Autophagy and other vacuolar protein degradation mechanisms

Autophagic degradation of cytoplasm (including protein, RNA etc.) is a non-selective bulk process, as indicated by ultrastructural evidence and by the similarity in autophagic sequestration rates of various cytosolic enzymes with different half-lives. The initial autophagic sequestration step, performed by a poorly-characterized organelle called a phagophore, is subject tofeedback inhibition by purines and amino acids, the effect of the latter being potentiated by insulin and antagonized by glucagon. Epinephrine and other adrenergic agonists inhibit autophagic sequestration through a prazosin-sensitive ₁-adrenergic mechanism. The sequestration is also inhibited by cAMP and by protein phosphorylation as indicated by the effects of cyclic nucleotide analogues, phosphodiesterase inhibitors and okadaic acid.Asparagine specifically inhibits autophagic-lysosomal fusion without having any significant effects on autophagic sequestration, on intralysosomal degradation or on the endocytic pathway. Autophaged material that accumulates in prelysosomal vacuoles in the presence of asparagine is accessible to endocytosed enzymes, revealing the existence of an amphifunctional organelle, the amphisome. Evidence from several cell types suggests that endocytosis may be coupled to autophagy to a variable extent, and that the amphisome may play a central role as a collecting station for material destined for lysosomal degradation.Protein degradation can also take place in a salvage compartment closely associated with the endoplasmic reticulum (ER). In this compartment unassembled protein chains are degraded by uncharacterized proteinases, while resident proteins roturn to the ER and assembled secretory and membrane proteins proceed through the Golgi apparatus. In thetrans-Golgi network some proteins are proteolytically processed by Ca²⁺-dependent proteinases; furthermore, this compartment sorts proteins to lysosomes, various membrane domains, endosomes or secretory vesicles/granules. Processing of both endogenous and exogenous proteins can occurr in endosomes, which may play a particularly important role in antigen processing and presentation. Proteins in endosomes or secretory compartments can either be exocytosed, or channeled to lysosomes for degradation. The switch mechanisms which decide between these options are subject to bioregulation by external agents (hormones and growth factors), and may play an important role in the control of protein uptake and secretion.     

非离子表面活性剂非均相光催化降解试验研究

以非离子型表面活性剂－脂肪醇聚氧乙烯醚为目标污染物,投加适量光敏半导体为催化剂,在高压汞灯照射下进行实验,在探讨各种影响因素作用的基础上,提出了在弱紫外辐照下使ＡＥＯ－９降解的最佳条件组合,为逐步利用自然光源催化氧化表面活性剂提供科学依据。     

药物盐酸曲普利啶热氧降解历程及动力学研究

采用热重法、微分热重法和差热分析法研究药物盐酸曲普利啶在空气流中的热氧降解历程及动力学,从而发现该药物的热氧降解过程由５个紧连步骤组成．用Ｃｏａｔｓ－Ｒｅｄｆｅｒｎ方程进行动力学处理,确定盐酸曲普利啶热氧降解的表观反应级数均为１．１,反应活化能分别为６６．５,１１３．７,１１６．２,１５３．８和１８０．６ｋＪ／ｍｏｌ．     

电化学降解含酚焦化废水的研究

选用Ti／Ir2O3／RuO2为阳极，C-PTFE气体扩散电极为阴极降解模拟含酚焦化废水。利用正交实验，求出最佳操作条件。考察了苯酚浓度、电流密度、电解质浓度、pH值等因素对苯酚去除效率的影响。对电化学降解苯酚进行动力学分析，蛄果证明了其反应为一级动力学反应。     

有毒生物难降解有机污染物的研究进展

对有毒生物难降解有机污染物（Persistent Toxic Substances,简称PTS）的特性、分布、迁移及来源进行了介绍,综述了目前对PTS的分析和控制处理方法,对光催化高级氧化技术处理PTS进行了阐述.     

醋酸对玻璃负载TiO2膜光催化的影响

以钛酸丁酯、乙醇、硝酸为原料,采用溶胶-凝胶法制备玻璃负载型TiO2膜,用醋酸浸渍对其进行表面修饰以增加其光催化活性,用直接耐晒蓝染料模拟废水中难降解的有机污染物.研究结果表明,醋酸浸渍可以增加坡璃负载型TiO2膜光催化活性,当采用0 25mol/L醋酸浸渍玻璃负载型TiO2膜1h,TiO2膜120min内降解率由13 8%提高到42%.     

H2O2氧化降解壳聚糖的动力学

为制备分子量分布较窄的可溶性低分子量壳聚糖，研究了简单均相体系下双氧水降解壳聚糖的过程与机理，考察了温度、双氧水浓度和时间对降解反应的影响，实验结果显示均相条件下壳聚糖的氧化降解符合无规降解动力学规律．同一降解体系中，同一反应时刻下，水解产物的分子量的倒数与反应温度成正比．     

TiO2薄膜光催化降解二氯乙酸和三氯乙酸水溶液

用常压化学气相沉积法镀TiO2薄膜,以紫外灯为光源,对二氯乙酸和三氯乙酸溶液进行光催化降解,并证实了此过程符合一级反应动力学方程。结果表明:卤代度以及不同的半导体化合物底物均对二氯乙酸和三氯乙酸溶液的降解有影响,卤代度低的二氯乙酸比卤代度高的三氯乙酸降解效果要好;同样条件下半导体的带隙能越低,降解效果越好。     

莠去津在填充土柱中的运移

用土柱实验模拟莠去津在土壤中的运移、实验结果表明相当浓度的莠去津被淋溶到土柱的底部，说明莠去津对地下水存在很大威胁、应用CXTFIT的平衡与非平衡模型模拟莠去津在土柱中的运移，模拟结果表明CXTFIT的非平衡模型能很好地模拟莠去津的穿透曲线．由CXTFIT率定得到的莠去津在土柱实验中的吸附和降解参数和从批次实验得到的吸附和降解参数有较好的一致性．     

聚联苯醚二甲酰十二碳二胺的热降解过程与机理

利用热重法研究了半芳香尼龙聚联苯醚二甲酰十二碳二胺(PA12-O)在N2气氛中以不同速率β升温时的热降解过程及热降解动力学.结果表明,PA12-O的热降解是一步反应,随着β的增大,降解温度呈指数关系升高.其起始平衡降解温度为439.4℃,终止时的平衡降解温度为468.33℃,最大降解速率时的平衡降解温度为459.17℃.为确定PA12-O的热降解机理,比较了用Kissinger、 Flynn-Wall-Ozawa和 Coats-Redfern方法求得的PA12-O的热降解表观活化能,证明PA12-O的热降解机理为减速类型.