratinocyte growth factor is a growth factor for type II pneumocytes in vivo[J]. J Clin Invest. 1994,93: 1298-1306.
Ware L B,Matthay M A.Keratinocyte and hepatocyte groth factors in the lung: roles in lung development,in flammation and repair[J].Am J Physiol Lung Mol Physiol,2002,282: L924-L940.
Werner S,Peters KG,Longaker MT,et al.Large induction of keratinocyte growth factor expression in the dermis during Wound healing[J]. Proc Natl Acad Sci,1992,89:6896~ 6900.
崔玉芳,丁彦青,徐菡等.大剂量γ线照射对小鼠免疫功能近期、远期的影响[J].细胞与分子免疫学杂志,2004,20(6):675-677.
崔玉芳,丁彦青,杜雪梅.细胞凋亡与辐射免疫损伤研究进展[J].国外医学·放射医学核医学分册,2002,26(6):271-274.
陈玉琴,俞诗源,张虎林等.红腹锦鸡肾的组织结构及EGFR,TGF-β,AQP-2在肾中的表达[J].动物学报,2008,54(2):332～341.
邓海平,俞诗源,陈玉琴等.X射线辐射对仔鼠体重、皮毛生长及肝、肾脏组织SOD、CAT活力及MDA含量的影响[J].动物学报,2008,54(6):1029-1037.
丁克祥.SOD应用研究集[M].原子能出版社,1991,181-207.
邓文,李毓琦.低剂量γ射线照射后骨髓细胞抗自由基损伤的兴奋效应[J].中国公共卫生学报,1997,16(1):56-58.
丁续红,吴小军,李清泉等.肺癌组织中bcl-2和Bax的表达[J].肿瘤研究与临床,1999,11(6):374-376.
封丽,邓大平.低剂量辐射对大鼠免疫功能影响的研究[J].中国辐射卫生,2007,16(1):26–27.
何淑杰,叶飞,刘树铮.X射线诱导转录因子活化与凋亡的关系[J]..中华放射医学与防护杂志,2002,22(1):4-6.
何中乾,蒋健,陆一鸣.氧自由基在大鼠肠缺血再灌流致肺损伤中的作用[J].同济大学学报(医学版),2002, 23(5):368-370.
金顺子,刘树铮,2002.X射线全身照射对免疫细胞共刺激分子表达的影响[J].中华放射医学与防护杂志,22(4):256-259.
李彩霞,卢晓晔,黄中新等.人胎肺发育过程中P53和Bax的表达及意义[J].中国组织化学与细胞化学杂志,2006,15(5):487-490.
刘婷婷.电磁辐射与电磁污染[J].现代物理知识,2006.18(1):30-31.
刘树铮.医学放射生物学[M].北京:原子能出版社,1998,256-270.
刘树铮.辐射免疫学研究的回顾与展望[J].中华放射医学与防护杂志,2005,25(2):193-200.
刘颖,刘永彪,高超等.超氧化物歧化酶对小鼠肝脏和免疫细胞的辐射防护作用[J].徐州医学院学报,2002,22(2):146-148.
刘亚宁.电磁辐射生物效应的机理研究述评[J].基础医学与临床,2000,20(1):20-23.
彭庆远,钟辉秀,尹朝伦.硒、GSH-PX、SOD、MDA测定在探测肝脏疾病过氧化脂质损伤中的临床应用[J].国外医学临床生物化学与检验学分册,2001,22(6):324.
庞轶兵,丁桂荣.2450 MHz微波辐照对小鼠脑组织SOD活性及GSH、MDA含量的影响[J].中华放射医学与防护杂志,2003,23(3):186-187.
孙存着.生物医学ESR研究论文集(I).北京:1989,67-70.
邵寒娟,陈亮,林涛.角质细胞生长因子研究进展[J].生命科学,2004,16(1):27-30.
王樯,黄中新,夏潮涌.小鼠肺发育中细胞增殖与凋亡及相关调控基因的表达[J].解剖学报,2000,31(4):372-375.
王小华,余争平,程天民.角质细胞生长因子.国外医学临床生物化学与检测学分册[J],2000,21(4):213-214.
王晓君,魏登邦,魏莲等.高原鼢鼠和高原鼠兔肺细叶的结构特征[J].动物学报,2008,54(3):531-539.
薛丽香,金顺子,刘建香等.电离辐射对小鼠免疫器官SOD基因转录以及蛋白活性的影响[J].中华放射医学与防护杂志,2002,12(5):347-349. 夏冰芝.X射线对花背蟾蜍胚胎发育的影响及肺蛋白的差异表达.西北师范大学硕士学位论文,2007:10-11.
夏寿萱.放射生物学[M].北京:军事医学科学出版社,1998,35-43.
谢漪,张红,党秉荣等. X射线低剂量多次辐射对小鼠外周血淋巴细胞的影响.辐射研究与辐射工艺学报,2007,25(6):368-370.
余鸿,刘敦玉,吴雨岭等.c-Fos和巢蛋白在鼠胚肺内的表达及缺氧对其影响[J].中国现代医学杂志,2006,16(16):2457-2460.
杨明建,孔福全,展永等.各种自由基清除剂在γ射线辐照DNA损伤中的作用[J].核技术, 2007,30(4):255-258.
张变英.60Co-γ射线对白腐真菌和黑曲霉的诱变效应以及对木质素降解的研究[J].广西大学硕士学位论文,2003:15-17.
邹国林,裘名宜,朱彤.超氧化物歧化酶研究的历史、现状及应用前景[J].氨基酸杂志,1991,3:28-32.
张欢乐,吴伟,吴兴中,2008.维生素A缺乏对大鼠肺脏发育的影响[J].中国实验动物学报,16(3):220-223.
赵卫平,张红,邱嵘等.碳离子全身辐照对小鼠血清及肝脏中超氧化物歧化酶活性、丙二醛含量和脑组织中还原性谷胱甘肽浓度的影响[J].辐射研究与辐射工艺学报,2007,25(2):33-36.
张弋,许松青,江慧琳等.纳洛酮对犬缺血再灌注损伤肺组织的MDA、SOD、NO的影响[J].广州医学院学报,2003,31(3):48-50.
赵琢道,1990.氧自由基与肺损伤[J].临床荟萃,5(4):31-32.
余鸿,刘敦玉,吴雨岭等.c-Fos和巢蛋白在鼠胚肺内的表达及缺氧对其影响[J].中国现代医学杂志,2006,16(16):2457-2460.
王彦良.电离辐射对人体健康的影响[J].科学之友,2008,23:103-105.
Anderson RE.Ionizing radiation and the immune response.Adv.Immunol.1976,4:215-235.
Alarid ET,Rubin JS,YoungP,etal.Keratinocyte growth factor function sinepithelial induction during seminal vesicle development[J]. Proc Natl Acad Sci,1994,91(3):1074~1078.
Bai C and Jones DP. GSH transport and GSH-dependent detoxication in small intestine of rats exposed in vivo to hypoxia[J]. Am J Physiol,1996,271(4): 701-706.
Bernecker OY,Huq F,Heist EK,et al.Apoptosis in heart failure and the senescent heart[J]. Cardiovasc Toxicol,2003,3(3):183-190.
Borok Z,Danto S I,Dimen L,et al.Na+-K+-ATPase expression in alveolar epithelial cells:upregulation of active ion transport by c-Fos[J]. Am J Physiol,1998,274:149-158.
Ciriolo MR,Palamara AT,Incerpi S,et al. Loss of GSH, oxidative stress, and decrease of intracellular PH as sequential steps in viral infection[J]. J Biol Chem,1997,272(5): 2700-2708.
Edwards MJ,Shiota K,Smith MS,et al. Hyperthermia and birth defects[J]. Reprod Toxicol,1995,9:411-425.
Freed BM,Rapoport R,Leempert N.Inhibition of early events in the human T-lymphocyte response to mitogens and alloantigens by hydrogen peroxide.Arch Surg,1987,122 (1):99–104.
Flanders KC, 2002. Mice lacking Smad3 are protected against cutaneous injury induced by ionizing radiation.AM.J.Pathol,160:1057-1068.
Goll DE,Thompson VF,Li HQ,et al. The calpain system[J]. Physiol Rev,2003,83(3): 731-801.
Harrington NP, Chambers KA, Rose WM, 1997. Radiation damage and immune suppression in splenic mononuclear cell populations.Clin.Exp.Immunol.107:417-424.
Hwang C,Sinskey AJ,Lodish HF. Oxidized redox state of glutathione in the endoplasmic reticulum[J]. Science,1992,257(5076): 1496-1502.
John J E,Kunal K.The ex vivo differential expression of apoptosis signaling cofactors in the developing perinatal lung:essential role of oxygenation during the transition from placental to pulmonary-based respiration[J].Biochemical and Biophysical Research Communications,2001,281 (2): 311-316.
Liu SZ,Qi J,Zhang YC.Signal transduction in lymphocytes after low-dose radiation[J].Int. J Occup Med Toxicol,1994,3:185-191.
Rubin JS,Osada H,Finch PW,et al. Purification and characterization of a newly identified growth factor specific for epithelial cells[J]. PNAS,1989,86(3):802-806.
Stark G. Biochimica Biophysica Acta, 1991, 1071(2):103-122.
Shibata M,Murray M,Tessler A,et al. Single injections of a DNA plasmid that contains the human bcl-2 gene prevent loss and atrophy of distinct neuronal populations after apinal cord injury in adult rats[J]. Neuroehabil Neural Repair,2000,14(4): 319-330.
Seaman WE,Gindhart TD,Blackman MA.Suppression of natural killing in vitro by monocyte and polymorph nuclear leukocytes : requirement for reactive metabolites for oxygen[J]. Clin. Invest,1982,69 (4):876–888.
Ulich T R,Yi E S,Longmuir K,et al. Keratinocyte growth factor is a growth factor for type II pneumocytes in vivo[J]. J Clin Invest. 1994,93: 1298-1306.
Ware L B,Matthay M A.Keratinocyte and hepatocyte groth factors in the lung: roles in lung development,in flammation and repair[J].Am J Physiol Lung Mol Physiol,2002,282: L924-L940.
Werner S,Peters KG,Longaker MT,et al.Large induction of keratinocyte growth factor expression in the dermis during Wound healing[J]. Proc Natl Acad Sci,1992,89:6896~ 6900.