五味子酚等三种抗氧化剂对氧化应激损伤中枢神经细胞的保护作用及其作用机理研究

氧化应激（ｏｘｉｄａｔｉｖｅｓｔｒｅｓ）在中枢神经系统退行性疾病,如帕金森氏病、老年性痴呆和多发性硬化等的发病机制中起重要作用。这些疾病严重影响着老年人的生活质量,因此寻找有效的抗氧化剂用于防治中枢神经系统退行性疾病的发生和发展是一个十分重要和迫切的问题。本文研究了五味子酚（Ｓａｌ）、丹酚酸Ａ（ＳａｌＡ）和ＳＹＬ三种化合物对氧化应激损伤中枢神经细胞的保护作用及其作用机理。Ｓａｌ和ＳａｌＡ分别为中药红花、五味子和丹参的有效成分,ＳＹＬ是新的、全合成的化合物,三者均有显著的抗氧化活性。本文研究结果显示三种化合物在体内外对多种氧化应激损伤脑组织模型都具有明显的保护作用。     

小麦秸秆的生化他感效应

小麦秸秆的生化他感效应马永清,毛仁钊,刘孟雨,刘小京,张玉铭（中国科学院石家庄农业现代化研究所,０５００２１）ＡｌｌｅｌｏｐａｔｈｉｃＥｆｆｅｃｔｓｏｆＷｈｅａｔＳｔｒａｗ￥ＭａＹｏｎｇｑｉｎｇ;ＭａｏＲｅｎｚｈａｏ;ＬｉｕＭｅｎｙｕ;ＬｉｕＸｉａｏｊｉｎｇ（ＳｈｉｊｉａｚｈｕａｎｇＩｎｓｔｉｔｕｔｅｏｆＡｇｒｉｃｕｌｔｕｒａｌＭｏｄｅｒｎｉｚａｔｉｏｎ,ＡｃａｄｅｍｉａＳｉｎｉｃａ,０５００２１）．ＣｈｉｎｅｓｅＪｏｕｒｎａｌｏｆＥｃｏｌｏｇｙ,１９９３,１２（５）;３６－３８。Ｔｈｅｗｏｒｌｄ－ｗｉｄｅｒｅｓｅａｒｃｈｅｓｏｎａｌｌｅｌｏｐａｔｈｉｃｅｆｆｅｃｔｓｏｆｗｈｅａｔｓｔｒａｗａｒｅｓｕｍｍａｒｉｚｅｄａｎｄｔｈｅｃｕｒｒｅｎｔｓｉｔｕａ－ｔｉｏｎｏｎｉｓｏｌａｔｉｏｎａｎｄｉｄｅｎｔｉｆｉｃａｔｉｏｎｏｆａｌｌｅｌｏｃｈｅｍｉｃａｌｓｆｒｏｍｉｔｉｓｐｒｅｓｅｎｔｅｄ．ｗｈｉｃｈｗｉｌｌｇｉｖｅａｇｕｉｄａｎｃｅｉｎｏｕｒｔｈｅｏｒｅｔｉｃａｌｓｔｕｄｙａｎｄｐｒｏｄｕｃｔｉｖｅｐｒａｃｔｉｃｅ。Ｋｅｙｗｏｒｄｓ：Ａｌｌｅｌｏｐａｔｈｙ,ａｌｌｅｌｏｃｈｅｍｉｃａｌｓ,ｗｈｅａｔｓｔｒａｗ。     

Regulation Culture on Cytological，Biochemical and Physiological Characteristics of Somatic Carrot Em

ＲｅｇｕｌａｔｉｏｎＣｕｌｔｕｒｅｏｎＣｙｔｏｌｏｇｉｃａｌ,ＢｉｏｃｈｅｍｉｃａｌａｎｄＰｈｙｓｉｏｌｏｇｉｃａｌＣｈａｒａｃｔｅｒｉｓｔｉｃｓｏｆＳｏｍａｔｉｃＣａｒｒｏｔＥｍｂｒｙｏｓＨＵＡＮＧＭｅｉ－ｊｕａｎ;（黄美娟）,ＨＵＡＮＧＳｈａｏ－...     

山东省引种乌桕的生态适应性分析

山东省引种乌桕的生态适应性分析王华田杨锦（山东农业大学,泰安２７１０１８）（山东日照港务局,２７６８２６）ＡｎａｌｙｓｉｓｏｆＥｃｏｌｏｇｉｃａｌＡｄａｐｔａｔｉｏｎｏｆＳａｐｉｕｍｓａｂｉｆｅｒｕｍＩｎｔｒｏｄｕｃｅｄｔｏＳｈａｎｄｏｎｇＰｒｏｖｉ...     

沈阳市东陵区丘陵坡地坡面太阳直射光的分布及其分析

沈阳市东陵区丘陵坡地坡面太阳直射光的分布及其分析郭林海（中国科学院沈阳应用生态研究所,１１００１５）ＤｉｓｔｒｉｂｕｔｉｏｎｏｆＤｉｒｅｃｔＳｏｌａｒＲａｄｉａｔｉｏｎｏｎＨｉｌｌｙＳｌｏｐｅｓｏｆＤｏｎｇｌｉｎｇＤｉｓｔｒｉｃｔｏｆＳｈｅｎｙａｎｇＭｕｎｉｃｉｐａｌｉｔｙａｎｄＩｔｓＡｎａｌｙｓｉｓ￥ＧｕｏＬｉｎｈａｉ（ＩｎｓｔｉｔｕｔｅｏｆＡｐｐｌｉｅｄＥｃｏｌｏｇｙ,ＡｃａｄｅｍｉａＳｉｎｉｃａ,Ｓｈｅｎｙａｎｇ１１００１５）．ＣｈｉｎｅｓｅＪｏｕｒｎａｌｏｆＥｃｏｌｏｇｙ,１９９３,１２（１）：５９－６１．Ｂａｓｅｄｏｎｔｈｅｌａｔｅｓｔ１：５００００ｔｏｐｏｇｒａｐｈｉｃｍａｐ,ｔｈｅ１：１０００００ｓｌｏｐｅｇｒａｄａｔｉｏｎｍａｐｉｓｄｒａｗｎｏｕｔａｎｄａｒｅａｃａｌｃｕｌａｔｉｏｎｉｓｍａｄｅ．Ｔｈｅｄｉｒｅｃｔｓｏｌａｒｒａｄｉａｔｉｏｎｉｎｔｙｐｉｃａｌｓｉｔｅｓｏｆｔｈｅｄｉｓｔｒｉｃｔｉｓｍｅａｓｕｒｅｄａｎｄｃａｌｃｕｌａｔｅｄ,ａｎｄｔｈｅｖａｒｉａｔｉｏｎｃｕｒｖｅｓｏｆａｎｎｕａｌｆｌｕｘｏｆｄｉｒｅｃｔｓｏｌａｒｒａｄｉａｔｉｏｎｏｎｖａｒｉｏｕｓｓｌｏｐｅｄｉｒｅｃｔｉ     

水稻内生联合固氮细菌的筛选,鉴定及其分布特性

利用乙炔还原法和固定１５Ｎ２ 活性测定法对分离自水稻（ Ｏｒｙｚａ ｓａｔｉｖａ Ｌ．）“越富”种子、根、茎和叶的内生细菌进行了筛选,获得２９ 株具有体外固氮能力的水稻内生联合固氮细菌。鉴定结果表明它们分属于根癌土壤杆菌（ Ａｇｒｏｂａｃｔｅｒｉｕｍ ｔｕｍｅｆａｃｉｅｎｓ （Ｓｍｉｔｈ ｅｔ Ｔｏｗｎｓｅｎｄ） Ｃｏｎｎ） ,放射土壤杆菌（ Ａ． ｒａｄｉｏｂａｃｔｅｒ （Ｂｅｉｊｅｒｉｎｃｋ ｅｔ ｖａｎ Ｄｅｌｄｅｎ） Ｃｏｎｎ） ;阴沟肠杆菌（ Ｅｎｔｅｒｏｂａｃｔｅｒ ｃｌｏａｃａｅ （Ｊｏｒｄａｎ） Ｈｏｒｍａｅｃｈｅ ｅｔ Ｅｄｗａｒｄｓ） ,成团肠杆菌（ Ｅ． ａｇｇｌｏｍｅｒａｎｓ （Ｂｅｉｊｅｒｉｎｃｋ） Ｅｗｉｎｇ ｅｔ Ｆｉｆｅ） ,坂崎肠杆菌（ Ｅ． ｓａｋａｚａｋｉｉ Ｆａｍｅｒ ｅｔ ａｌ．） ;皮氏产碱菌（ Ａｌｃａｌｉｇｅｎｅｓ ｐｉｅｃｈａｕｄｉｉ Ｋｉｒｅｄｊｉａｎ ｅｔ ａｌ．） ,反硝化产碱菌（ Ａ． ｄｅｎｉｔｒｉｆｉｃａｎｓ （Ｌｅｉｆｓｏｎ ｅｔ Ｈｕｇｈ） Ｒｕｇｅｒ ｅｔ Ｔａｎ） ;类产碱假单胞菌（ Ｐｓｅｕｄｏｍｏｎａｓ ｐｓｅｕｄｏａｌｃａｌｉｇｅｎｅｓ Ｓｔａｎｉｅｒ） ,产碱假单胞菌（ Ｐ． ａｌｃａｌ     

三唑酮对绿豆幼苗叶片衰老的延缓作用

三唑酮处理可提高离体绿豆（ＰｈａｓｅｏｌｕｓｒａｄｉａｔｕｓＬ．）幼苗叶片叶绿素和蛋白质含量。叶片衰老过程中超氧物歧化酶（ＳＯＤ）、过氧化物酶（ＰＯＤ）、过氧化氢酶（ＣＡＴ）和抗坏血酸过氧化物酶（ＡｓＡＰＯＤ）活性及抗坏血酸（ＡｓＡ）和还原型谷胱甘肽（ＧＳＨ）含量降低。２０ｍｇ／Ｌ三唑酮可提高ＰＯＤ、ＡｓＡＰＯＤ活性和ＡｓＡ、ＧＳＨ含量,对ＳＯＤ、ＣＡＴ活性无影响。丙二醛（ＭＤＡ）含量在叶片衰老过程中提高,并与ＰＯＤ、ＡｓＡＰＯＤ活性和ＡｓＡ、ＧＳＨ含量呈显著负相关,三唑酮可降低ＭＤＡ含量。表明三唑酮有提高植物对膜脂过氧化作用的保护能力,延缓叶片的衰老作用。     

牙形刺分子的组织化学染色

牙形刺分子的组织化学染色ＡｎｎｅＫｅｍｐ（ＤｅｐａｒｔｍｅｎｔｏｆＡｎａｔｏｍｉｃａｌＳｃｉｅｎｃｅｓ,ＵｎｉｖｅｒｓｉｔｙｏｆＱｕｅｅｎｓｌａｎｄ,Ｓｔｏｌｕｃｉａ,Ｑｕｅｅｎｓｌａｎｄ４０７２,Ａｕｓｔｒａｌｉａ）一、技术条件未交代变化的牙形刺。...     

农业气象灾害地域组合规律的初步研究

农业气象灾害地域组合规律的初步研究石忆邵（西北农业大学经贸学院,陕西杨陵７１２１００）ＰｒｅｌｉｍｉｎａｒｙＳｔｕｄｙｏｎＡｒｅａＣｏｍｂｉｎａｔｉｏｎＬａｗｏｆＡｇｒｏ－ＭｅｔｅｏｒｏｌｏｇｉｃａｌＤｉｓａｓｔｅｒｓ￥,ＳｈｉＹｉｓｈａｏ（Ｎｏｒｔ...     

土壤—植物根际磷的生物有效性研究

土壤－植物根际磷的生物有效性研究李法云高子勤（辽宁大学生物系,沈阳１１００３６）（中国科学院沈阳应用生态研究所,１１００１５）ＳｔｕｄｙｏｆＰｈｏｓｐｈｏｒｕｓＢｉｏｌｏｇｉｃａｌＡｖａｉｌａｂｉｌｉｔｙｉｎｔｈｅＳｏｉｌ＿ｐｌａｎｔＲｈｉｚｏｓｐｈ...     

Salvianolic acid A protects human SH-SY5Y neuroblastoma cells against H₂O₂-induced injury by increasing stress tolerance ability

Salvianolic acid A (Sal A) is a polyphenol extracted from the root of the Salvia miltiorrhiza bunge. Hydrogen peroxide (H(2)O(2)) is a major reactive oxygen species (ROS), which has been implicated in stroke and other neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease. In this study, we investigated the neuroprotective effects of Sal A in human SH-SY5Y neuroblastoma cells against H(2)O(2)-induced injury. Our results showed that cells pretreated with Sal A exhibited enhanced neuronal survival and that this protection was associated with an increase in adenosine triphosphate (ATP) and the stabilization of mitochondrial membrane potential. In addition, Sal A markedly decreased the excessive activation AMP-activated protein kinase (AMPK) and the serine-threonine protein kinase, Akt, in SH-SY5Ycells induced by H(2)O(2). In conclusion, our results demonstrated that Sal A protects SH-SY5Y cells against H(2)O(2)-induced oxidative stress and these protective effects are related to stress tolerance and not energy depletion via inhibition of the AMPK and Akt signaling pathway.     

Protective activity of aromatic amines and imines against oxidative nerve cell death.

Oxidative stress is a widespread phenomenon in the pathology of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. Neuronal cell death due to oxidative stress may causally contribute to the pathogeneses of these diseases. Therefore, neuroprotective antioxidants are considered to be a promising approach to slow down disease progression. We have investigated different aromatic amine and imine compounds for neuroprotective antioxidant functions in cell culture, and found that these compounds possess excellent cytoprotective potential in diverse paradigms of oxidative neuronal cell death, including clonal cell lines, primary cerebellar neurons, and organotypic hippocampal slice cultures. Aromatic amines and imines are effective against oxidative glutamate toxicity, glutathione depletion, and hydrogen peroxide toxicity. Their mode of action as direct antioxidants was experimentally confirmed by electron spin resonance spectroscopy, cell-free brain lipid peroxidation assays, and intracellular peroxide measurements. With half-maximal effective concentrations of 20-75 nM in different neuroprotection experiments, the aromatic imines phenothiazine, phenoxazine, and iminostilbene proved to be about two orders of magnitude more effective than common phenolic antioxidants. This remarkable efficacy could be directly correlated to calculated properties of the compounds by means of a novel, quantitative structure-activity relationship model. We conclude that bridged bisarylimines with a single free NH-bond, such as iminostilbene, are superior neuroprotective antioxidants, and may be promising lead structures for rational drug development.     

Mitochondrial Enzymes and Endoplasmic Reticulum Calcium Stores as Targets of Oxidative Stress in Neurodegenerative Diseases

Considerable evidence indicates that oxidative stress accompanies age-related neurodegenerative diseases. Specific mechanisms by which oxidative stress leads to neurodegeneration are unknown. Two targets of oxidative stress that are known to change in neurodegenerative diseases are the mitochondrial enzyme alpha-ketoglutarate dehydrogenase complex (KGDHC) and endoplasmic reticulum calcium stores. KGDHC activities are diminished in all common neurodegenerative diseases and the changes are particularly well documented in Alzheimer's disease (AD). A second change that occurs in cells from AD patients is an exaggerated endoplasmic reticulum calcium store [i.e., bombesin-releasable calcium stores (BRCS)]. H(2)O(2), a general oxidant, changes both variables in the same direction as occurs in disease. Other oxidants selectively alter these variables. Various antioxidants were used to help define the critical oxidant species that modifies these responses. All of the antioxidants diminish the oxidant-induced carboxy-dichlorofluorescein (cDCF) detectable reactive oxygen species (ROS), but have diverse actions on these cellular processes. For example, alpha-keto-beta-methyl-n-valeric acid (KMV) diminishes the H(2)O(2) effects on BRCS, while trolox and DMSO exaggerate the response. Acute trolox treatment does not alter H(2)O(2)-induced changes in KGDHC, whereas chronic treatment with trolox increases KGDHC almost threefold. The results suggest that KGDHC and BRCS provide targets by which oxidative stress may induce neurodegeneration and a useful tool for selecting antioxidants for reversing age-related neurodegeneration.     

Mitochondrial matters of the brain: mitochondrial dysfunction and oxidative status in epilepsy

Epilepsy is a neurological disorder characterized by spontaneous, recurrent and paroxysmal cerebral discharge, clinically leading to persistent alterations in function and morphology of neurons. Oxidative stress is one of possible mechanisms in the pathogenesis of epilepsy. Oxidative stress resulting from mitochondrial dysfunction gradually disrupts the intracellular calcium homeostasis, which modulates neuronal excitability and synaptic transmission making neurons more vulnerable to additional stress, and leads to neuronal loss in epilepsy. In addition, the high oxidative status is associated with the severity and recurrence of epileptic seizure. Hence, treatment with antioxidants is critically important in epileptic patients through scavenging the excessive free radicals to protect the neuronal loss. In this review, we reviewed the recent findings that focus on the role for antioxidants in prevention of mitochondrial dysfunction and the correlation between oxidative status and disease prognosis in patients with epilepsy.     

Redox nanoparticles: synthesis,properties and perspectives of use for treatment of neurodegenerative diseases

Oxidative stress (OS) and nitrative stress (NS) accompany many diseases, including Alzheimer’s disease (AD) and Parkinson’s disease (PD). Antioxidants have been proposed to counteract OS/NS in these diseases. Nevertheless, the effects of antioxidants are limited and new, more efficient antioxidants are searched for. Redox-active nanoparticles (RNPs), containing antioxidants create a new therapeutical perspective. This review examines the recent literature describing synthesis and potential applications of cerium oxide RNPs, boron cluster-containing and silica containing RNPs, Gd₃N_@C₈₀ encapsulated RNPs, and concentrates on nitroxide-containing RNPs. Nitroxides are promising antioxidants, preventing inter alia glycation and nitration, but their application poses several problems. It can be expected that application of RNPs containing covalently bound nitroxides, showing low toxicity and able to penetrate the blood–brain barrier will be more efficient in the treatment of neurodegenerative disease, in particular AD and PD basing on their effects in cellular and animal models of neurodegenerative diseases.     

Oxidative stress and mitochondrial dysfunction in neurodegeneration; cardiolipin a critical target?

Oxidative stress and subsequent impairment of mitochondrial function is implicated in the neurodegenerative process and hence in diseases such as Parkinson's and Alzheimer's disease. Within the brain, neuronal and astroglial cells can display a differential susceptibility to oxidant exposure. Thus, astrocytes can up regulate glutathione availability and, in response to mitochondrial damage, glycolytic flux. Whilst neuronal cells do not appear to possess such mechanisms, neuronal glutathione status may be enhanced due to the trafficking of glutathione precursors from the astrocyte. However, when antioxidants reserves are not sufficient or the degree of oxidative stress is particularly great, mitochondrial damage occurs, particularly at the level of complex IV (cytochrome oxidase). Whilst the exact mechanism for the loss of activity of this enzyme complex is not know, it is possible that loss and/or oxidative modification of the phospholipid, cardiolipin is a critical factor. Consequently, in this short article, we also consider (a) cardiolipin metabolism and function, (b) the susceptibility of this molecule to undergo oxidative modification following exposure to oxidants such as peroxynitrite, (c) loss of mitochondrial cardiolipin in neurodegenerative disorders, (d) methods of detecting cardiolipin and (e) possible therapeutic strategies that may protect cardiolipin from oxidative degradation.     

Neuroprotective effect of carvedilol and melatonin on 3-nitropropionic acid-induced neurotoxicity in neuroblastoma

In neurodegenerative diseases, progressive oxidative stress is a major event that precedes neuronal death. Oxidative stress is characterized by an imbalance between oxidants and antioxidants. This imbalance induced oxidative molecular and cell damage, reducing cellular viability. 3-Nitropropionic acid (3NP) causes oxidative stress and other molecular and cellular changes similar to those observed in neurons of patients with Huntington’s disease. Since carvedilol and melatonin act as free-radical scavengers, this study examined the effect of carvedilol (10^?5 M) and melatonin (10^?5 M) on oxidative and cell damage induced by 3NP in N1E-115 neuroblastoma cells. Carvedilol and melatonin prevented the increases in lipid peroxidation and total LDH activity, as well as the depletion of reduced glutathione (GSH) and the reduction of antioxidative enzymes activities in N1E-115 cells incubated with 100 mM 3NP. All these carvedilol and melatonin effects were more intense when the drugs were added before rather than after inducing the damage by 3NP. These results also provided evidence supporting the hypothesis that carvedilol and melatonin can be useful for treating neurodegenerative diseases, such as Huntington’s disease.     

The preventive and therapeutic effects of molecular hydrogen in ocular diseases and injuries where oxidative stress is involved

Oxidative stress initiates, accompanies and contributes to the development of several human diseases and injuries, including ocular diseases. Reactive oxygen species (ROS) can generate oxidative stress via excessive ROS production and/or decreased physiologically occurring antioxidants. To replace these weakened antioxidants, substances with effective antioxidant properties are needed in order to suppress oxidative stress and enable healing. Molecular hydrogen (H₂) is very suitable for this purpose due to its unique properties. H₂ is the only antioxidant that crosses the blood–brain and blood-ocular barriers. It quickly penetrates through tissue due to its small molecular size and effectively removes ROS, mainly hydroxyl radicals and peroxynitrite. Apart from its antioxidant effects, H₂ also displays anti-inflammatory, antiapoptotic, cytoprotective and mitohormetic properties. A significant advantage of H₂ is its nontoxicity, even when applied at high concentrations. In this review, we present the results of studies utilising H₂ in the treatment of ocular diseases involving oxidative stress. These results, obtained in experimental animals as well as in human clinical studies, show that the suppression of oxidative stress by H₂ treatment leads to the prevention or improvement of ocular diseases. In severe degenerative diseases, H₂ slows disease progression.     

The specificity of neuroprotection by antioxidants

Background  

Reactive oxygen species (ROS) play an important role in aging and age-related diseases such as Parkinson's disease and Alzheimer's disease. Much of the ROS production under conditions of toxic stress is from mitochondria, and multiple antioxidants prevent ROS accumulation. The aim of this study is to examine the specificity of the interaction between the antioxidants and ROS production in stressed cells.     

Water-soluble fractions from defatted sesame seeds protect human neuroblast cells against peroxyl radicals and hydrogen peroxide-induced oxidative stress

Oxidative stress is involved in the development of aging-related diseases, such as neurodegenerative diseases. Dietary antioxidants that can protect neuronal cells from oxidative damage play an important role in preventing such diseases. Previously, we reported that water-soluble fractions purified from defatted sesame seed flour exhibit good antioxidant activity in vitro. In the present study, we investigated the protective effects of white and gold sesame seed water-soluble fractions (WS-wsf and GS-wsf, respectively) against 2,2′-azobis(2-amidinopropane) dihydrochloride (AAPH) and hydrogen peroxide (H₂O₂) induced oxidative stress in human neuroblast SH-SY5Y cells. Pretreatment with WS-wsf and GS-wsf did not protect cells against AAPH-induced cytotoxicity, while simultaneous co-treatment with AAPH significantly improved cell viability and inhibited membrane lipid peroxidation. These results suggest that WS-wsf and GS-wsf protect cells from AAPH-induced extracellular oxidative damage via direct scavenging of peroxyl radicals. When oxidative stress was induced by H₂O₂, pretreatment WS-wsf and GS-wsf significantly enhanced cell viability. These results suggest that in addition to radical scavenging, WS-wsf and GS-wsf enhance cellular resistance to intracellular oxidative stress by activation of the Nrf-2/ARE pathway as confirmed by the increased Nrf2 protein level in the nucleus and increased heme oxygenase 1 (HO-1) mRNA expression. The roles of ferulic and vanillic acids as bioactive antioxidants in these fractions were also confirmed. In conclusion, our results indicated that WS-wsf and GS-wsf, which showed antioxidant activity in vitro, are also efficient antioxidants in a cell system protecting SH-SY5Y cells against both extracellular and intracellular oxidative stress.