工业氧化过程中过氧化物的生成及其防治

本文着重讨论工业生产直接氧化过程中有机过氧化物(organic Pe-roxides)的形成、检测、及由有机过氧化物引起的爆炸事故的防治方法。     

辣根过氧化物酶在有机合成中的应用

综述了辣根过氧化物酶在有机合成中作为催化剂使用,其催化机理为过氧化循环过程;以及辣根过氧化物酶催化合成苯胺、苯胺衍生物、酚类的研究进展,其特点为催化效率高。用酶的催化聚合作用来处理酚类、芳香胺类化合物的污染,显示了广阔的应用前景。     

过氧化物在橡胶硫化中的交联机理

概述了过氧化物交联机理中的三个方面，讨论了一些常用的添加剂对交联效果的影响。为了使最终产品获得良好的性能，需选择合适的过氧化物、矿物油、填充剂、抗氧剂及活性助剂等配合剂。     

过氧化物酶的应用研究进展

过氧化物酶在过氧化物氧化底物的过程中起着重要的作用,广泛应用于生物技术领域.过氧化物酶的热不稳定性是抑制其应用的主要因素,现正设计成新的催化剂形式来克服其稳定性问题,增加其热稳定系数.     

高密度燃料HDF-1中过氧化物生成的研究

研究了在升温加速氧化条件下高密度燃料HDF-1的储存温度、气氛和燃料纯度对过氧化物生成量的影响。结果表明,在130￣170℃,过氧化物的生成可划分为抑制段和增长段2个阶段,HDF-1的抑制期随温度升高显著缩短,其定量关系为τ=2×1010×e-0.1188T;HDF-1的抑制期随气氛中氧气浓度的降低而延长;杂质桥式四氢双环戊二烯(endo-THDCPD)能显著缩短HDF-1生成过氧化物的抑制期,质量分数1%endo-THDCPD使抑制期缩短约47.4%。     

过氧化物交联聚烯烃弹性体的性能

采用过氧化物交联,讨论了交联剂、共交联剂、补强填充剂以及增地采用茂金属催化剂合成的乙烯－辛烯共聚物（ＰＯＥ）的物理机械性能的影响。和过氧化物交联后,ＰＯＥ的拉伸强度、扯断伸长率和扯断永久变形大幅度下降。加入共交联剂,可以提高交联程度,缩短硫化时间。加入炭黑,可以起到补强作用。提高１００％定伸应力、撕裂强度、伸强度和硬度,减小扯断伸长率和扯断永久变形。加入增塑剂降低了某些力学性能,但扯断伸长率增加,     

琼脂糖膜固载辣根过氧化物酶催化还原过氧化物的研究

用琼脂糖(agarose)水凝胶将辣根过氧化物酶(HRP)固定在玻碳电极(GCE)表面,制备了HRP-Agarose膜修饰电极。在水-乙醇混合溶液中,包埋在琼脂糖水凝胶中的HRP可以与电极直接传递电子,并且能催化还原H2O2、过氧化丁酮、氢过氧化叔丁基、氢过氧化异丙基苯等过氧化物和NO。HRP-Agarose膜修饰电极具有较好的稳定性和重现性,可用于上述过氧化物和亚硝酸盐的定量检测。     

超高压处理对橙汁中过氧化物酶活性的影响

为了推进超高压钝酶技术的工业化进程,以橙汁中的过氧化物酶（POD）为研究对象,通过实验对影响超高压钝酶效果的处理条件（压力、保压时间、pH、温度）进行了考察与评价.在处理温度为室温、保压时间分别为5和20 m in的条件下,200 MPa以下压力范围内POD被激活,其活性随压力的增加出现上升趋势,当压力大于200MPa,随着处理压力增加酶活性下降;压力较高时（500 MPa）酶的活性随着保压时间的增加而降低,而在较低的压力（200 MPa）,其活性随着保压时间的增加而升高;酶活性随pH的增大先上升后下降;随着温度的上升,酶活性降低.实验结果表明,压力、保压时间、pH值、温度是影响超高压钝酶效果的重要因素.     

过氧化物酶应用的生物技术进展

介绍了过氧化物酶可以催化的四种反应类型 :氧化去氢反应、氧化卤化反应、双氧水歧化反应、氧传递反应。综述了过氧化物酶在有机合成等反应中的应用前景。认为氯过氧化物酶是一种应用最广的过氧化物酶 ,在催化有机反应时 ,具有更高的手性选择性和酶稳定性     

Nitric Oxide and Reactive Oxygen Species in the Pathogenesis of Preeclampsia

Preeclampsia (PE) is characterized by disturbed extravillous trophoblast migration toward uterine spiral arteries leading to increased uteroplacental vascular resistance and by vascular dysfunction resulting in reduced systemic vasodilatory properties. Its pathogenesis is mediated by an altered bioavailability of nitric oxide (NO) and tissue damage caused by increased levels of reactive oxygen species (ROS). Furthermore, superoxide (O₂⁻) rapidly inactivates NO and forms peroxynitrite (ONOO⁻). It is known that ONOO⁻ accumulates in the placental tissues and injures the placental function in PE. In addition, ROS could stimulate platelet adhesion and aggregation leading to intravascular coagulopathy. ROS-induced coagulopathy causes placental infarction and impairs the uteroplacental blood flow in PE. The disorders could lead to the reduction of oxygen and nutrients required for normal fetal development resulting in fetal growth restriction. On the other hand, several antioxidants scavenge ROS and protect tissues against oxidative damage. Placental antioxidants including catalase, superoxide dismutase (SOD), and glutathione peroxidase (GPx) protect the vasculature from ROS and maintain the vascular function. However, placental ischemia in PE decreases the antioxidant activity resulting in further elevated oxidative stress, which leads to the appearance of the pathological conditions of PE including hypertension and proteinuria. Oxidative stress is defined as an imbalance between ROS and antioxidant activity. This review provides new insights about roles of oxidative stress in the pathophysiology of PE.     

Peroxisome-Mediated Reactive Oxygen Species Signals Modulate Programmed Cell Death in Plants

Peroxisomes are a class of simple organelles that play an important role in plant reactive oxygen species (ROS) metabolism. Experimental evidence reveals the involvement of ROS in programmed cell death (PCD) in plants. Plant PCD is crucial for the regulation of plant growth, development and environmental stress resistance. However, it is unclear whether the ROS originated from peroxisomes participated in cellular PCD. Enzymes involved in the peroxisomal ROS metabolic pathways are key mediators to figure out the relationship between peroxisome-derived ROS and PCD. Here, we summarize the peroxisomal ROS generation and scavenging pathways and explain how peroxisome-derived ROS participate in PCD based on recent progress in the functional study of enzymes related to peroxisomal ROS generation or scavenging. We aimed to elucidate the role of the peroxisomal ROS regulatory system in cellular PCD to show its potential in terms of accurate PCD regulation, which contribute to environmental stress resistance.     

Faradaic Fenton Pixel: Reactive Oxygen Species Delivery Using Au/Cr Electrochemistry

Reactive oxygen species (ROS) are an integral part of many anticancer therapies. Fenton-like processes involving reactions of peroxides with transition metal ions are a particularly potent and tunable subset of ROS approaches. Precise on-demand dosing of the Fenton reaction is an area of great interest. Herein, we present a concept of an electrochemical faradaic pixel that produces controlled amounts of ROS via a Fenton-like process. The pixel comprises a cathode and anode, where the cathode reduces dissolved oxygen to hydrogen peroxide. The anode is made of chromium, which is electrochemically corroded to yield chromium ions. Peroxide and chromium interact to form a highly oxidizing mixture of hydroxyl radicals and hexavalent Cr ions. After benchmarking the electrochemical properties of this type of device, we demonstrate how it can be used under in vitro conditions with a cancer cell line. The faradaic Fenton pixel is a general and scalable concept that can be used for on-demand delivery of redox-active products for controlling a physiological outcome.     

Extracellular Inorganic Phosphate-Induced Release of Reactive Oxygen Species: Roles in Physiological Processes and Disease Development

Inorganic phosphate (Pi) is an essential nutrient for living organisms and is maintained in equilibrium in the range of 0.8–1.4 mM Pi. Pi is a source of organic constituents for DNA, RNA, and phospholipids and is essential for ATP formation mainly through energy metabolism or cellular signalling modulators. In mitochondria isolated from the brain, liver, and heart, Pi has been shown to induce mitochondrial reactive oxygen species (ROS) release. Therefore, the purpose of this review article was to gather relevant experimental records of the production of Pi-induced reactive species, mainly ROS, to examine their essential roles in physiological processes, such as the development of bone and cartilage and the development of diseases, such as cardiovascular disease, diabetes, muscle atrophy, and male reproductive system impairment. Interestingly, in the presence of different antioxidants or inhibitors of cytoplasmic and mitochondrial Pi transporters, Pi-induced ROS production can be reversed and may be a possible pharmacological target.     

Mitochondria-Derived Reactive Oxygen Species Play an Important Role in Doxorubicin-Induced Platelet Apoptosis

Doxorubicin (DOX) is an effective chemotherapeutic agent; however; its use is limited by some side effects; such as cardiotoxicity and thrombocytopenia. DOX-induced cardiotoxicity has been intensively investigated; however; DOX-induced thrombocytopenia has not been clearly elucidated. Here we show that DOX-induced mitochondria-mediated intrinsic apoptosis and glycoprotein (GP)Ibα shedding in platelets. DOX did not induce platelet activation; whereas; DOX obviously reduced adenosine diphosphate (ADP)- and thrombin-induced platelet aggregation; and impaired platelet adhesion on the von Willebrand factor (vWF) surface. In addition; we also show that DOX induced intracellular reactive oxygen species (ROS) production and mitochondrial ROS generation in a dose-dependent manner. The mitochondria-targeted ROS scavenger Mito-TEMPO blocked intracellular ROS and mitochondrial ROS generation. Furthermore; Mito-TEMPO reduced DOX-induced platelet apoptosis and GPIbα shedding. These data indicate that DOX induces platelet apoptosis; and impairs platelet function. Mitochondrial ROS play a pivotal role in DOX-induced platelet apoptosis and GPIbα shedding. Therefore; DOX-induced platelet apoptosis might contribute to DOX-triggered thrombocytopenia; and mitochondria-targeted ROS scavenger would have potential clinical utility in platelet-associated disorders involving mitochondrial oxidative damage.     

Alliin Attenuated RANKL-Induced Osteoclastogenesis by Scavenging Reactive Oxygen Species through Inhibiting Nox1

The healthy skeleton requires a perfect coordination of the formation and degradation of bone. Metabolic bone disease like osteoporosis is resulted from the imbalance of bone formation and/or bone resorption. Osteoporosis also reflects lower level of bone matrix, which is contributed by up-regulated osteoclast-mediated bone resorption. It is reported that monocytes/macrophage progenitor cells or either hematopoietic stem cells (HSCs) gave rise to multinucleated osteoclasts. Thus, inhibition of osteoclastic bone resorption generally seems to be a predominant therapy for treating osteoporosis. Recently, more and more natural compounds have been discovered, which have the ability of inhibiting osteoclast differentiation and fusion. Alliin (S-allyl-l-cysteine sulfoxides, SACSO) is the major component of aged garlic extract (AGE), bearing broad-spectrum natural antioxidant properties. However, its effects on bone health have not yet been explored. Hence, we designed the current study to explore its effects and role in receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast fusion and differentiation. It was revealed that alliin had an inhibitory effect in osteoclasteogenesis with a dose-dependent manner via blocking the c-Fos-NFATc1 signaling pathway. In addition, alliin decreased the generation of reactive oxygen species (ROS) and down-regulated the expression of NADPH oxidase 1 (Nox1). The overall results revealed that alliin could be a potential therapeutic agent in the treatment of osteoporosis.     

Damaged DNA Binding Protein 2 in Reactive Oxygen Species (ROS) Regulation and Premature Senescence

Premature senescence induced by DNA damage or oncogene is a critical mechanism of tumor suppression. Reactive oxygen species (ROS) have been implicated in the induction of premature senescence response. Several pathological disorders such as cancer, aging and age related neurological abnormalities have been linked to ROS deregulation. Here, we discuss how Damaged DNA binding Protein-2 (DDB2), a nucleotide excision repair protein, plays an important role in ROS regulation by epigenetically repressing the antioxidant genes MnSOD and Catalase. We further revisit a model in which DDB2 plays an instrumental role in DNA damage induced ROS accumulation, ROS induced premature senescence and inhibition of skin tumorigenesis.     

Reactive Oxygen Species: Modulators of Phenotypic Switch of Vascular Smooth Muscle Cells

Reactive oxygen species (ROS) are natural byproducts of oxygen metabolism in the cell. At physiological levels, they play a vital role in cell signaling. However, high ROS levels cause oxidative stress, which is implicated in cardiovascular diseases (CVD) such as atherosclerosis, hypertension, and restenosis after angioplasty. Despite the great amount of research conducted to identify the role of ROS in CVD, the image is still far from being complete. A common event in CVD pathophysiology is the switch of vascular smooth muscle cells (VSMCs) from a contractile to a synthetic phenotype. Interestingly, oxidative stress is a major contributor to this phenotypic switch. In this review, we focus on the effect of ROS on the hallmarks of VSMC phenotypic switch, particularly proliferation and migration. In addition, we speculate on the underlying molecular mechanisms of these cellular events. Along these lines, the impact of ROS on the expression of contractile markers of VSMCs is discussed in depth. We conclude by commenting on the efficiency of antioxidants as CVD therapies.