洋葱种子含水量与贮藏温度对其寿命的影响

不同含水量（MC 7．1％－1．2）的洋葱种子贮藏在35℃、室温、15℃和5℃条件下1－3年,适度超于处理能延长种子的贮藏寿命;种子的贮藏寿命与种子含水量和贮藏温度密切相关。种子贮藏的最适含水量随温度的改变而发生相应的变化,35℃时MC为3．4％;室温时为3．4％－3．5％;15℃时为4．5％－5．1％。MC≤2．2％不利于延长种子寿命。在室温自然条件下贮藏1－3年,适度超干种子（MC3．4％）内MDA和H2O2含量、O2^-产生速率和LOX活性明显地低于未超干种子（MC7．1％）和高度超干种子（MC1．2％）,而抗氧化酶AsA-POD 、CAT和SOD的活性显著地高于未超干种子（MC7．1％）和高度超干种子（MC1．2％）。据此认为对脂质过氧化的抑制作用是适度超干种子耐贮藏的生理原因之一。     

洋葱种子含水量与贮藏温度对其寿命的影响

不同含水量（MC7.1％～1.2％）的洋葱种子贮藏在35℃、室温、15℃和5℃条件下1～3年,适度超干处理能延长种子的贮藏寿命;种子的贮藏寿命与种子含水量和贮藏温度密切相关。种子贮藏的最适含水量随温度的改变而发生相应的变化,35℃时MC为3.4％;室温时为3.4％～4.5％;15℃时为4.5%～5.1％。MC≤2.2％不利于延长种子寿命。在室温自然条件下贮藏1～3年,适度超干种子（MC3.4％）内MDA和H2O2含量、O－*2产生速率和LOX活性明显地低于未超干种子（MC7.1％）和高度超干种子（MC1.2％）,而抗氧化酶AsA-POD、CAT和SOD的活性显著地高于未超干种子（MC7.1％）和高度超干种子（MC1.2％）。据此认为对脂质过氧化的抑制作用是适度超干种子耐贮藏的生理原因之一。     

营养缺乏与脂质过氧化的关系

人体必需的营养素如含硫氨基酸、维生素A、B_2、C、E、辅酶Q等以及微量元素铜、锌、锰、硒等均有抗氧化作用;果糖能加重脂质过氧化作用,葡萄糖或淀粉则有减轻脂质过氧化作用。这些抗氧化营养素缺乏时,机体抗氧化能力下降,多不饱和脂肪酸发生脂质过氧化而导致组织、细胞等损害。因此,在治疗这些营养缺乏病时,不仅要补给所缺乏的营养素,而且还要给予其他抗氧化剂,以协同作用,取得较好的治疗效果。     

贮藏温度和种子含水量对洋葱种子发芽率的影响

贮藏温度低于15℃时,温度对洋葱种子发芽率影响变小,种子含水量低于8.8%时,其衰老过程变慢,高含水量种子在高温下贮存,衰老过程加快,含水量为100%和13%的种子在25℃下贮存分别不到5个月和2个月就失去商品性。     

脂质过氧化与癌肿形成

脂质过氧化与癌肿形成许小波（浙江医科大学医学系,杭州３１０００３）关键词脂质过氧化,癌肿形成自从１９５４年Ｈｏｒｇｅｒ和Ｐｈｉｌｐｏｔ认识到生物脂质过氧化和自由基形成在细胞膜损伤中的可能重要作用后,其在生化、营养、药理等各个领域都得到了广泛而深入的研...     

黄皮种子脱水敏感性与脂质过氧化作用

黄皮种子自然脱水时,种子的发芽率和发芽指数迅速下降;种子浸泡液的电导率和可溶性物质的量大大增加;线粒体膜和质膜ＡＴＰａｓｅ的活性下降,种子中ＳＯＤ活性先上升,然后下降;脂质过氧化产物ＭＤＡ和脂质氢过氧化物的量大大增加。     

亚油酸体系脂质过氧化引起的DNA损伤研究

用含两个双键的不饱和脂肪酸-亚油酸作为模型化合物,分析其过氧化程度,同时检测了由于脂质过氧化而引起的DNA损伤,结果表明:在脂质过氧化过程中,DNA与亚油酸过氧化产物反应生成一种荧光物质、其最大激发波长315nm最大发射波长410nm并随着氧化时间增加而增加,与此同时,双链DNA百分含量明显下降,DNA-溴乙锭复合物荧光显著降低,反映了DNA二级结构受到破坏.上述结果揭示了脂质过氧化产物在自由基引起DNA的损伤中可能起重要作用     

亚油酸体系脂质过氧化起动机理的ESR研究

本研究直接用含两个双键的不饱和脂肪酸一亚油酸(LH)作为模型化台物,利用自旋捕集ESR技术鉴测脂质过氧化反应的中间自由基L·.研究结果表明:0H自由基,H O,0(?)自由基都不能起动亚油酸的过氧化,即使这种亚油酸含有过氧化成份-LOOH.Fe(Ⅱ)和Fe(Ⅲ)都能使含有过氧化成份的亚油酸产生进一步的过氧化,但不能起动纯的亚油酸的过氧化.     

体外循环下牛磺酸对家兔心肌脂质过氧化的影响

采用家兔微型体外循环模型观察牛磺酸对心肌脂质过氧化的影响,研究提示：体外循环下术后心肌组织脂质过氧化物含量明显增高,而牛磺酸组则接近于正常,说明牛磺酸具有抗心肌脂质过氧化损伤作用。     

小麦种子在不同保存条件下的生活力丧失特性研究

近年来种子在低温种质库和室温保存条件下的生活力丧失特性研究日益受到关注,但是与其重要性相比,目前很少见有文献报道此方面进展。本文中我们监测了在中期库、室温和人工加速老化条件下小麦种子的生活力变化,以了解种子在这些保存条件下的生活力变化特性。结果表明,三种条件下所有种子的存活曲线均呈反S形,这种特点不受保存条件的影响。随着保存温度的降低,种子生活力丧失速度降低,反S形曲线的平台期和种子寿命延长。我们采用T检验来判断平台期和种子生活力快速下降期之间的转折点（Pt）,发现小麦种子在不同条件下保存时,其Pt均十分接近,在82.2%到83.6%之间。本文讨论了将Pt以及其他生理指标作为种子保存过程中生活力快速下降的预警指标的可能性。     

Sex-dependent Antioxidant Enzyme Activities and Lipid Peroxidation in Ageing Mouse Brain

We investigated whether oxidant status and antioxidant enzyme activities during ageing of mouse brain are regulated in sex-dependent manner. In the homogenate from the brain of 1, 4, 10 and 18 months old male and female CBA mice, lipid peroxidation (LPO), total superoxide dismutase (tSOD), catalase (CAT) and glutathione peroxidase (Gpx) were determined. LPO was age- and sex-related, favoring males over females throughout the lifespan with the peak in both sexes at 10 months of age. Throughout ageing, no difference in tSOD activity between male and female brains was observed, except in immature 1 month old mice. Gender-related difference in Gpx activity was observed, with higher level in females comparing to males, reaching statistical significance in senescent (18 months old) animals. CAT activity was drastically changed with ageing in both the male and female brain. We found different age associated trends in CAT activity in males and females: decreased with age in males and increased with age in females. Taken together, the present findings indicate that brains of female mice have lower oxidant and higher antioxidant capacity mostly related to CAT and to a lesser extent to Gpx activity.     

年龄相关性白内障晶状体脂质过氧化及抗氧化能力的变化

摘要目的：观察年龄相关性白内障晶状体中脂质过氧化及抗氧化能力的变化,探讨脂质过氧化与年龄相关性白内障的关系。方法：选择2010年8月至2011年10月我院收治的年龄相关性白内障患者35例（35眼）和透明晶状体15例（15眼）作为白内障纽和对照组,测定其维生素C（VitC）、脂质过氧化物丙二醛（MDA）含量及超氧化物歧化酶（SOD）活性的改变。结果：与对照组相比,白内障组晶状体内VitC含量和SOD酶活性均显著下降,分别降低了39．30％（P〈0．01）和63．50％（P〈0．01）,MDA含量较明显升高（P〈O．01）。Pearson相关分析显示,对照组透明晶状体中MDA含量与SOD活性、VitC含量均呈显著负相关（r=-0．858,P〈0．01;r-=．0．883,P〈0．01）,而白内障组晶状体中三者未发现明显的直线相关关系（P〉0．05）。结论：脂质过氧化参与了年龄相关性白内障的形成,SOD和VitC对晶状体氧化损伤具有一定的保护作用。     

四氧嘧啶致大鼠糖尿病与脂类过氧化

四氧嘧啶致SD大白鼠糖尿病的过程中,首先引起体内多种组织器官广泛发生脂类过氧化作用。脂类过氧化物分解产生一些醛类物质,故血清、胰腺、肝和肾组织中TBA反应物(主要成分为丙二醛)含量升高;生成的其它醛类物质与蛋白质结合形成的水溶性荧光物质含量亦增多。抗氧化剂维生素E的抗脂类过氧化作用对机体起保护作用;而维生素C在大量氧化剂四氧嘧啶存在的条件下起氧化强化剂的作用,并使机体对维生素E的消耗增多。     

Protective Effect of Dehydroepiandrosterone Against Copper-Induced Lipid Peroxidation in the Rat

This study investigates the effectiveness and multitargeted activity of dehydroepiandrosterone (DHEA) as antioxidant in vivo. A single dose of DHEA was given IP to male rats. Liver and brain microsomes, and plasma low density lipoprotein (LDL), were isolated from rats sacrified 17 h later. Liver and brain microsomes were challenged with CuSO₄ and, as index of lipid peroxidation, the production of thiobarbituric acid reactive substances (TBARS) was measaured. Also, plasma low-density lipoprotein (LDL) were challenged with copper and the time course of lipid peroxidation was evaluated following the formation of conjugated dienes. The onset of TBARS generation induced by copper was marked delayed in both liver and brain microsomes from DHEA-treated animals. Also, the resistance of LDL to oxidation, expressed by the duration of the lag-phase of the kinetic curve, was significantly enhanced in DHEA-treated rats. Results indicate that in vivo DHEA supplementation makes subcellular fractions isolated from different tissues and plasma constituents (LDL) more resistant to lipid peroxidation triggered by copper. The antioxidant effect on plasma LDL might be of special relevance to the proposed antiatherogenic activity of DHEA. Moreover, multitargeted antioxidant activity of DHEA might protect tissues from oxygen radicals damage. © 1997 Elsevier Science Inc.     

Lipid Peroxidation in Rat Brain Cortical Slices as Measured by the Thiobarbituric Acid Test

Abstract: Malonaldehyde formation by cortical brain slices from rat brain was determined as a function of incubation time and of oxygen pressure. This substance, a byproduct of lipid peroxidation, was detected by the thiobarbituric acid test. Significant amounts of malonaldehyde were formed by brain slices during incubation in the 0.2 (air) to 10 atm oxygen range, and a portion of it was released into the medium. The rate of malonaldehyde formation was the highest during the first 10 min. Elevation of oxygen pressure above 1 atm caused further increments in malonaldehyde production with kinetic properties similar to that seen at 1 atm pressure, but the increments per additional oxygen pressure were diminishing. The formation of a given amount of malonaldehyde can be expressed as a function of atm oxygen × min. This function has the shape of a saturation curve approaching a maximum at around 300 atm × min. The results indicate extensive lipid peroxidation in brain slices under standard incubation conditions.     

Occurrence of Lipid Peroxidation in Brain Microsomes in the Presence of NADH and Vanadate

Oxidation of NADH by rat brain microsomes was stimulated severalfold on addition of vanadate. During the reaction, vanadate was reduced, oxygen was consumed, and H2O2 was generated with a stoichiometry of 1:1 for NADH/O2, as in the case of other membranes. Extra oxygen was found to be consumed over that needed for H2O2 generation specifically when brain microsomes were used. This appears to be due to the peroxidation of lipids known to be accompanied by a large consumption of oxygen. Occurrence of lipid peroxidation in brain microsomes in the presence of NADH and vanadate has been demonstrated. This activity was obtained specifically with the polymeric form of vanadate and with NADH, and was inhibited by the divalent cations Cu2+, Mn2+, and Ca2+, by dihydroxyphenolic compounds, and by hemin in a concentration-dependent fashion. In the presence of a small concentration of vanadate, addition of an increasing concentration of Fe2+ gave increasing lipid peroxidation. After undergoing lipid peroxidation in the presence of NADH and vanadate, the binding of quinuclidinyl benzylate, a muscarinic antagonist, to brain membranes was decreased.     

Iron (III) Stimulation of Lipid Hydroperoxide-Dependent Lipid Peroxidation

In an experimental system where both Fe²⁺ autoxidation and generation of reactive oxygen species is negligible, the effect of FeCl₂ and FeCl₃ on the peroxidation of phosphatidylcholine (PC) liposomes containing different amounts of lipid hydroperoxides (LOOH) was studied; Fe²⁺ oxidation, oxygen consumption and oxidation index of the liposomes were measured. No peroxidation was observed at variable FeCl₂/FeCl₃ ratio when PC liposomes deprived of LOOH by triphenyl-phosphine treatment were utilized. By contrast, LOOH containing liposomes were peroxidized by FeCl₂. The FeCl₂ concentration at which Fe²⁺ oxidation was maximal, defined as critical Fe²⁺ concentration [Fe²⁺]*, depended on the LOOH concentration and not on the amount of PC liposomes in the assay. The LOOH-dependent lipid peroxidation was stimulated by FeCl₃, addition; the oxidized form of the metal increased the average length of radical chains, shifted to higher values the [Fe²⁺]* and shortened the latent period. The iron chelator KSCN exerted effects opposite to those exerted by FeCl₃ addition. The experimental data obtained indicate that the kinetics of LOOH-dependent lipid peroxidation depends on the Fe²⁺/Fe³⁺ ratio at each moment during the time course of lipid peroxidation. The results confirm that exogenously added FeCl₃ does not affect the LOOH-independent but the LOOH-deendent lipid peroxidation; and suggest that the Feg, endogenously generated exerts a major role in the control of the LOOH-dependent lipid peroxidation.     

Iron (III) Stimulation of Lipid Hydroperoxide-Dependent Lipid Peroxidation

In an experimental system where both Fe²⁺ autoxidation and generation of reactive oxygen species is negligible, the effect of FeCl₂ and FeCl₃ on the peroxidation of phosphatidylcholine (PC) liposomes containing different amounts of lipid hydroperoxides (LOOH) was studied; Fe²⁺ oxidation, oxygen consumption and oxidation index of the liposomes were measured. No peroxidation was observed at variable FeCl₂/FeCl₃ ratio when PC liposomes deprived of LOOH by triphenyl-phosphine treatment were utilized. By contrast, LOOH containing liposomes were peroxidized by FeCl₂. The FeCl₂ concentration at which Fe²⁺ oxidation was maximal, defined as critical Fe²⁺ concentration [Fe²⁺]*, depended on the LOOH concentration and not on the amount of PC liposomes in the assay. The LOOH-dependent lipid peroxidation was stimulated by FeCl₃, addition; the oxidized form of the metal increased the average length of radical chains, shifted to higher values the [Fe²⁺]* and shortened the latent period. The iron chelator KSCN exerted effects opposite to those exerted by FeCl₃ addition. The experimental data obtained indicate that the kinetics of LOOH-dependent lipid peroxidation depends on the Fe²⁺/Fe³⁺ ratio at each moment during the time course of lipid peroxidation. The results confirm that exogenously added FeCl₃ does not affect the LOOH-independent but the LOOH-deendent lipid peroxidation; and suggest that the Feg, endogenously generated exerts a major role in the control of the LOOH-dependent lipid peroxidation.     

Basal Lipid Peroxidation in Substantia Nigra Is Increased in Parkinson''s Disease

Polyunsaturated fatty acid (PUFA) levels (an index of the amount of substrate available for lipid peroxidation) were measured in several brain regions from patients who died with Parkinson's disease and age-matched control human postmortem brains. PUFA levels were reduced in parkinsonian substantia nigra compared to other brain regions and to control tissue. However, basal malondialdehyde (MDA; an intermediate in the lipid peroxidation process) levels were increased in parkinsonian nigra compared with other parkinsonian brain regions and control tissue. Expressing basal MDA levels in terms of PUFA content, the difference between parkinsonian and control substantia nigra was even more pronounced. Stimulating MDA production by incubating tissue with FeSO4 plus ascorbic acid, FeSO4 plus H2O2, or air alone produced lower MDA levels in the parkinsonian substantia nigra, probably reflecting the lower PUFA content. These results may indicate that an increased level of lipid peroxidation continues to occur in the parkinsonian nigra up to the time of death, perhaps because of continued exposure to excess free radicals derived from some endogenous or exogenous neurotoxic species.