采后两种不同果肉类型油桃软化相关酶活性的变化

以软质油桃“秦光”和非软质油桃“阿姆肯”为原料,研究了果实软化过程中果实硬度和果实软化相关酶活性变化。在果实硬度迅速下降期淀粉酶和蔗糖酶活性较高,以后酶活性下降。纤维素酶多聚半乳糖醛酸酶在果实软化前期活性很低,只在要果实呼吸跃变期这两种酶活性才明显升高。果胶果酯酶活性极低而且变化不大。“秦光”油桃的这几种酶酶活化性“阿姆肯”高,因而果实软化较快。     

冷害对贮藏油桃膜脂脂肪酸及相关酶活性的影响

以秦光2号油桃为试材,研究了1℃和5℃贮藏温度下油桃果实的膜脂脂肪酸及相关酶活性的变化.结果表明:油桃果实的SOD、CAT和APX活性在冷害发生后迅速下降;冷害果实的相对膜透性和MDA含量显著高于对照;冷害促使油桃果实LOX活性的增强,使棕榈酸相对含量高于对照,油酸、亚麻酸相对含量低于对照,降低了膜脂脂肪酸的不饱和指数.     

外源一氧化氮供体硝普钠对干旱胁迫下小麦幼苗叶中ATP酶活性和膜脂过氧化的影响

研究外源一氧化氮（NO）供体硝普钠（sNP）对干旱胁迫下小麦幼苗叶片ATP酶活性和膜脂过氧化影响的结果表明,15％聚乙二醇．6000（PEG-6000）模拟的干旱胁迫下小麦幼苗叶中H^＋-ATP酶和Ca^2＋．ATP酶活性显著升高后迅速下降,硫代巴比妥酸反应产物（TBARs）和质量膜透性增加;0．1mm01．L^-1 SNP可提高干旱胁迫下小麦幼苗叶中超氧化物歧化酶（SOD）、过氧化物酶（POD）和过氧化氢酶（cAT）活性,降低超氧阴离子（O2^-）和过氧化氢（H2O2）水平,缓解膜脂过氧化,稳定生物膜的结构和功能,H^＋-ATP酶和Ca^2＋-ATP酶也可以保持更高的活性。     

桃果实采后微粒体膜Ca2+-ATPase活性与膜脂过氧化

以常温（25℃）和低温（4℃）贮藏的迎庆桃果实为试验材料,对其果实硬度、呼吸强度进行了测定,并对微粒体膜Ca^2＋-ATPase、超氧化物歧化酶（SOD）活性、氧自由基变化和膜的伤害程度进行了研究.结果表明,随桃果实衰老,常温贮藏的果实硬度迅速下降、微粒体膜上的Ca^2＋-ATPase活性、SOD活性和O2-产生速率均呈跃变式变化,先升高后降低;膜脂过氧化产物MDA的含量逐渐增加;与常温相比,低温可以抑制果实硬度的下降、呼吸速率、Ca^2＋-ATPase和SOD活性的下降及推迟峰值的出现,同时降低O2^-产生速率和MDA含量.以上结果表明,桃果实衰老与细胞质内Ca^2＋稳态的破坏和膜脂过氧化作用的加强有密切关系.     

冷激处理对油桃贮藏品质和抗氧化酶活性的影响

以‘秦光2号’油桃为材料。研究了冷激处理对果实冷藏中品质及相关酶活性的影响。结果表明,0℃冷空气．处理3．5h可明显延迟油桃的后熟衰老;同时有推迟乙烯释放高峰和呼吸高峰。提高膜脂过氧化保护酶SOD、CAT、POD的活性,保持果肉硬度。减轻冷害发生的作用。但对可溶性固形物和可滴定酸含量无明显影响。     

垃圾填埋场渗滤液尾水灌溉下百慕大草抗氧化系统的反应

通过盆栽试验,研究了渗滤液尾水灌溉下百慕大草的膜脂过氧化及酶促、非酶促抗氧化系统的反应.结果表明,低稀释比的渗滤液尾水(<25%)灌溉下,随着稀释比增大,百慕大草叶绿素a/b提高,丙二醛(MDA)、H₂O₂含量及膜透性降低,膜脂过氧化水平较轻;但中、高稀释比(>25%)下,随稀释比的增大则显示出一定的负效应,表现为叶绿素a/b降低,MDA、H₂O₂含量及膜透性提高,从而导致膜脂过氧化水平提高.非酶抗氧化剂抗坏血酸(AsA)、还原型谷胱甘肽(GSH)、类胡萝卜素(Car)含量的变化趋势相同,即低稀释比下含量升高,中高稀释比胁迫下明显降低.抗氧化酶中,超氧化物岐化酶(SOD)和过氧化物酶(POD)的活性变化同抗氧化剂变化趋势相似,但POD对胁迫的反应更敏感;而过氧化氢酶(CAT)活性变化趋势则先减弱后增强;MDA含量和抗氧化剂含量、抗氧化酶SOD、POD活性间的显著负相关,表明3种抗氧化剂和SOD、POD在防止百慕大草膜脂过氧化上可能起到更重要的作用.     

脱水速率对黄皮胚轴脱水敏感性及膜膜过氧化的影响

以黄皮种子离体胚轴为材料,研究了不同于燥速率对胚轴脱水反应和膜脂过氧化的影响。在脱水过程中,胚轴的萌发率,活力指数,电解质渗漏速率,超氧化物歧化酶（SOD）,过氧化物酶（POD）和过氧化氢酶（CAT）活性逐渐降低,膜脂过氧化产物MDA的含量不断增加,脱水速率愈快,胚轴的半致死含水量就愈低。快速干燥的胚轴能在较低的含水量存活是因为顾中间含量下发生的膜脂过氧化作用的时间,以及保持较高的SOD,POD和CAT活性,缓慢干燥的胚轴当与周围环境达到水分平衡后,生活力的丧失将与保持在水分平衡后的时间有关,。因此,脱水速率是一种影响顽拗性种子或者胚轴脱水敏感性的重要因子。     

三唑酮对黄瓜子叶抗氧化酶活力的影响

黄瓜子叶衰老过程中超氧物歧化酶（ＳＯＤ）、过氧化氢酶（ＣＡＴ）和抗坏血酸－过氧化物酶（ＡＳＡ－ＰＯＤ）活性降低,而过氧化物酶（ＰＯＤ）活性升高。２０ｍｇ／Ｌ三唑酮右明显提高ＳＯＤ,ＡＳＡ－ＰＯＤ,ＣＡＴ活性,抑制ＰＯＤ活性升高。膜脂过氧化产物丙二醛（ＭＤＡ）含量在叶片衰老过程中提高,三唑酮可降低ＭＤＡ含量。表明三唑酮减轻脂氧化程度,延缓了叶片的衰老。     

He-Ne激光对增强UV-B辐射下小麦幼苗膜脂过氧化的缓解作用

采用He-Ne激光(5 mW/mm2)辐照增强UV-B辐射(10.08 kJ/m2.d)的晋麦8号小麦幼苗,通过测定小麦幼苗叶片细胞质膜透性、丙二醛(MDA)的含量以及脂氧合酶(LOX)、过氧化氢酶(CAT)、抗坏血酸过氧化物酶(APX)和谷光苷肽过氧化物酶(GPX)的活性变化,研究He-Ne激光对增强UV-B辐射的小麦幼苗膜脂过氧化的影响。结果显示,He-Ne激光辐照可使经UV-B辐射后小麦幼苗叶片质膜相对透性、MDA含量、LOX活性降低,而使CAT、APX和GPX的活性均升高。分析表明UV-B辐射增强可导致膜脂过氧化加剧,而一定剂量的He-Ne激光能够通过促进酶促抗氧化系统酶的活性来缓解紫外线辐射下小麦幼苗的膜脂过氧化作用。     

采后荔枝果实中氧化和过氧化作用的变化

采后的荔枝（Litchi chinensts)果实的果皮和果汁中的抗坏血酸及果汁的谷胱甘肽含量逐渐下降,果皮的谷胱甘肽甘肽含量先增多（采后3天）接着减少,超氧化物歧化酶活性随采后时间加长而降低,膜脂过氧化产物丙二醛及过氧化物酶活性显著增高,采收7天后果皮中丙二醛含量增加2倍,过氧化物酶活性增高6－7倍,超氧物歧化酶活性只为原来的44％,内源清除活性氧能力的减弱与膜脂过氧化产物的积累表明,荔枝果实的衰老与活性氧的伤害有关,过氧化物酶活性增高可作为果实衰老的一个指标。     

Nitric oxide counteracts the senescence of rice leaves induced by abscisic acid

In the present study, we evaluate the protective effect of nitric oxide (NO) against senescence of rice leaves promoted by ABA. Senescence of rice leaves was determined by the decrease of protein content. ABA treatment resulted in (1) induction of leaf senescence, (2) increase in H2O2 and malondialdehyde (MDA) contents, (3) decrease in reduced form glutathione (GSH) and ascorbic acid (AsA) contents, and (4) increase in antioxidative enzyme activities (superoxide dismutase, ascorbate peroxidase, glutathione reductase, and catalase). All these ABA effects were reduced by free radical scavengers such as sodium benzoate and GSH. NO donors [N-tert-butyl-alpha-phenylnitrone (PBN), sodium nitroprusside, 3-morpholinosydonimine, and AsA + NaNO2] were effective in reducing ABA-induced leaf senescence. PBN prevented ABA-induced increase in the contents of H2O2 and MDA, decrease in the contents of GSH and AsA, and increase in the activities of antioxidative enzymes. The protective effect of PBN on ABA-promoted senescence, ABA-increased H2O2 content and lipid peroxidation, ABA-decreased GSH and AsA, and ABA-increased antioxidative enzyme activities was reversed by 2-(4-carboxy-2-phenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, a NO-specific scavenger, suggesting that the protective effect of PBN is attributable to NO released. Reduction of ABA-induced senescence by NO in rice leaves is most likely mediated through its ability to scavenge active oxygen species including H2O2.     

Evalution of toxicity of abcisic acid and gibberellic acid in rats: 50 days drinking water study

In the present study, the influence of subchronic effects of two plant growth regulators (PGRs) [Abcisic acid (ABA) and Gibberellic acid (GA3)] on antioxidant defense systems [reduced glutathione (GSH), glutathione reductase (GR), superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT)] and lipid peroxidation level (malondialdehyde = MDA) in various tissues of the rat were investigated during treatment as a drinking water model. 75 ppm of ABA and GA3 in drinking water were continuously administered orally to rats (Sprague-Dawley albino) ad libitum for 50 days. The PGRs treatments caused different effects on the antioxidant defense systems and MDA content of dosed rats compared to controls. The lipid peroxidation end product MDA significantly increased in the lungs, heart and kidney of rats treated with GA3 without significant change in the spleen. ABA caused also a significant increase in MDA content in the spleen, lungs, heart and kidney. The GSH levels were significantly depleted in the spleen, lungs and stomach of rats treated with ABA without any change in the tissues of rats treated with GA3 except the kidney where it increased. Antioxidant enzyme activities such as SOD significantly increased in the lungs and stomach and decreased in the spleen and heart tissues of rats treated with GA3. Meanwhile, SOD significantly decreased in the spleen, heart and kidney and increased in the lungs of rats treated with ABA. While CAT activity significantly decreased in the lungs of rats treated with GA3, a significant increase occurred in the heart of rats treated with both PGRs. On the other hand, the ancillary enzyme GR activity in the tissues were either significantly depleted or not changed with PGRs treatment. The drug metabolizing enzyme GST activity significantly decreased in the lungs of rats treated with ABA but increased in the stomach of rats treated with both PGRs. As a conclusion, the rats resisted oxidative stress via the antioxidant mechanism. But the antioxidant mechanism could not prevent the increases in lipid peroxidation in rat's tissues. This data, along with changes, suggests that PGRs produced substantial systemic organ toxicity in the spleen, lungs, stomach, heart and kidney during a 50-day period of subchronic exposure.     

锌硼营养对苦瓜产量品质与叶片多胺、激素及衰老的影响

采用田间试验、植株生理生化测定方法,研究了锌硼营养对苦瓜(株洲长白)产量品质与叶片多胺、激素及衰老的影响。结果表明,在锌硼缺乏的土壤中施用硫酸锌和硼砂均可提高苦瓜产量,并可提高苦瓜蛋白质、Vc和17种氨基酸含量,尤其是人体必需氨基酸含量,降低NO3^-含量,改善苦瓜品质。这与锌硼提高了叶片多胺(PAs)、腐胺(Put)、亚精胺(Spd)、精胺(Spm)、抗坏血酸(ASA)、吲哚乙酸(IAA)、赤霉素(GA3)含量以及超氧化物歧化酶(SOD)、过氧化物酶(POD)、过氧化氢酶(CAT)酶的活性,减少脱落酸(ABA)、丙二醛(MDA)含量,从而抑制膜脂过氧化有关试验结果同时表明苦瓜产量与叶片PAs、Put、Spd、Spm、GA3、SOD、POD、CAT呈极显著正相关,与叶片MDA与ABA含量呈极显著负相关。叶片MDA含量与ABA呈极显著正相关,而与PAs、Put、Spd、Spm、ASA、IAA、CA3、SOD、POD、CAT呈极显著负相关。     

渗透胁迫下稻苗中铁催化的膜脂过氧化作用

在－０．７ＭＰａ渗透胁迫下,水稻幼苗体内和Ｈ２Ｏ２大量产生,Ｆｅ２＋积累,膜脂过氧化作用加剧。水稻幼苗体内Ｆｅ２＋含量与膜脂过氧化产物ＭＤＡ含量呈极显著的正相关。外源Ｆｅ２＋、Ｆｅ３＋、Ｈ２Ｏ２、Ｆｅ２＋＋Ｈ２Ｏ２、ＤＤＴＣ均能刺激膜脂过氧化作用,而铁离子的螯合剂ＤＴＰＡ则有缓解作用。ＯＨ的清除剂苯甲酸钠和甘露醇能明显地抑制渗透胁迫下Ｆｅ２＋催化的膜脂过氧化作用。这都表明渗透胁迫下水稻幼苗体内铁诱导的膜脂过氧化作用主要是由于其催化Ｆｅｎｔｏｎ型Ｈａｂｅｒ－Ｗｅｉｓｓ反应形成ＯＨ所致。     

Thermal recovery after passage of the pulmonary circulation assessed by deconvolution

We determined the effect of H2O2 on both the physiological and biochemical lung changes seen in the adult sheep after endotoxin. Fourteen unanesthetized adult sheep with chronic lung lymph fistula were given Escherichia coli endotoxin (1 microgram/kg) over 30 min. Seven sheep were given catalase (32,500 U/kg body wt) as an intravenous bolus 30 min before endotoxin. Four sheep were given catalase alone. Oxidant lung changes were measured using arterial plasma conjugated dienes and lung tissue malondialdehyde (MDA) content, both reflecting the lipid peroxidation process. Animals were killed 5 h after endotoxin. We found that endotoxin alone caused an early increase in pulmonary arterial pressure lung lymph flow (QL), plasma thromboxane B2, 6-keto-prostaglandin F1 alpha, and plasma conjugated dienes. A decrease in cardiac output and arterial PO2 was also seen. A three- to four-fold increase in protein-rich QL was noted at 3-4 h as well as a continued increase in arterial conjugated dienes. Lung MDA and water content were also significantly increased from base line. Catalase pretreatment significantly attenuated both the physiological changes and the prostanoid and conjugated diene release. Lung MDA and water content also remained at base line. We conclude that H2O2 plays a major role in endotoxin-induced lung injury as well as the resulting lipid peroxidation process.     

Mechanisms of the killing of cultured hepatocytes by hydrogen peroxide

Mechanisms of H2O2-induced cell injury were explored in primary cultures of rat hepatocytes. Cells prepared from male rats and cultured for 1 day prior to treatment were killed by H2O2 either added directly to the medium at 0.25-2 mM or generated in situ by glucose oxidase (0.25-2 U/ml) or xanthine oxidase (20-120 mM/ml) and 2 mM xanthine. Catalase protected the cells in each case. Lipid peroxidation as measured by the accumulation of malondialdehyde (MDA) preceded the cell death due to H2O2 added directly to the cultures or generated in the medium. The antioxidants N,N'-diphenyl-p-phenylenediamine (DPPD) and promethazine prevented the accumulation of MDA in both cases and protected the cells treated with H2O2 directly. DPPD and promethazine did not react directly with H2O2. Other antioxidants including butylated hydroxytoluene, vitamin E, and N-propylgallate had varied protective activity against the addition of H2O2 in proportion to their ability to reduce MDA accumulation. In glucose oxidase-treated cultures, DPPD and promethazine prevented the cell killing during the first hour but failed to protect between 1 and 3 h despite prevention of lipid peroxidation. The cell killing between 1 and 3 h in the presence of DPPD was prevented by catalase indicating its dependence upon continued generation of H2O2. Further addition of H2O2 in the presence of DPPD also increased the number of dead cells without lipid peroxidation. The data are consistent with at least two mechanisms of hepatocyte killing by H2O2. The first pathway is prevented by the antioxidants DPPD and promethazine and is very likely related to the peroxidation of membrane phospholipids. The second is independent of lipid peroxidation yet dependent upon the continued presence of H2O2.     

Active Oxygen Damage Effect of Chlorophyll Degradation in Rice Seedlings Under Osmotic Stress

The changes of chlorophyll (Chl) content and contents of protochlorophyllide (Pchl), superoxide radical (O2-) and hydrogen peroxide (H2O2), malondialdehyde (MDA), ascorbic acid (ASA), glutathione (GSH), carotenoid (CAR) and the binding capacity of chlorophyll-protein (Chl-Pro) in rice (Oryza sativa L. ) seedlings exposed to osmotic stress induced by PEG 6000 (–0. 5 MPa, –0.8 MPa) were investigated to explore the relationship between Chl degradation and active oxygen effect. Under osmotic stress, Chl degradation was accompanied by the increase of contents of O2-, H2O2 and MDA and the decrease of contents of antioxidants AsA, GSH and CAR. The binding of Chl-Pro was loosened with the change of time and intensity of osmotic stress. Pretreatment with scavengers for active oxygen, such as AsA, α-tocopherol and mannitol retarded lipid peroxidation and reduced the oxidative injury of Chl, but Fe2+, H2O2 and Fenton reaction promoted the formation of MDA. The Fenton reaction accelerated the degradation of Chl. The results indicate that Chl degradation in rice seedlings induced by osmotic stress may be mainly due to the formation of more active hydroxyl radicals ('OH) through Fenton reaction and Haber-Weiss reaction.     

A comparative study on the effect of homobrassinolide and gibberellic acid on lipid peroxidation and antioxidant status in normal and diabetic rats

Dietary content of phytohormones may potentially influence metabolic processes in animal cells. This study therefore aimed to investigate the effect of two plant growth regulators homobrassinolide (HB) and gibberellic acid (GBA) on the antioxidant defense status and lipid peroxidation level in the tissues of normal and streptozotocin- induced diabetic rats. Normal and diabetic rats (Albino –wistar strain) were administered 50μg HB and GBA intradermally each day for seven days and their tissue and blood levels of malondialdehyde (MDA), 4-hydroxy-2-nonenol (4-HNE), reduced glutathione (GSH) content and catalase (CAT) activity were determined. Subchronic treatment of rats with HB reduced lipid perioxidation and elevated antioxidant defense whereas GBA caused enhancement of lipid peroxidation and reduction of antioxidant defense in treated animals compared to the control rats.     

水杨酸调节决明根系铝诱导的氧化胁迫

水杨酸(Salicylicacid,SA)在调节生物和非生物胁迫,诱导植物氧化胁迫中起着重要的作用,但对铝诱导的氧化胁迫的调节作用尚不清楚。本文研究了SA对决明(CassiatoraL.)根系铝诱导的H2O2和O2-含量变化,包括抗氧化酶活性以及细胞质膜过氧化胁迫变化的影响。介质中20mmol/L铝处理增加质膜透性,导致MDA含量上升及根尖细胞Evansblue染色加重(测定细胞死亡),而外源供给5mmol/LSA能缓解铝诱导的氧化胁迫。SA处理能明显降低根尖H2O2和O2-的含量,但两者含量与CAT、APX和GR的活性变化没有相关性,而与POD活性增加有关。水杨酸诱导H2O2含量的下降与抑制O2-积累和SOD活性有关。结果表明,SA可能激活一条由H2O2介导的、依赖于POD的抗氧化机制来缓解脂质的过氧化作用。     

Biochemical mechanisms accounting for the toxic action of oxygen on living organisms: the key role of superoxide dismutase.

It seems that superoxide dismutase plays the key role in protecting aerobes against O2 toxicity, but there is a whole range of ancillary mechanisms: enzymes to remove H2O2 (catalase, peroxidases) and hence to control formation of .OH from O2, which requires H2O2; antioxidants (ascorbate, GSH, alpha-tocopherol, carotenoids), which also react with singlet oxygen and/or .OH and often inhibit lipid peroxidation and last, but not least in animals, glutathione peroxidase, which controls the rate of lipid peroxidation. These mechanisms cope well at normal O2 concentrations but are insufficient at higher levels.