添加外源锌对大杯香菇子实体细胞保护酶活性的影响

摘要：【目的】本实验研究了添加外源锌（Zn）对大杯香菇子实体保护酶活性的影响。【方法】以硫酸锌为外源锌,添加到培养料中,制成0、10、20、30、40、50 mg/kg 6个浓度。采用分光光度法测定大杯香菇子实体超氧化物岐化酶（SOD）活性、过氧化物酶（POD）活性、多酚氧化酶（PPO）活性、丙二醛（MDA）含量和可溶性蛋白含量,采用高锰酸钾滴定法过氧化氢酶（CAT）活性。【结果】添加外源 Zn浓度为30 mg/kg处理大杯香菇子实体内可溶性蛋白含量、SOD、POD和CAT活性极显著提高（P＜0.01）,PPO活性极显著减少（P＜0.01）,而MDA含量显著下降（P＜0.05）。随着Zn水平进一步升高,可溶性蛋白含量、SOD、POD和CAT活性呈下降趋势,而MDA含量极显著和显著上升（P＜0.01和P＜0.05）。【结论】高用量的Zn浓度能使大杯香菇子实体中的MDA含量上升,SOD、POD、CAT活性均下降,对保护酶系统有破坏作用,促进自由基的积累,从而导致膜脂过氧化作用的加剧。适宜Zn浓度能提高保护酶的活性,从而抑制了大杯香菇子实体中细胞膜脂过氧化水平,减轻膜伤害。     

光敏掩蔽基团在化学生物学中的应用

光敏掩蔽基团技术是通过运用一种由光子控制的光敏化合物,在光子激发后,被该化合物掩蔽处于惰性状态的生物活性分子重新被激活、释放以调节生理功能的化学生物学研究方法,它对生命活动的控制具有实时、原位、精确、快速的优势。该文综述了不同光敏基团的结构与功能,包括硝基苄基类、香豆素类、喹啉类、吲哚类、硝基二苯并呋喃类等,它们通过掩蔽神经递质、钙离子、蛋白质、缩氨酸、核苷酸、遗传物质等重要的生理活性物质来高选择性地调控不同的生物学过程。     

颈髓损伤后线粒体系列酶活性变化与线粒体功能的关系

为了探讨颈髓损伤后颈髓线粒体系列酶活性变化与线粒体功能的关系,采用Ａｌｅｎ法造成猫颈髓损伤,观察颈髓损伤后线粒体Ｃａ２＋,Ｍｇ２＋－ＡＴＰ酶、Ｎａ＋,Ｋ＋－ＡＴＰ酶、超氧化物歧化酶（ＳＯＤ）活性及线粒体呼吸功能的变化。结果显示：颈髓损伤后２ｈ至７２ｈ,Ｃａ２＋,Ｍｇ２＋－ＡＴＰ酶、Ｎａ＋,Ｋ＋－ＡＴＰ酶活性、ＳＯＤ活性明显降低,而线粒体呼吸控制率（ＲＣＲ）、磷氧比值（Ｐ／Ｏ）、氧化磷酸化效率（ＯＰＲ）也明显下降。表明颈髓损伤后Ｃａ２＋,Ｍｇ２＋－ＡＴＰ酶、Ｎａ＋,Ｋ＋－ＡＴＰ酶、ＳＯＤ活性与线粒体功能密切相关,提示颈髓线粒体的病理生理改变在颈髓损伤后继发性损害过程中起重要作用。     

厌氧发酵液中溶解性有机物对活性污泥合成聚羟基脂肪酸酯影响的研究进展

利用活性污泥微生物将剩余污泥发酵液中的挥发性脂肪酸(Volatile fatty acids,VFAs)转化为聚羟基脂肪酸酯(Polyhydroxyalkanoates,PHA)是目前环境生物技术领域的研究热点.但针对发酵液中非VFAs物质(主要是溶解性有机物,Dissolved organic matter,DOM)...     

ApoA-II maintains HDL levels in part by inhibition of hepatic lipase. Studies In apoA-II and hepatic lipase double knockout mice.

High density lipoprotein (HDL) cholesterol levels are inversely related to the risk of developing coronary heart disease. Apolipoprotein (apo) A-II is the second most abundant HDL apolipoprotein and apoA-II knockout mice show a 70% reduction in HDL cholesterol levels. There is also evidence, using human apoA-II transgenic mice, that apoA-II can prevent hepatic lipase-mediated HDL triglyceride hydrolysis and reduction in HDL size. These observations suggest the hypothesis that apoA-II maintains HDL levels, at least in part, by inhibiting hepatic lipase. To evaluate this, apoA-II knockout mice were crossbred with hepatic lipase knockout mice. Compared to apoA-II-deficient mice, in double knockout mice there were increased HDL cholesterol levels (57% in males and 60% in females), increased HDL size, and decreased HDL cholesteryl ester fractional catabolic rate. In vitro incubation studies of plasma from apoA-II knockout mice, which contains largely apoA-I HDL particles, showed active lipolysis of HDL triglyceride, whereas similar studies of plasma from apoA-I knockout mice, which contains largely apoA-II particles, did not. In summary, these results strongly suggest that apoA-II is a physiological inhibitor of hepatic lipase and that this is at least part of the mechanism whereby apoA-II maintains HDL cholesterol levels.     

Expression profile of IGF system during lung injury and recovery in rats exposed to hyperoxia: a possible role of IGF-1 in alveolar epithelial cell proliferation and differentiation

Although several studies have shown that an induction of insulin-like growth factor (IGF) components occurs during hyperoxia-mediated lung injury, the role of these components in tissue repair is not well known. The present study aimed to elucidate the role of IGF system components in normal tissue remodeling. We used a rat model of lung injury and remodeling by exposing rats to > 95% oxygen for 48 h and allowing them to recover in room air for up to 7 days. The mRNA expression of IGF-I, IGF-II, and IGF-1 receptor (IGF-1R) increased during injury. However, the protein levels of these components remained elevated until day 3 of the recovery and were highly abundant in alveolar type II cells. Among IGF binding proteins (IGFBPs), IGFBP-5 mRNA expression increased during injury and at all the recovery time points. IGFBP-2 and -3 mRNA were also elevated during injury phase. In an in vitro model of cell differentiation, the expression of IGF-I and IGF-II increased during trans-differentiation of alveolar epithelial type II cells into type-I like cells. The addition of anti-IGF-1R and anti-IGF-I antibodies inhibited the cell proliferation and trans-differentiation to some extent, as evident by cell morphology and the expression of type I and type II cell markers. These findings demonstrate that the IGF signaling pathway plays a critical role in proliferation and differentiation of alveolar epithelium during tissue remodeling.     

糖基化终产物对原代培养乳鼠肾脏细胞损伤的影响

糖基化终产物(AGEs)在糖尿病肾病的发生发展过程中起着重要的作用.但目前其作用机制还不太清楚.通过体外乳鼠肾脏细胞的原代培养,探讨AGEs对肾细胞的损伤作用及可能的作用机制.取出生3天的SD大鼠的乳鼠肾脏进行体外原代细胞培养,并取传代到4-6代的细胞进行实验研究.分别用不同浓度的AGEs(0、1.2、2.5、5、10、20 mg/ml),不同的作用时间(6、12、18、24 h)作用于体外培养的肾细胞,用MTT法检测AGEs对肾细胞的增殖情况,用酶试剂盒法检测AGEs对肾细胞培养液中乳酸脱氢酶(LDH)、β-N-乙酰氨基葡萄糖苷酶(NAG)的含量,以及肾细胞内还原型谷胱甘肽(GSH)和超氧化物歧化酶(SOD)的含量.实验结果表明随着AGEs作用肾细胞时间的延长和浓度的增加,细胞存活率、细胞内GSH含量和SOD活性均逐渐下降,而细胞培养液中LDH和NAG的含量则逐渐升高,与正常培养的对照组细胞相比差异非常显著(P＜0.001),并且AGEs对细胞的作用与其浓度和作用时间呈显著的量效关系.实验结果说明AGEs对原代培养的肾细胞有明显的损伤作用,并随着AGEs作用浓度的增加和作用时间的延长对肾细胞的损伤越来越严重,实验结果也表明.肾细胞对AGEs的作用很敏感,其损伤细胞的途径和作用机制可能是由于改变了肾细胞膜的通透性和降低肾细胞抗氧化能力,该实验研究也进一步提示了AGEs是导致糖尿病肾脏并发症发生的重要原因之一.     

氨氧化古菌的生态学研究进展

上百年来细菌一直被认为是地球氨氧化过程的主要驱动者,2005年海洋中分离到迄今唯一的非极端环境泉古菌,发现其氧化氨态氮获得能源生长,是氨氧化古菌。氨氧化古菌和细菌对地球氨氧化过程的相对贡献率,是目前全球氮循环研究最重要的微生物生态学问题之一。已有的证据表明古菌在海洋氨氧化过程中发挥了重要作用,细菌则是土壤氨氧化过程的主要驱动者。本文重点探讨了原位自然环境下氨氧化古菌的生态学研究进展。