一氧化氮对增强的UV_B胁迫下螺旋藻生物损伤的减缓作用

为了探讨一氧化氮对增强的UV_B胁迫下螺旋藻生物学特性的影响,通过色素含量、蛋白质含量和生物量3个方面的变化证实了05mmol/L的一氧化氮(Nitric oxide, NO)供体硝普钠(Sodium nitroprusside, SNP)对增强UV_B胁迫下的螺旋藻(Spirulina platensis)794细胞生物损伤有明显的减缓作用。实验结果显示,NO能够显著诱导增强的UV_B胁迫下螺旋藻细胞内蛋白质含量、脯氨酸含量的提高,促进正常生长条件下螺旋藻(Spirulina platensis)794细胞内抗氧化物质GSH含量的增多,但外源NO又可以降低增强UV_B胁迫下螺旋藻细胞中GSH含量的增加。说明NO对增强UV_B胁迫下的螺旋藻794细胞有保护作用,可以减轻UV_B胁迫对螺旋藻(S. platensis)细胞引起的生物损伤。首次研究报道了增强UV_B胁迫下NO信号分子对蓝细菌——螺旋藻细胞生物损伤调节能力的影响,为进一步探讨NO信号及其与其它信号分子之间相互作用、相互关联来调节细胞的生理生化过程,以减缓UV_B胁迫下的生物损伤机理奠定了基础。     

螺旋藻对增强的UV-B胁迫的响应

本文研究了实验室条件下增强的uv-B（280-320nm）胁迫对一种蓝藻一钝顶螺旋藻（Spirulina platensis）794生物量、色素和蛋白、细胞内MDA含量及活性氧产生的影响。结果表明,在增强的uV-B胁迫下,螺旋藻的生物量减少,细胞内叶绿素a和类胡萝卜素含量降低,从而使螺旋藻的生长发育受到一定程度的抑制,而细胞浆蛋白质含量增加,这可能是螺旋藻对逆境胁迫的一种适应性反应。增强UV-B胁迫下,螺旋藻细胞内MDA含量增加,与之相对应,活性氧的产生速率也增加,进一步证实了逆境胁迫下,植物细胞内叶绿素含量的下降、MDA的积累主要与UV-B胁迫下活性氧的产生及其对细胞的氧化损伤有关。     

外源过氧化氢对 UV-B 胁迫下蓝藻生理的影响

以青海湖粘球藻 (Gloeocapsa sp.)为研究材料, 通过生物化学和对比分析的方法 , 研究了外源添加过氧化氢(H2O2)(0.5 mmol·L −1 )对长期增强 UV-B(2.4 W·m-2)胁迫下其生理的影响。研究结果显示, 与增强 UV-B 胁迫下的藻细胞相比 , 加入 0.5 mmol·L − 1 H2O2 减缓了藻体生物量的减少 , 提高了其蛋白质含量, 表明 H2O2 对增强 UV-B 胁迫给藻体带来的损伤有一定的缓解作用。进一步研究发现, 加入 0.5 mmol·L − 1 H2O2 明显(P<0.05)提高了增强UV-B 胁迫下藻体细胞内脯氨酸和类黄酮含量及 CAT 与 SOD 的活性, 并降低了藻体细胞内 MDA 含量, 表明 H2O2 可以通过增加细胞抗氧化物质及抗逆物质的含量来缓解 UV-B 胁迫对藻体造成的损伤。说明 H2O2 不仅对高等真核生物在抵御逆境胁迫中可以起到信号分子的作用 , 在原核生物中也具有此功能。为将来的逆境胁迫抵御机制的研究途径提供参考。     

Te(Ⅳ)胁迫对两种螺旋藻生长及抗氧化酶系统的影响

在钝顶螺旋藻(Spirulina platensis)和极大螺旋藻(Spirulina maximum)接种的第5天至第10天添加不同浓度的亚碲酸钠,研究Te(Ⅳ)胁迫对两种螺旋藻的生长、抗氧化活性系统和脂质过氧化作用的影响。结果表明,通过调节添加碲的时间,可以有效地调节碲胁迫强度,随着加碲时间依次后移,碲胁迫强度逐渐减小,螺旋藻的最终生物量递增。碲对螺旋藻的生物效应与碲胁迫强度有关,也与添加碲时藻所处的生长期有关。实验组Ⅲ(分别在第7、8、第9天三天添加碲)的碲胁迫强度并不是最低的,两种螺旋藻的最终生物量也不是最大,但MDA的含量却是最低的,表明该实验组的生长状态是最佳的。各种抗氧化酶(SOD、GPX、CAT、APX和POD)的活性变化情况较复杂。其中,在碲胁迫下,GPX的活性显著提高。       

大螺旋藻的形态观察和培养试验

蓝藻—螺旋藻(Spirulina)作为大规模工业化培养的对象,以其高的蛋白质含量和合理的氨基酸组成,极大地吸引了国内外生物学工作者的注意,他们对原产于非洲的钝顶螺旋藻(S.platensis)或墨西哥的极大螺旋藻(S.maxima)进行了广泛的研究3-6。笔者在我国广州珠江河畔一个小池塘里发现采集了一种螺旋藻——大螺旋藻(Spirulina major)1,2,进行了分离和单种培养。       

外源NO对NaCl胁迫下黄瓜（Cucumis sativus L.）幼苗生长和谷胱甘肽抗氧化酶系统的影响

采用营养液水培,研究了外源一氧化氮(NO)对黄瓜(Cucumis sativus L.)幼苗生长和叶片谷胱甘肽抗氧化酶系统的影响.结果表明,正常生长条件下添加NO能促进黄瓜幼苗生长,而添加NO信号传递途径关键酶鸟苷酸环化酶(cGC)抑制剂亚甲基蓝(MB-1)显著抑制了黄瓜幼苗的生长;添加NO显著缓解了盐胁迫对黄瓜幼苗生长的抑制,提高了叶片谷胱甘肽还原酶(GR)活性、脱氢抗坏血酸还原酶(DHAR)活性、抗坏血酸过氧化物酶(APX)及还原型谷胱甘肽(GSH)、抗坏血酸(ASA)含量,降低了氧化型谷胱甘肽(GSSG)含量,提高了GSH/GSSG,对单脱氢抗坏血酸还原酶(MDAR)活性无显著影响;NaCl胁迫下添加NO的同时添加MB-1抑制了GR活性的提高,GSH和ASA含量、GSH/GSSG均降低,GSSG含量提高,但对MDAR、APX和DHAR活性无显著影响,表明NaCl胁迫下NO对GR活性、GSH和ASA含量、GSH/GSSG的调节可能是通过cGC介导的,对MDAR无明显的调节作用,对DHAR、APX的调节还存在其它途径.     

一氧化氮对植物重金属胁迫抗性的影响研究进展

一氧化氮(NO)作为一种重要的信号分子,在调节植物重金属胁迫抗性方面上起着非常重要的作用。综述了NO在植物体内的产生途径,重金属胁迫下植物体内内源NO含量的变化以及外源NO与内源NO对植物重金属胁迫抗性的影响。大量研究表明外源NO能够增强植物对重金属胁迫的抗性,一方面是通过增强植物细胞的抗氧化系统或直接清除活性氧,另一方面是通过影响植物对重金属的吸收以及重金属在植物细胞内的分布。然而内源NO在调节植物重金属胁迫抗性上的功能角色仍存在争议。有些研究表明内源NO是有益的,能够缓解重金属胁迫诱导的毒性;但是也有证据表明内源NO是有害的,能够通过促进植物对重金属的吸收以及对植物螯合素进行S-亚硝基化弱化其解毒功能,从而参与重金属诱导的毒害反应和细胞凋亡过程。     

NO在植物中的调控作用

一氧化氮(NO)是一种易扩散的生物活性分子,是生物体内重要的信号分子.植物细胞通过NO合酶、硝酸还原酶、或非生化反应途径产生NO.NO参与植物生长发育调控和对生物与非生物环境胁迫的应答反应,大量证据表明NO是植物防御反应中的关键信使,其信号转导机制也受到越来越多的关注.本文主要通过讨论NO的产生、对植物生长周期的影响、在植物代谢中的信号调节以及参与细胞凋亡来阐述NO在植物中的作用.     

外源NO介导Cu胁迫下番茄GSH-PCs合成途径

一氧化氮(NO)作为生物活性分子,广泛参与各种生物和非生物胁迫.采用营养液培养,研究了Cu胁迫下外源NO介导的番茄还原型谷胱甘肽 植物螯合肽(GSH PCs)合成途径中相关酶活性及代谢产物的变化.结果表明: 与对照(CK)相比,Cu胁迫可以显著激活番茄体内γ-谷氨酰半胱氨酸合成酶(γ-ECS)、谷胱甘肽合成酶(GS)活性,根系GSH、PCs含量急剧升高,且随着处理时间的延长,γ-ECS、GS活性和GSH、PCs含量呈持续上升趋势;添加外源硝普钠(SNP, NO供体)可以进一步提高Cu胁迫下番茄根系γ-ECS、GS活性,促进GSH、PCs的合成,增强清除过氧化物的能力,并螯合过多的Cu²⁺,降低其生物毒性.叶片中的GSH-PCs代谢变化在一定程度上滞后于根系.外源丁硫氨酸-亚砜亚胺(BSO,GSH合成抑制剂)显著抑制根系γ-ECS活性,添加SNP可以显著逆转根系中BSO对GSH和PCs合成的抑制,对叶片中PCs合成的影响较小.Cu胁迫下,外源NO可能启动了某些信号机制,并通过激活或增强GSH-PCs合成途径中的酶促和非酶促系统,降低过多的Cu²⁺的生物毒性和氧化伤害.     

NO在植物生长发育和环境胁迫响应中的作用

一氧化氮(NO)是具有生物活性和信号转导作用的气体活性分子,它不仅对植物的许多生命活动如种子萌发、生长和衰老等具有直接的生理调节功能,而且作为防御反应中的关键信使,参与了植物对外界环境胁迫的响应,如干旱胁迫、热胁迫、盐胁迫、UV-B辐射、臭氧胁迫、重金属胁迫、机械损伤以及植物抗病反应。NO与各种激素如乙烯、脱落酸、水杨酸、生长素和细胞分裂素等,在调节植物的生理活动与信号转导方面有明显的协同作用,通过激素起作用可能是植物内源NO作用的机理之一。探明在正常生长状况下植物内源NO对植物生长发育的调控机制及其参与信号转导的生理机制是目前研究的重点。     

Nitric Oxide Alleviates Oxidative Damage Induced by Enhanced Ultraviolet-B Radiation in Cyanobacterium

To study the role of nitric oxide (NO) on enhanced ultraviolet-B (UV-B) radiation (280–320 nm)-induced damage of Cyanobacterium, the growth, pigment content, and antioxidative activity of Spirulina platensis-794 cells were investigated under enhanced UV-B radiation and under different chemical treatments with or without UV-B radiation for 6 h. The changes in chlorophyll-a, malondialdehyde content, and biomass confirmed that 0.5 mM sodium nitroprusside (SNP), a donor of nitric oxide (NO), could markedly alleviate the damage caused by enhanced UV-B. Specifically, the biomass and the chlorophyll-a content in S. platensis-794 cells decreased 40% and 42%, respectively under enhanced UV-B stress alone, but they only decreased 10% and 18% in the cells treated with UV-B irradiation and 0.5 mM SNP. Further experiments suggested that NO treatment significantly increased the activities of superoxide dismutase (SOD) and catalase (CAT), and decreased the accumulation of O ₂ ⁻ in enhanced UV-B-irradiated cells. SOD and CAT activity increased 0.95- and 6.73-fold, respectively. The accumulation of reduced glutathione (GSH) increased during treatment with 0.5 mM SNP in normal S. platensis cells, but SNP treatment could inhibit the increase of GSH in enhanced UV-B-stressed S. platensis cells. Thus, these results suggest that NO can strongly alleviate oxidative damage caused by UV-B stress by increasing the activities of SOD, peroxidase, CAT, and the accumulation of GSH, and by eliminating O ₂ ⁻ in S. platensis-794 cells. In addition, the difference of NO origin between plants and cyanobacteria are discussed.     

Counteractive action of nitric oxide on the decrease of nitrogenase activity induced by enhanced ultraviolet-B radiation in cyanobacterium

The experimental enhancement of UV-B radiation resulted in damage to chlorophyll-a in Spirulina platensis 794, and the degree of this damage was modified by chemical treatments. The addition of 0.5 mM sodium nitroprusside (SNP), a donor of nitric oxide (NO), to cultures of Spirulina platensis 794 could markedly alleviate the damage to chlorophyll-a caused by enhanced ultraviolet-B radiation. Exposure of N₂-fixing cyanobacterium Spirulina platensis 794 to enhanced ultraviolet-B radiation resulted in an intensity-dependent inhibition of nitrogenase activity. In cultured cells that were treated with 0.5 mM SNP and enhanced UV-B for 6 h, nitrogenase activity increased by 47.3% compared with UV-B treated control cells. SNP apparently counteracted the decrease in nitrogenase activity caused by UV-B stress. NAC (a free radical scavenger) significantly increased nitrogenase activity, but PTIO (a nitric oxide scavenger) decreased nitrogenase activity in UV-B treated S. platensis 794. Thus, the free radical scavenger NAC and NO may counteract the effects of enhanced UV-B radiation. The activity of UV-B-inhibited nitrogenase did not recover upon transfer of exposed cells to fluorescent light, suggesting that the inhibition may be due to specific inactivation of the enzyme. By experimentally manipulating the inhibitors of photosystem-II activity, it was demonstrated that nitrogenase activity in cyanobacterium S. platensis 794 is limited by the amount of reductant and ATP. This result further confirmed that nitrogenase activity requires a continued and abundant supply of suitable reductant and ATP for conversion of N₂ to NH₃. The effects of UV-B treatment on nitratase activity were also examined, and enhanced UV-B radiation increased nitratase activity. In addition, enhanced UV-B in combination with SNP and NAC resulted in significant increases in the activity of nitratase.     

The impact of nitrite and antioxidants on ultraviolet-A-induced cell death of human skin fibroblasts

Nitrite (NO(2)(-)) occurs ubiquitously in biological fluids such as blood and sweat. Ultraviolet A-induced nitric oxide formation via decomposition of cutaneous nitrite, accompanied by the production of reactive oxygen (ROS) or nitrogen species (RNS), represents an important source for NO in human skin physiology. Examining the impact of nitrite and the antioxidants glutathione (GSH), Trolox (TRL), and ascorbic acid (ASC) on UVA-induced toxicity of human skin fibroblasts (FB) we found that NO(2)(-) concentration-dependently enhances the susceptibility of FB to the toxic effects of UVA by a mechanism comprising enhanced induction of lipid peroxidation. While ASC completely protects FB cultures from UVA/NO(2)(-)-induced cell damage, GSH or TRL excessively enhances UVA/NO(2)(-)-induced cell death by a mechanism comprising nitrite concentration-dependent TRL radical formation or GSH-derived oxidative stress. Simultaneously, in the presence of GSH or TRL the mode of UVA/NO(2)(-)-induced cell death changes from apoptosis to necrosis. In summary, during photodecomposition of nitrite, ROS or RNS formation may act as strong toxic insults. Although inhibition of oxidative stress by NO and other antioxidants represents a successful strategy for protection from UVA/NO(2)(-)-induced injuries, GSH and TRL may nitrite-dependently aggravate the injurious impact by TRL or GSH radical formation, respectively.     

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。     

Protective effect of nitric oxide against oxidative stress under ultraviolet-B radiation.

The response of bean leaves to UV-B radiation was extensively investigated. UV-B radiation caused increase of ion leakage, loss of chlorophyll, and decrease of the maximum efficiency of PSII photochemistry (Fv/Fm) and the quantum yield of PSII electron transport (PhiPSII) of bean leaves. H2O2 contents and the extent of thylakoid membrane protein oxidation increased, indicated by the decrease of thiol contents and the increase of carbonyl contents with the duration of UV-B radiation. Addition of sodium nitroprusside, a nitric oxide (NO) donor, can partially alleviate UV-B induced decrease of chlorophyll contents, Fv/Fm and PhiPSII. Moreover, the oxidative damage to the thylakoid membrane was alleviated by NO. The potassium salt of 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, a specific NO scavenger, arrested NO mediated protective effects against UV-B induced oxidative damage. Incubation of thylakoid membrane with increasing H2O2 concentrations showed a progressive enhancement in carbonyl contents. H2O2 contents were decreased in the presence of NO under UV-B radiation through increased activities of superoxide dismutases, ascorbate peroxidases, and catalases. Taken together, the results suggest that NO can effectively protect plants from UV-B damage mostly probably mediated by enhanced activities of antioxidant enzymes.     

Nitric oxide alleviates oxidative damage in the green alga<Emphasis Type="Italic">Chlorella pyrenoidosa</Emphasis> caused by UV-B radiation

The effect of ultraviolet-B radiation (UV-B; 280-320 nm) on induction of nitric oxide was estimated in the suspensions of green alga Chlorella pyrenoidosa with or without the NO scavenger N-acetyl-L-cysteine, and reductants such as 1,4-dithiothreitol, glutathione (reduced form), and ascorbic acid. Exogenously added sodium nitroprusside (NO donor), glutathione, 1,4-dithiothreitol, and ascorbic acid were able to prevent chlorophyll loss mediated by UV-B. Addition of NO to algal suspensions irradiated by UV-B increased the activity of catalase and superoxide dismutase but lowered the activity of phenylalanine ammonia-lyase. UV-B thus appears to be a strong inducer of NO production, exogenously added NO and reductants protecting the green alga against UV-B-induced oxidative damage.     

Interaction of regular exercise and chronic nitroglycerin treatment on blood pressure and rat aortic antioxidants

Many cardiac patients undergo exercise conditioning with or without medication. Therefore, we investigated the interaction of exercise training and chronic nitroglycerin treatment on blood pressure (BP), aortic nitric oxide (NO), oxidants and antioxidants in rats. Fisher 344 rats were divided into four groups and treated as follows: (1) sedentary control, (2) exercise training (ET) for 8 weeks, (3) nitroglycerin (15 mg/kg, s.c. for 8 weeks) and (4) ET+nitroglycerin. BP was monitored with tail-cuff method. The animals were sacrificed 24 h after the last treatments and thoracic aorta was isolated and analyzed. Exercise training on treadmill for 8 weeks significantly increased respiratory exchange ratio (RER), aortic NO levels, and endothelial nitric oxide synthase (eNOS) protein expression. Training significantly enhanced aortic glutathione (GSH), reduced to oxidized glutathione (GSH/GSSG) ratio, copper/zinc-superoxide dismutase (CuZn-SOD), Mn-SOD, catalase (CAT), glutathione peroxidase (GSH-Px) glutathione disulfide reductase (GR) activities and protein expressions. Training significantly depleted aortic malondialdehyde (MDA) and protein carbonyls without change in BP. Nitroglycerin administration for 8 weeks significantly increased aortic NO levels and eNOS protein expression. Nitroglycerin significantly enhanced aortic Mn-SOD, CAT, GR and glutathione-S-transferase (GST) activities and protein expressions with decreased MDA levels, protein carbonyls and BP. Interaction of training and nitroglycerin treatment significantly increased aortic NO levels, eNOS protein expression, GSH/GSSG ratio, antioxidant enzymes and normalized BP. The data suggest that the interaction of training and nitroglycerin maintained BP by up-regulating the aortic NO and antioxidants and reducing the oxidative stress in rats.     

Glyceryl trinitrate,a nitric oxide donor,abrogates ferric nitrilotriacetate-induced oxidative stress and renal damage

Ferric nitrilotriacetate (Fe-NTA), a common water pollutant and a known renal carcinogen, acts through the generation of oxidative stress and hyperproliferative response. In the present study, we show that the nitric oxide (NO) generated by the administration of glyceryl trinitrate (GTN) affords protection against Fe-NTA-induced oxidative stress and proliferative response. Administration of Fe-NTA resulted in a significant (P<0.001) depletion of renal glutathione (GSH) content with concomitant increase in lipid peroxidation and elevated tissue damage marker release in serum. Parallel to these changes, Fe-NTA also caused down-regulation of GSH metabolizing enzymes including glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione-S-transferase and several fold induction in ornithine decarboxylase (ODC) activity and rate of DNA synthesis. Subsequent exogenous administration of GTN at doses of 3 and 6mg/kg body weight resulted in significant (P<0.001) recovery of GSH metabolizing enzymes and amelioration of tissue GSH content, in a dose-dependent manner. GTN administration also inhibited malondialdehyde (MDA) formation, induction of ODC activity, enhanced rate of DNA synthesis, and pathological deterioration in a dose-dependent fashion. Further, administration of NO inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), exacerbated Fe-NTA-induced oxidative tissue injury, hyperproliferative response, and pathological damage. Overall, the study suggests that NO administration subsequent to Fe-NTA affords protection against ROS-mediated damage induced by Fe-NTA.     

Selenium-induced changes in activities of antioxidant enzymes and content of photosynthetic pigments in Spirulina platensis

Spirulina platensis exposed to various selenium （Se） concentrations （0, 10, 20, 40, 80, 150, 175, 200, 250 mg/L） accumulated high amounts of Se in a dose- and time-dependent manner. Under low Se concentrations （〈150 mg/L）, Se induced increases in biomass concentration, content of photosynthetic pigments, and activities of glutathione peroxidase （GPX）, superoxide dismutase （SOD）, catalase （CAT） and Gua-dep peroxidases （POD）, which indicates that antioxidant enzymes play an important role in protecting cells from Se stress. Higher Se concentrations （≥175 mg/L） led to higher Se accumulation and increases in activities of GPX, SOD, CAT and POD, but also induced lipid peroxidation （LPO） coupled with potassium leakage and decreases in biomass concentration and contents of photosynthetic pigment. The results indicate that increases in activities of the antioxidant enzymes were not sufficient to protect cell membranes against Se stress. Time-dependent variations in the activities of antioxidant enzymes, contents of chlorophyll a and carotenoid and the LPO level were also investigated under representative Se concentrations of 40 and 200mg/L. Opposite variation trends between SOD-CAT activities, and GPX-POD-APX activities were observed during the growth cycles. The results showed that the prevention of damage to cell membranes of S. platensis cells could be achieved by cooperative effects of SOD-CAT and GPX-POD-APX enzymes. This study concludes that S. platensis possessed tolerance to Se and could protect itself from phytotoxicity induced by Se by altering various metabolic processes.     

乙烯与NO互作对镉胁迫下荷花的抗坏血酸-谷胱甘肽循环的影响

以荷花‘微山湖红莲’实生苗为试验材料,研究镉(Cd,50 μmol·L^-1)胁迫下,外源乙烯前体1-氨基环丙烷羧酸(ACC,100 μmol·L^-1)、ACC与一氧化氮合酶(NOS)抑制剂N-硝基-L-精氨酸(L-NNA,200 μmol·L^-1)、ACC与硝酸还原酶(NR)抑制剂钨酸钠(Tu,1 mmol·L^-1),ACC与一氧化氮(NO)清除剂2-苯基-4,4,5,5-四甲基咪唑啉-3-氧代-1-氧(PTIO,200 μmol·L^-1),外源NO供体硝普钠(SNP,500 μmol·L^-1)、SNP与乙烯信号转导抑制剂硫代硫酸银(STS,100 μmol·L^-1)处理下荷花幼苗叶片的受害程度及抗坏血酸(AsA)-谷胱甘肽(GSH)循环的变化情况.结果表明: Cd胁迫下,荷花叶片受害症状明显,其相对电导率、丙二醛(MDA)、AsA和GSH含量显著上升,抗坏血酸过氧化物酶(APX)、谷胱甘肽还原酶(GR)、单脱氢抗坏血酸还原酶(MDHAR)和脱氢抗坏血酸还原酶(DHAR)活性明显降低;ACC的添加进一步增加了Cd对荷花叶片的毒害症状,并加剧了4种抗氧化酶活性的降低,但增加了抗氧化剂的含量;SNP的添加对荷花叶片的伤害起到加重作用,并导致GR和MDHAR活性降低以及AsA和GSH含量的升高;PTIO可显著提高Cd和ACC复合处理下荷花叶片APX、GR、MDHAR和DHAR的活性并降低AsA和GSH的含量,而L-NNA和Tu效果不如PTIO明显;STS可显著缓解Cd和SNP复合处理下荷花叶片的毒害症状,并提高4种抗氧化酶的活性、降低AsA和GSH的含量.由此说明,乙烯和NO在AsA-GSH循环中存在互作,二者相互促进,共同调控AsA-GSH循环,进而参与调控荷花对Cd胁迫的响应.