Protective effect of electroacupuncture and moxibustion on gastric mucosal damage and its relation with nitric oxide in rats

INTRODUCTION Gastric mucosal injury is one of the common disorders,there are many reports subjicted to its pathogenesis treatment and prevention.We investigated the protective effect

Inflammatory cytokines promote inducible nitric oxide synthase-mediated DNA damage in hamster gallbladder epithelial cells

AIM: To investigate the link between chronic biliary inflammation and carcinogenesis using hamster gallbladder epithelial cells. METHODS: Gallbladder epithelial cells were isolated from hamsters and cultured with a mixture of inflammatory cytokines including interleukin-1β,interferon-γ,and tumor necrosis factor-α. Inducible nitric oxide synthase (iNOS) expression,nitric oxide (NO) generation,and DNA damage were evaluated. RESULTS: NO generation was increased significantly following cytokine stimulation,and suppressed by an iNOS inhibitor. iNOS mRNA expression was demonstrated in the gallbladder epithelial cells during exposure to inflammatory cytokines. Furthermore,NO-dependent DNA damage,estimated by the comet assay,was significantly increased by cytokines,and decreased to control levels by an iNOS inhibitor. CONCLUSION: Cytokine stimulation induced iNOS expression and NO generation in normal hamster gallbladder epithelial cells,which was sufficient to cause DNA damage. These results indicate that NO-mediated genotoxicity induced by inflammatory cytokines through activation of iNOS may be involved in the process of biliary carcinogenesis in response to chronic inflammation of the biliary tree.

Spatio-temporal expression of inducible nitric oxide synthase in and surrounding a region of rat frontal lobe damaged with a sharp instrument

BACKGROUND： Inducible nitric oxide synthase （iNOS） cannot be detected in the neurons and glial cells of normal rats, but iNOS can be found in some neurons and glial cells of rats following ischemic, traumatic, neurotoxic or inflammatory damage. OBJECTIVE： To investigate iNOS expression and iNOS-positive cell types at various time points following damage to the rat frontal lobe using a sharp instrument. DESIGN： A nerve molecular biology, randomized, controlled study. TIME AND SETTING： This experiment was performed at the Department of Human Anatomy, Institute of Neurobiology, Medical School of Nantong University, between April 2006 and December 2007. MATERIALS： Rabbit anti-iNOS antibody （Santa Cruz, USA）, biotin labeled goat anti-rabbit antibody （Sigma, USA）, reverse transcription kit （Biouniquer, Hong Kong, China） and horseradish peroxidase labeled goat anti-rabbit antibody （Pierce, USA） were used for this study. METHODS： A total of 112 healthy rats aged 3 months were randomly assigned into a sham operation group （n = 28） and a damage group （n = 84）. Rat models of frontal lobe damage were induced in the damage group using a sharp instrument to make an incision in the frontal lobe cortex. In the sham operation group, the rat bone window was opened but brain tissues were left intact. MAIN OUTCOME MEASURES： Parameters were measured at 3, 6, 12, 24, 72, 120 and 168 hours following damage in both groups. Pathological changes were observed using Nissl staining and hematoxylin-eosin staining. Expression of iNOS mRNA, iNOS protein and iNOS-positive cells were examined by RT-PCR, Western blot analysis and immunohistochemistry, respectively. RESULTS： A large number of inflammatory cells infiltrated the damaged region 12 and 24 hours following damage, iNOS mRNA and iNOS protein expression increased in and around the damaged region 3 hours following damage, reached a peak at 24 hours, and then gradually decreased. The changes in iNOS-positive cell number reflected the changes in iNOS mRNA and iNOS protein expression after damage, iNOS was mainly found in neural cells at 3 and 6 hours, in macrophages at 12 and 24 hours, and in glial cells at 72 and 120 hours after damage. iNOS-positive cells were few in and surrounding the damaged region at 168 hours. There were a few iNOS-positive neural cells in the rat frontal lobe cortex in the sham operation group. CONCLUSION： Neurons, macrophages and glial cells can express iNOS following rat frontal lobe damage caused by a sharp instrument. The levels of iNOS expression, and the cell types expressing iNOS, change with time.

Abnormal Reactions of Free Radicals and Oxidative Damages in the Bodies of Patients With Chronic Glomerulonephritis

Objective To study the abnormal reactions of a series of free radicals and the oxidative damages induced by free radical abnormal reactions in the bodies of patients with chronic glomerulonephritis. Methods Eighty chronic glomerulonephritis patients (CGNP) and eighty healthy adult volunteers (HAV) were enrolled in a random control study, in which concentrations of nitric oxide (NO) in plasma, lipoperoxides (LPO) in plasma and in erythrocytes, and vitamin C (VC), vitamin E (VE) and beta-carotene (?CAR) in plasma as well as activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined with spectrophotometric assays. Results Compared with the average values of the above biochemical parameters in the HAV group, the average values of NO in plasma, and LPO in plasma and erythrocytes in the CGNP group were significantly increased (P = 0.0001), while those of VC, VE and -CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the CGNP group were significantly decreased (P = 0.0001). Pearson product-moment correlation analysis showed that with increase of the concentration of blood creatinine as well as prolongation of the course of disease in the CGNP, the concentrations of NO in plasma, and LPO in plasma and erythrocytes in the CGNP increased gradually, while the concentrations of VC, VE and ?CAR in plasma as well as the activities of SOD, CAT and GPX in erythrocytes in the CGNP decreased gradually (P = 0.002454 0.000001). The relative risk ratio (RR) of the above biochemical parameters reflecting oxidative damages in the bodies of CGNP ranged from 6.061 to 72.429. The reliability coefficient (alpha) that the above biochemical parameters were used to reflect the oxidative damages of the CGNP was 0.8137, standardized item alpha = 0.9728, Hotelling抯 T-Squared = 1135680.191, F = 53274.6478, P = 0.000001. Conclusions The findings in this study show that in the bodies of CGNP a series of free radical chain reactions result in severe pathological aggravation and induce oxidative damages in their bodies. Therefore, suitable dose of antioxidants should be supplemented to them so as to alleviate oxidative damages in their bodies.

Increased oxidative stress and oxidative damage associated with chronic bacterial prostatitis

Aim： To investigate whether chronic bacterial prostatitis might increase oxidative stress and oxidative damage in chronic bacterial prostatitis patients （CBPP）, and to explore its possible mechanism. Methods： Enrolled in a casecontrol study were 70 randomly sampled CBPP and 70 randomly sampled healthy adult volunteers （HAV）, on whom plasma nitric oxide （NO）, vitamin C （VC）, vitamin E （VE） and β-carotene （β-CAR） level, erythrocyte malondialdehyde （MDA） level, as well as erythrocyte superoxide dismutase （SOD）, catalase （CAT） and glutathione peroxidase （GPX） activities were determined by spectrophotometry. Results： Compared with the HAV group, values of plasma NO and erythrocyte MDA in the CBPP group were significantly increased （P 〈 0.001）; those of plasma VC, VE and β-CAR as well as erythrocyte SOD, CAT and GPX activities in the CBPP group were significantly decreased （P 〈 0.001）. Findings from partial correlation for the 70 CBPP showed that with prolonged course of disease, values of NO and MDA were gradually increased （P 〈 0.001）, and those of VC, VE, β-CAR, SOD, CAT and GPX were gradually decreased （P 〈 0.05- 0.001）. The findings from stepwise regression for the 70 CBPP suggested that the model was Y= -13.2077 ＋ 0.1894MDA ＋ 0.0415NO - 0.1999GPX, F = 18.2047, P 〈 0.001, r = 0.6729, P 〈 0.001. Conclusion： The findings suggest that there exist increased oxidative stress and oxidative damage induced by chronic bacterial prostatitis in the patients, and such phenomenon was closely related to the course of disease.

Increased Oxidative Stress and Damage in Patients With Chronic Bacterial Prostatitis

Objective To investigate whether chronic bacterial prostatitis （CBP） increases oxidative stress and damage in patients with CBP, and to explore its possible mechanism. Methods Eighty patients with CBP and 80 healthy adults as controls were enrolled in a case-control study, in which levels of nitric oxide （NO）, vitamin C （VC）, and vitamin E （VE） in plasma, as well as malondialdehyde （MDA）, activities of superoxide dismutase （SOD）, and eatalase （CAT） in erythrocytes were determined by spectrophotometry. Results Compared with the average values of NO, VC, VE, MDA, SOD, and CAT in the healthy control group, those of plasma N O and erythrocyte MDA in the CBP group were significantly increased （P〈0.00 1）, and those of plasma VC and VE as well as erythrocyte SOD and CAT in the CBP group were significantly decreased （P〈0.001）. Findings from partial correlation analysis for course of the disease and NO, VC, VE, MDA, SOD, and CAT in 80 patients with CBP, adjusted for age, suggested that with prolonged course of the disease, values of NO and MDA were gradually increased （P〈0.001）, and those of VC, VE, SOD, and CAT were gradually decreased （P〈0.05-0.001）. The findings from stepwise regression analysis for course of the disease and NO, VC, VE, MDA, SOD, and CAT in CBP group suggested that the model of stepwise regression was Y = -19.1160 ＋0.3112MDA ＋ 0.0337NO, F = 22.1734, P〈0.001, r = 0.6045, P〈0.001. The findings from the reliability analysis for VC, VE, SOD, CAT, NO, and MDA in the CBP group showed that the reliability coefficients＇ alpha （6 items） was 0.7195, P〈0.0001, and the standardized item alpha was 0.9307, P〈0.0001. Conclusion There exist increased oxidative stress and damage induced by chronic bacterial prostatitis in patients, and such a phenomenon is closely related to the course of disease.

Oxidative damage of primary cultured hippocampal neurons Does androgen have an antagonistic effect?

BACKGROUND： Evidence illustrates that androgen has a neuroprotective role. However, whether androgen also has the protective effect on hippocampal neurons during free radical mediated injury remains unclear. OBJECTIVE： To investigate the neuroprotective effect of androgen on hippocampal neurons during free radical damage. DESIGN, TIME AND SETTING： A controlled in vitro experiment was performed at the Department of Human Anatomy, Cell Culture Lab, and Neuroendocrinology Lab, Basic Medical School, Hebei Medical University from February to June 2009. MATERIALS： Testosterone was provided by Tianjin Jinyao Amino Acid Company, China. METHODS： Primary cultured neurons from 24 Sprague Dawley rats were randomly assigned into four groups： control, H202, testosterone, and testosterone （pre-added） plus H2O2 groups. MAIN OUTCOME MEASURES： The positive cell ratio of microtubule associated protein-Ⅱ and neuron specific enolase was determined by immunocytochemistry. Neuronal morphology was observed by hematoxylin-eosin staining and Nissl staining. Cell vitality and viability were determined using an inverted phase contrast microscope. The content of nitric oxide synthase, malondialdehyde, and superoxide dismutase were measured with a spectrophotometer. RESULTS： As compared with the control group, cell vitality and viability, and superoxide dismutase level were significantly decreased in the H202 group （P 〈 0.05）, while nitric oxide synthase and malondialdehyde levels were significantly increased （P 〈 0.05）. Neuronal vitality and viability as well as superoxide dismutase level in the testosterone plus H2O2 group were significantly greater than in the H2O2 group （P 〈 0.05）, and nitric oxide synthase and malondialdehyde levels were significantly less than in the H2O2 group （P〈 0.05）. CONCLUSION： Androgen partially reversed H2O2-induced neuronal damage and protected neurons.

Oxidative stress and damage induced by abnormal free radical reactions and IgA nephropathy

Objective: To estimate the oxidative stress and oxidative damage induced by abnormal free radical reactions in IgA nephropathy (IgAN) patients' bodies. Methods: Seventy-two IgA N patients (IgANP) and 72 healthy adult volunteers (HAV) were enrolled in a random control study design, in which the levels of nitric oxide (NO) in plasma, lipoperoxide (LPO) in plasma and in erythrocytes, and vitamin C (VC), vitamin E (VE) and β-carotene (β-CAR) in plasma as well as the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined with spectrophotometric mothods. Results: Compared with the HAV group, the averages of NO in plasma, and LPO in plasma and in erythrocytes in the IgANP group were significantly increased (P＜0.0001), while those ofVC, VE and β-CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the IgANP group were significantly decreased (P＜0.0001). Linear correlation analysis showed that with the increase of the values of NO, and LPO in plasma and in erythrocytes, and with the decrease of those ofVC, VE, β-CAR,SOD, CAT and GPX in the IgAN patients, the degree of histological damage of tubulointerstitial regions was increased gradually (P＜0.0001); and that with the prolongation of the duration of disease the values of NO, and LPO in plasma and erythrocytes were increased gradually, while those of VC, VE, β-CAR, SOD, CAT and GPX were decreased gradually (P＜0.005). The discriminatory correct rates of the above biochemical parameters reflecting oxidative damage of the IgAN patients were 73.8%-92.5%, and the correct rates for the HAV were 70.0%-91.3% when independent discriminant analysis was used; and the correct rate for the IgAN patients was increased to 98.8%, the correct rate for the HAV was increased to 100% when stepwise discriminant analysis was used. The above biochemical parameters' reliability coefficient (alpha) were used to estimate the oxidative damage of the IgAN patients as 0.8145, the standardized item alpha=0.9730, F=53273.5681, P＜0.0001. Conclusions: A series of free radical chain reactions caused serious pathological aggravation in the IgANP' bodies, thus resulting in oxidative damage in their bodies. In treating IgANP, therefore, it is necessary that suitable dose antioxidants should be supplemented to them so as to alleviate the oxidative damage in their bodies.

Estrogen inhibits lipid peroxidation after hypoxic-ischemic brain damage in neonatal rats

Sprague-Dawley neonatal rats within 7 days after birth were used in this study. The left common carotid artery was occluded and rats were housed in an 8% O2 environment for 2 hours to establish a hypoxic-ischemic brain damage model. 17β-estradiol （1 × 10-5 M） was injected into the rat abdominal cavity after the model was successfully established. The left hemisphere was obtained at 12, 24, 48, 72 hours after operation. Results showed that malondialdehyde content in the left brain of neonatal rats gradually increased as modeling time prolonged, while malondialdehyde content of 17β-estrodial-treated rats significantly declined by 24 hours, reached lowest levels at 48 hours, and then peaked at 72 hours after injury. Nicotinamide-adenine dinucleotide phosphate histochemical staining showed the nitric oxide synthase-positive cells and fibers dyed blue/violet and were mainly distributed in the cortex, hippocampus and medial septal nuclei. The number of nitric oxide synthase-positive cells peaked at 48 hours and significantly decreased after 17β-estrodial treatment. Our experimental findings indicate that estrogen plays a protective role following hypoxic-ischemic brain damage by alleviating lipid peroxidation through reducing the expression of nitric oxide synthase and the content of malondialdehyde.

Increased oxidative stress and oxidative damage associated with chronic bacterial prostatitis

Aim:To investigate whether chronic bacterial prostatitis might increase oxidative stress and oxidative damage in chronic bacterial prostatitis patients(CBPP),and to explore its possible mechanism.Methods:Enrolled in a case- control study were 70 randomly sampled CBPP and 70 randomly sampled healthy adult volunteers(HAV),on whom plasma nitric oxide(NO),vitamin C(VC),vitamin E(VE)and β-carotene(β-CAR)level,erythrocyte malondialdehyde (MDA)level,as well as erythrocyte superoxide dismutase(SOD),catalase(CAT)and glutathione peroxidase(GPX) activities were determined by spectrophotometry.Results:Compared with the HAV group,values of plasma NO and erythrocyte MDA in the CBPP group were significantly increased(P<0,001);those of plasma VC,VE and β-CAR as well as erythrocyte SOD,CAT and GPX activities in the CBPP group were significantly decreased(P<0.001).Findings from partial correlation for the 70 CBPP showed that with prolonged course of disease,values of NO and MDA were gradually increased(P<0.001),and those of VC,VE,β-CAR,SOD,CAT and GPX were gradually decreased(P<0.05- 0.001).The findings from stepwise regression for the 70 CBPP suggested that the model was Y=-13.2077 + 0.1894MDA + 0.0415NO-0.1999GPX.F=18.2047,P<0.001,r=0.6729,P<0.001.Conclusion:The findings suggest that there exist increased oxidative stress and oxidative damage reduced by chronic bacterial prostatitis in the patients,and such phenomenon was closely related to the course of disease.

ONE PROBABLE MECHANISM OF THE LEARNING-MEMORY DAMAGE BY LEAD:THE CHANGES OF NOS IN HIPPOCAMPUS

Objective To study the effects of lead on the activity and expression of nitric oxide synthase (NOS) and relationship between the effects of lead on learning memory and changes of NOS in subfields of hippocampus. Methods Y maze test was used to study the effects of lead on ability of learning memory; NADPH d histochemistry and immunohistochemistry methods were used to investigate the changes of NOS in subfields of hippocampus. Results Compared with the control group, the ability of learning memory in lead exposed rats was significantly decreased ( P < 0.05 ); the number of NOS positive neurons in CA1 region and dentate gyrus of lead exposed rats was significantly decreased( P < 0.05 ), but no marked changes in CA3 region; the number of nNOS positive neurons in CA1 of lead exposed rats was also significantly decreased( P < 0.05 ), but no obvious changes in CA3. Conclusion Lead could damage the ability of learning memory in rats. Lead could decrease the activity and expression of NOS in hippocampus and had different effects on NOS in different subfields of hippocampus. The changes of NOS in hippocampus induced by lead may be the mechanism of the learning memory damage by lead.

Protective effects of nitric oxide on salt stress-induced oxidative damage to wheat (Triticum aestivum L.)leaves

The changes of chlorophyll and malondialde-hyde (MDA) contents, plasma membrane permeability confirmed that 0.1 and 1 mmol/L sodium nitroprusside (SNP), a donor of nitric oxide (NO) in vivo, could markedly alleviate the oxidative damage to wheat (Triticum aestivum L.) leaves induced by 150 and 300 mmol/L NaCl treatments, respectively. Further results proved that NO significantly enhanced the activities of superoxide dismutase (SOD) and catalase (CAT), both of which separately contributed to the delay of O2- and H2O2 accumulation in wheat leaves under saltstress. Meanwhile, the accumulation of proline was apparently accelerated. Therefore, these results suggested that NO could strongly protect wheat leaves from oxidative damage caused by salt stress.

非线粒体辅酶Q10在线粒体损伤所致心血管疾病中治疗机制研究进展

线粒体损伤与心血管疾病(CVD)的发生密切相关,减少线粒体损伤能够显著减少心血管事件发生。近年研究发现,非线粒体辅酶Q10(CoQ10)对防治线粒体损伤所致CVD具有一定作用,其机制可能与降低内皮型一氧化氮合酶解耦联状态以及活性氧积聚等作用来减少线粒体结构和功能损伤有关。因此,非线粒体Co Q10在线粒体损伤所致CVD治疗方面有良好的开发利用前景,值得引起重视。

外源一氧化氮对NaCl胁迫下番茄幼苗生理影响

【目的】探明NO对NaCl胁迫下番茄(LycopersiconesculentumMill.)幼苗的生长和叶片氧化损伤具有保护作用。【方法】在100mmol·L-1NaCl胁迫下,研究了0.05～0.8mmol·L-1外源NO供体硝普钠(SNP)处理对番茄幼苗生长、叶片保护酶活性和氧化损伤的影响。【结果】0.1mmol·L-1SNP处理缓解NaCl胁迫伤害的效果最好,显著提高了番茄幼苗生长,叶片叶绿素含量,保护酶SOD、POD、CAT、APX活性,脯氨酸和可溶性糖含量。显著降低了MDA和O2.-含量。【结论】外源NO缓解番茄幼苗NaCl胁迫具有剂量效应,以0.1mmol·L-1SNP的效果最好,从而增强植株的耐盐性。

外源一氧化氮对盐胁迫下水稻根部脂质过氧化的缓解作用

在100 mmol/L NaCl的胁迫条件下,研究了两种浓度的一氧化氮供体硝普钠(sodium nitroprusside,SNP)处理对水稻幼苗根部脂质过氧化的影响。低浓度(10 μmol/L)的SNP处理明显缓解盐胁迫下水稻幼苗根组织膜脂过氧化产物MDA的累积,显著提高可溶性蛋白含量,并诱导根系APX、POD和SOD活性的上升;而高浓度(50 μmol/L)SNP处理的效果则基本相反。表明外源低浓度NO可以通过提高盐胁迫下水稻幼苗根组织的抗氧化能力来缓解氧化损伤。

NO在甲醛介导的氧化损伤中的协同作用

为了探讨NO在甲醛介导的氧化损伤中的协同作用,用不同剂量的气态甲醛对小鼠进行连续动态染毒处理72h后,测定小鼠脑、心和肝组织一氧化氮合酶活力和总抗氧化能力.结果显示,吸入甲醛后,小鼠的脑、心和肝组织一氧化氮合酶活力升高,总抗氧化能力下降.当甲醛浓度为0.5mg·m-3时,脑和肝的一氧化氮合酶活力与阴性对照组相比有显著性差异(p<0.05),脑和肝的总抗氧化能力与阴性对照组相比,有极显著性差异(p<0.01),而心的总抗氧化能力与阴性对照组相比有显著性差异(p<0.05).当甲醛浓度上升为3.0mg·m-3时,脑、心和肝组织的一氧化氮合酶活力和总抗氧化能力与阴性对照组相比均有极显著性差异(p<0.01).结果表明,过量生成的NO是甲醛导致机体氧化损伤可能的机理.

外源NO对渗透胁迫下黄瓜种子萌发、幼苗生长和生理特性的影响

【目的】探究外源NO对渗透胁迫下黄瓜(Cucumis sativus L.)种子萌发、幼苗生长和生理特性的作用。【方法】在25%PEG-6000胁迫下,研究0.1和0.5 mmol.L-1SNP(硝普钠)对黄瓜种子萌发、幼苗生长、叶片氧化损伤和保护酶活性的影响。【结果】0.1 mmol.L-1 SNP处理能显著缓解25%PEG-6000的胁迫伤害,使黄瓜种子萌发率提高0.24倍,发芽指数提高0.86倍,活力指数提高3.01倍;幼苗株高、根长和干重分别提高1.15,2.17和1.16倍;叶片Pro含量提高50.99%,SOD,CAT,POD和APX活性分别提高42.39%,66.58%,79.03%和116.39%,MDA含量降低80.50%。与0.1 mmol.L-1 SNP处理相比,0.5 mmol.L-1 SNP处理促进黄瓜种子萌发和幼苗生长,缓解叶片氧化损伤和提高保护酶活性的作用明显或显著降低。【结论】0.1 mmol.L-1 SNP能显著促进渗透胁迫下黄瓜种子萌发和幼苗生长,明显缓解叶片氧化损伤,显著提高SOD等保护酶活性;0.5 mmol.L-1 SNP的有效作用减弱,甚至抑制SOD活性。

一氧化氮对杨树耐旱性的影响

探讨了外源NO对水分胁迫下杨树叶片质膜相对透性、叶片光合作用和氧化伤害保护酶的影响.结果表明,NO供体硝普钠(sodiumnitroprusside,SNP)能提高杨树叶片的含水率,在水分胁迫(PEG6000渗透液处理)下,能缓解叶片的水分丢失.NO对杨树叶片光合作用具有双重性,低浓度SNP(200、500μmol·L-1)能促进叶片的光合,高浓度SNP(1000、2000μmol·L-1)则明显抑制叶片的光合.较短时间水分处理胁迫(1h))的杨树叶片SOD和POD活性显著高于较长时间(3h)水分胁迫下叶片的酶活性.经SNP处理后,各处理组POD、SOD活性明显上升.同时,随SNP浓度的增加,POD和SOD活性表现出先上升后下降的趋势.外源NO可通过诱导POD和SOD活性的上升,延缓活性氧的积累,从而减轻水分胁迫对杨树的伤害,增强树木的耐旱能力.

外源NO对NaCl胁迫下燕麦幼苗氧化损伤的保护作用

用不同浓度的外源一氧化氮(NO)供体SNP处理100 mmol/L NaCl胁迫下一年生燕麦草幼苗,研究了外源NO对NaCl胁迫下燕麦幼苗氧化损伤的影响。结果表明,外源NO可缓解NaCl胁迫造成的燕麦幼苗膜质过氧化产物丙二醛(MDA)含量的升高,促进脯氨酸(Pro)积累,提高超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和过氧化物酶(POD)活性,并能缓解叶绿素含量的降解,提高可溶性糖的含量。而且NO的这种作用存在明显的剂量效应,其中以0.2 mmol/L SNP处理效果最为显著。

外源NO对NaCl胁迫下辣椒幼苗氧化损伤的保护效应

以辣椒品种陇椒2号为试验材料,研究了外源NO供体硝普钠(SNP)对辣椒幼苗氧化损伤的影响.结果显示,在100 mmol/L NaCl胁迫下,辣椒叶片的MDA含量、质膜相对透性和脯氨酸含量均增加,保护酶SOD、CAT活性降低,而POD活性只在胁迫18 d时降低.0.1 mmol/L SNP处理可减缓NaCl胁迫下辣椒幼苗叶片MDA含量的上升,降低叶片质膜相对透性,并诱导SOD、POD和CAT活性增加,提高脯氨酸含量,表明外源NO可以通过提高盐胁迫下辣椒幼苗叶片组织的抗氧化能力来缓解氧化损伤.而SNP相似物NaNO2和K3Fe(CN)6处理对盐胁迫引起的氧化损伤并没有起到明显的缓解作用,进一步证实了NO对辣椒幼苗耐盐性具有专一性的调节作用.