稀土镧致小鼠睾丸氧化损伤的分子机制

摘要：诸多研究以表明稀土可导致动物睾丸的氧化性损伤，但其分子机制仍不明朗。本文通过不同剂量的LaCl3连续灌胃雄性小鼠90d, 研究Nrf-2/AREs (抗氧化反应元件)通路在睾丸毒性氧化应激中的调控作用。结果表明LaCl3连续染毒可导致睾丸组织严重病变和生精细胞凋亡。进一步分析表明损伤的睾丸中ROS大量积累、SOD、GSH-PX、GST活性和GSH下降, 脂质、蛋白质和DNA过氧化;与Nrf-2/AREs通路有关的因子Nrf2及其靶基因产物HO-1、GCLC、NQO1、PKC和PI3K表达显著下调，Keap1表达显著上调。由此表明LaCl3染毒引起的睾丸氧化性损伤与Nrf-2/AREs通路活化的抑制有关。94035

毕业论文关键词：LaCl3；雄性小鼠；睾丸；细胞凋亡；氧化应激；Nrf-2/AREs通路

Abstract: Numerous studies have shown that rare earths can cause oxidative damage in animal testis, but its molecular mechanism is still unclear。 In this paper, male mice were fed with different doses of LaCl3 for 90 consecutive days, the regulatory role of Nrf-2/AREs (antioxidant response element) pathway in testicular oxidative stress was investigated。 The results showed that the continuous exposure of LaCl3 could lead to severe testicular pathological changes and spermatogenic cell apoptosis。 Furthermore, LaCl3 resulted in over ROS production, reductions of SOD, GSH-PX, GST activities and GSH content, peroxidation of lipids, proteins and DNA, downregulation of Nrf2 and its target gene products including HO-1,GCLC, NQO1, PKC and PI3K expression, and upregulation of Keap1 expression in damaged testes of mice induced by LaCl3。 It implies that the oxidative damage of testis induced by LaCl3 was related to the inhibition of Nrf-2/AREs pathway activation。源C于H优J尔W论R文M网WwW.youeRw.com 原文+QQ752-018766

Key words: Lanthanum chloride; Male mice; Testis; Apoptosis; Nrf-2/AREs pathway

题目稀土镧致小鼠睾丸氧化损伤的分子机制 1

第一部分：研究背景 4

1。稀土元素的概述及应用 4

1。1概念及性质 4

1。2稀土的应用 4

2。稀土镧进入体内的方式 5

2。1 皮肤吸收 5

2。2 鼻腔吸入 5

2。3 其他吸入方式 5

3。稀土的生物学毒性 6

3。1脑神经毒性 6

3。2肝、肺等器官毒性 6

3。3生殖毒性 6

4。研究思路 8

5。研究内容 8

第二部分稀土镧对小鼠睾丸氧化损伤的分子机制 12

1。前言 12

2。材料与方法 14

2。1 动物饲养和处理 14

2。2睾丸的组织病理学评估 14

2。3 TEM观察睾丸细胞超显微结构 14

2。4睾丸组织氧化应激指标测定 14

2。5 Western blot分析 15

2。6 统计学分析 15

3。结果稀土镧致小鼠睾丸氧化损伤的分子机制:http://www.youerw.com/shengwu/lunwen_202001.html