水杨酸对黄瓜叶片抗氧化剂酶系的调节作用

分析了水杨酸（ＳＡ）对黄瓜（ＣｕｃｕｍｉｓｓａｔｉｖｕｓＬ．）叶片抗氧化剂酶系活性及活性氧水平的调节作用。不同浓度的ＳＡ（０．５ｍｍｏｌ／Ｌ、１ｍｍｏｌ／Ｌ、２．５ｍｍｏｌ／Ｌ、５ｍｍｏｌ／Ｌ）均能显著地提高被处理叶片超氧化物歧化酶（ＳＯＤ）和过氧化物酶（ＰＯＤ）活性,而且还能诱导同株的非处理叶片中ＳＯＤ和ＰＯＤ活性增加。用１ｍｍｏｌ／ＬＳＡ处理第一片真叶,在处理后６～７２ｈ,ＰＯＤ活性增加了２２％～６７％,同株非处理的第二片真叶ＰＯＤ活性增加了１４％～８６％,但是,在ＳＡ处理后３ｈ之前以及处理９６ｈ之后,ＰＯＤ活性没有变化。ＳＡ能够显著降低超氧物阴离子含量和提高过氧化氢水平,但它对过氧化氢酶（ＣＡＴ）活性的抑制作用很弱,表明ＳＡ提高体内过氧化氢含量的原因主要是通过提高ＳＯＤ活性而不是抑制ＣＡＴ活性。同工酶分析表明,ＳＡ不能诱导新的ＳＯＤ同工酶,但可以诱导新的ＰＯＤ同工酶。     

钙对水稻幼苗抗冷性的影响

ＣａＣｌ２浸种提高水稻幼苗叶片中结合态钙、内源抗氧化剂（ＧＳＨ、ＡｓＡ）含量和膜保护酶（ＣＡＴ、ＳＯＤ和ＰＯＤ）活性,也增加可溶性蛋白质中煮沸稳定蛋白质（ｂｏｉｌｉｎｇ－ｓｔａｂｌｅｐｒｏｔｅｉｎ）的含量。冷胁迫期间,ＣａＣｌ２并能减少因冷胁迫引起的ＧＳＨ、ＡｓＡ含量,ＣＡＴ、ＳＯＤ和ＰＯＤ活性以及煮沸稳定蛋白质下降的程度。在恢复期间,经ＣａＣｌ２处理的幼苗其ＧＳＨ、ＡＳＡ、ＣＡＴ、ＳＯＤ和ＰＯＤ以及煮沸稳定蛋白质水平均有回升。     

冷型小麦旗叶衰老和活性氧代谢特性研究

以典型的冷型小麦和暖型小麦为试验材料,研究了同一环境背景下不同温度型小麦开花后的旗叶衰老和活性氧代谢特性。结果表明,与暖型小麦相比,冷型小麦籽料灌浆期旗叶叶绿素和可溶性蛋白质含量下降缓慢、含量高,整个业粒形成和灌浆期ＭＤＡ积累速度慢、含量低,籽粒灌浆期防御活性氧伤害的关键性保护酶（ＳＯＤ、ＣＡＴ和ＰＯＤ）活性下隆幅度小,灌浆中后期活性水平高。由此认为,小麦旗叶衰老和活性氧代谢特性与其温度型的归属关     

冷锻炼和ABA诱导水稻幼苗提高抗冷性期间膜保护系统的变化

冷锻炼和ＡＢＡ处理提高了水稻幼苗叶绿体ＳＯＤ和ＧＲ活性及叶片抗氧化剂ＡｓＡ和ＧＳＨ的含量,降低了膜电解质泄漏,增强了幼苗的抗冷性．等电聚焦电泳分析表明,冷锻炼和ＡＢＡ处理苗叶绿体ＳＯＤ三条同工酶带和ＧＲ１、２、３和６同工酶带都有不同程度的增强．低温胁迫后,处理和未处理首的ＳＯＤ、ＧＲ活性和ＡＳＡ、ＧＳＨ含量均有所下降．但处理苗的水平仍维持在未处理苗之上．亚胺环已酮可抑制因冷锻炼和ＡＢＡ诱导增加的ＳＯＤ和ＧＲ活性,并使叶片电解质泄漏增大．本试验结果表明冷锻炼或ＡＢＡ诱导水稻幼苗抗冷性提高时,对防御活性氧的保护系统有类似的影响。     

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。     

久效磷对扁藻的损伤作用Ⅱ.叶绿素a降解与活性氧损伤的相关性

扁藻细胞在久效磷的毒性胁迫下,随着胁迫强度的增加,叶绿素ａ降解加剧,其含量逐渐降低．分析表明,叶绿素ａ含量的降低与活性氧Ｏ２－含量、膜脂过氧化产物丙二醛（ＭＤＡ）含量及细胞的电解质外渗率呈显著负相关;而与细胞超氧化物歧化酶（ＳＯＤ）活性及过氧化物酶（ＰＯＤ）活性的降低呈显著正相关,说明久效磷胁迫下扁藻细胞叶绿素ａ降解与其活性氧的损伤有明显相关性．     

渗透胁迫下水稻幼苗中叶绿素降解的活性氧损伤作用

水稻（Ｏｒｙｚａ ｓａｔｉｖａ Ｌ．）幼苗在渗透胁迫下,随着胁迫强度的增加及时间的延长,Ｃｈｌ降解加剧,活性氧Ｏ－·２ 、Ｈ２Ｏ２ 及脂质过氧化产物丙二醛（ＭＤＡ）含量明显增加,抗氧化剂抗坏血酸（ＡｓＡ）还原型谷胱甘肽（ＧＳＨ）及胡萝卜素（ＣＡＲ）含量显著降低,叶绿素蛋白复合体（Ｃｈｌ－Ｐｒｏ）结合度松弛． Ｃｈｌ含量的降低和Ｏ－·２ 、Ｈ２Ｏ２ 及ＭＤＡ 含量呈显著的负相关,与ＡｓＡ、ＧＳＨ及ＣＡＲ含量的下降呈良好的正相关性．ＡｓＡ、α－生育酚（ＶｉｔＥ）及甘露醇预处理可使胁迫诱导的ＭＤＡ 增多及Ｃｈｌ降解延缓,而Ｆｅ２＋ 、Ｈ２Ｏ２ 及Ｆｅｎｔｏｎ 反应则刺激ＭＤＡ 增加． Ｆｅｎｔｏｎ 反应可加速Ｃｈｌ降解． 渗透胁迫下水稻幼苗Ｃｈｌ的降解可能主要是由Ｏ－·２ 和Ｈ２Ｏ２ 的代谢产物·ＯＨ氧化损伤之故     

紫外线B对水稻叶组织中活性氧代谢及膜系统的影响

增强ＵＶ－Ｂ处理下,水稻叶片的Ｏ净产生速率、Ｈ２Ｏ２和ＭＤＡ含量以及膜透性都显著增加,敏感性弱的品种Ｏ２净产生速率和膜伤害程度较低。在ＵＶ－Ｂ处理初期活性氧清除系统的水平增高,但随着处理时间的延长,ＳＯＤ、ＣＡＴ和ＡＰ活性以及ＡＳＡ含量降低,其中ＡＰ和ＳＯＤ活性的下降最为明显,而敏感性弱的品种ＳＯＤ活性始终高于敏感性强的品种。处理１４ｄ后去掉ＵＶ－Ｂ,再经则１４ｄ上述各指标均恢复到与对照相近的水平。根据这些结果推测,水稻的ＵＶ－Ｂ伤害可能主要是由于ＳＯＤ活性的降低而导致Ｏ增生和膜脂过氧化。     

UVB对水稻幼苗膜脂过氧化作用的影响

ＵＶ－Ｂ处理的水稻幼苗,叶片的膜透性、Ｏ２－净产生速率及ＭＤＡ含量显著增加。在ＵＶ－Ｂ处理初期,活性氧防御系统中的ＳＯＤ和ＣＡＴ活性比对照增强,但随着处理时间的延长,ＳＯＤ和ＣＡＴ活性明显下降;ＰＯＤ活性受ＵＶ－Ｂ处理抑制。这一结果表明,ＵＶ－Ｂ降低了细胞内活性氧自由基的清除能力,膜脂过氧化作用加剧,最终导致伤害效应。     

中性粒细胞内的NADPH氧化酶

中性粒细胞内的ＮＡＤＰＨ氧化酶周剑涛（湖北省黄冈地区卫校,４３６１００）关键词ＮＡＤＰＨ氧化酶中性粒细胞受刺激,出现呼吸突发,产生０－２、·ＯＨ、Ｏ２、Ｈ２Ｏ２等活性氧类物质。其中,Ｏ－２是ＮＡＤＰＨ氧化酶催化Ｏ２与ＮＡＤＰＨ之间发生单电子还原反应的...     

Mitochondrial damage by active oxygen species in vitro

Under in vitro conditions involving formation of active oxygen species, rat liver mitochondria were found to undergo swelling, peroxidative decomposition of lipids, and distinct disorganization of ultrastructure. Supplementation with free radical scavengers such as superoxide dismutase (SOD), methionine, histidine, and tryptophan accorded considerable protection to the organelle. A possible correlation between oxygen radicals, membrane integrity, and calcium functions is indicated.     

Increased expression of SERCA in the hearts of transgenic mice results in increased oxidation of glucose

While several transgenic mouse models exhibit improved contractile characteristics in the heart, less is known about how these changes influence energy metabolism, specifically the balance between carbohydrate and fatty acid oxidation. In the present study we examine glucose and fatty acid oxidation in transgenic mice, generated to overexpress sarco(endo)plasmic reticulum calcium-ATPase (SERCA), which have an enhanced contractile phenotype. Energy substrate metabolism was measured in isolated working hearts using radiolabeled glucose and palmitate. We also examined oxygen consumption to see whether SERCA overexpression is associated with increased oxygen utilization. Since SERCA is important in calcium handling within the cardiac myocyte, we examined cytosolic calcium transients in isolated myocytes using indo-1, and mitochondrial calcium levels using pericam, an adenovirally expressed, mitochondrially targeted ratiometric calcium indicator. Oxygen consumption did not differ between wild-type and SERCA groups; however, we were able to show an increased utilization of glucose for oxidative metabolism and a corresponding decreased utilization of fatty acids in the SERCA group. Cytosolic calcium transients were increased in myocytes isolated from SERCA mice, and they show a faster rate of decay of the calcium transient. With these observations we noted increased levels of mitochondrial calcium in the SERCA group, which was associated with an increase in the active form of the pyruvate dehydrogenase complex. Since an increase in mitochondrial calcium levels leads to activation of the pyruvate dehydrogenase complex (the rate-limiting step for carbohydrate oxidation), the increased glucose utilization observed in isolated perfused hearts in the SERCA group may reflect a higher level of mitochondrial calcium.     

Reactive oxygen-mediated contraction in pulmonary arterial smooth muscle: cellular mechanisms.

Reactive oxygen species (at least relatively high doses) cause contraction of pulmonary arterial smooth muscle. The objective of the present study was to elucidate the possible cellular mechanisms involved in reactive oxygen-mediated contraction. Isolated arterial rings from Sprague-Dawley rats were placed in tissue baths containing Earle's balanced salt solution. The maximum active force production (Po) in response to 80 mM KCl was obtained. All other responses were normalized as percentages of Po for comparative purposes. Exposure to reactive oxygen (generated from either the xanthine oxidase reaction (XO) or the glucose oxidase reaction) resulted in pulmonary arterial muscle developing mean active tension of 17.1 +/- 3.0% Po. This contraction was independent of extracellular calcium, since it was not affected by verapamil (a calcium channel blocker) or by placement of the arterial muscle in calcium-free media. Phentolamine (an alpha 1-receptor blocker) and propranolol (a beta-receptor blocker) did not diminish the response to XO. Ryanodine (a SR calcium release inhibitor), while reducing the response to norepinephrine, did not affect the response to XO. However, H-7 (an inhibitor of protein kinase C) decreased the XO-mediated contraction by 49%. These results indicate that while Ca2+ may not be involved as a second messenger, protein kinase C activity appears to play a role in the transduction pathway of reactive oxygen species mediated contraction of pulmonary arterial smooth muscle.     

The effects of haloalkene cysteine conjugates on cytosolic free calcium levels in suspensions of rat renal proximal tubules

Disturbances in intracellular calcium homeostasis may play a role in the injury induced by various haloalkene cysteine conjugates. The effects of S-(1,2,3,4,4-pentachloro-1,3-butadienyl)-L-cysteine (PCBC), S-(1,2-dichlorovinyl)-L-cysteine (DCVC), and S-(1,1,2,2-tetrafluoroethyl)-L-cysteine (TFEC) on cytosolic free calcium levels were examined in suspensions of rat renal proximal tubules. Cytosolic free calcium levels, measured with fura 2, in control tubules, were 112 +/- 3 nM and increased more than 200% within 1 minute after exposure to the calcium ionophore ionomycin (0.005 mM). PCBC (0.1 mM) increased cytosolic free calcium levels 18% after 5 minutes, while tubular oxygen consumption was unaffected. DCVC (1 mM) did not alter tubular cytosolic free calcium levels or oxygen consumption under similar conditions. TFEC (1 mM) increased cytosolic free calcium levels 36%, had no effect on basal oxygen consumption, and decreased nystatin-stimulated oxygen consumption 30% after 5 minutes. TFEC increased cytosolic free calcium levels in tubules incubated in a nominally calcium-free buffer but not in a calcium containing buffer in the presence of EGTA. The data suggest that the TFEC-induced increase in cytosolic free calcium levels may result from an influx of extracellular calcium or from inhibition of calcium efflux. The increase in cytosolic free calcium levels preceded changes in basal oxygen consumption in tubules exposed to PCBC and TFEC. This study shows that an increase in cytosolic free calcium levels is an early event following PCBC and TFEC but not DCVC exposure.     

Ca2+ binding in the active site of HincII: implications for the catalytic mechanism

The 2.8 A crystal structure of the type II restriction endonuclease HincII bound to Ca(2+) and cognate DNA containing GTCGAC is presented. The DNA is uncleaved, and one calcium ion is bound per active site, in a position previously described as site I in the related blunt cutting type II restriction endonuclease EcoRV [Horton, N. C., Newberry, K. J., and Perona, J. J. (1998) Proc. Natl. Acad. Sci. U.S.A. 95 (23), 13489-13494], as well as that found in other related enzymes. Unlike the site I metal in EcoRV, but similar to that of PvuII, NgoMIV, BamHI, BglII, and BglI, the observed calcium cation is directly ligated to the pro-S(p) oxygen of the scissile phosphate. A calcium ion-ligated water molecule is well positioned to act as the nucleophile in the phosphodiester bond cleavage reaction, and is within hydrogen bonding distance of the conserved active site lysine (Lys 129), as well as the pro-R(p) oxygen of the phosphate group 3' of the scissile phosphate, suggesting possible roles for these groups in the catalytic mechanism. Kinetic data consistent with an important role for the 3'-phosphate group in DNA cleavage by HincII are presented. The previously observed sodium ion [Horton, N. C., Dorner, L. F., and Perona, J. J. (2002) Nat. Struct. Biol. 9, 42-47] persists in the active sites of the Ca(2+)-bound structure; however, kinetic data show little effect on the single-turnover rate of DNA cleavage in the absence of Na(+) ions.     

Involvement of anion channel in signal transduction of early defense responses elicited by harpinPss in tobacco]

No matter when anion channel inhibitors, DIDS (4, 4'-diisothiocyanatostilbene-2, 2'-disulfonic acid) and A9C (anthracene-9-carboxylic acid) added (before, at the same time of or after harpinPss treatment), they can inhibit harpinPss-induced hypersensitive response in tobacco seedlings and release of active oxygen and extracellular alkalinization in tobacco suspension cells. DIDS and A9C also inhibit harpinPss-induced Ca2+ influx. In all these cases, DIDS is more efficient than A9C. It is postulated that anion channel positively regulates calcium channel in plasma membrane, and harpinPss may function through signal transduction mediated by anion channel and calcium channel to regulate cellular Ca2+ concentration and defense responses.     

THE EFFECT OF CALCIUM WITHDRAWAL ON THE STRUCTURE AND FUNCTION OF THE TOAD BLADDER

Previous reports have indicated that calcium is necessary to support active sodium transport by the toad bladder, and may be required as well in the action of vasopressin on both toad bladder and frog skin. The structure and function of the toad bladder has been studied in the absence of calcium, and a reinterpretation of the previous findings now appears possible. When calcium is withdrawn from the bathing medium, epithelial cells detach from one another and eventually from their supporting tissue. The short-circuit current (the conventional means of determining active sodium transport) falls to zero, and vasopressin fails to exert its usual effect on short-circuit current and water permeability. However, employing an indirect method for the estimation of sodium transport (oxygen consumption), it is possible to show that vasopressin exerts its usual effect on Q_oo2 when sodium is present in the bathing medium. Hence, it appears that the epithelial cells maintain active sodium transport when calcium is rigorously excluded from the bathing medium, and continue to respond to vasopressin. The failure of conventional techniques to show this can be attributed to the structural alterations in the epithelial layer in the absence of calcium. These findings may provide a model for the physiologic action of calcium in epithelia such as the renal tubule.     

Calcium-dependent allosteric modulation of the giant hemoglobin from the terrestrial oligochaete, Eisenia foetida

The effect of calcium and magnesium ions on the oxygen equilibrium of Eisenia hemoglobin was investigated by using an automatic oxygenation apparatus. On addition of calcium chloride (20 mM, pH 7.5), oxygen affinity and cooperativity (nmax) of the hemoglobin increased markedly (p 50:3.82 mmHg, nmax :9.76). The effect of magnesium on the oxygen equilibrium was weaker than that of calcium. The top asymptotes of the oxygen equilibrium curve shifted to the left by adding cations whereas the bottom asymptotes remained almost unchanged. The free energy of heme-heme interaction (delta GR,T) also increased remarkably. These results imply the binding of calcium to Eisenia hemoglobin in the oxygenated form and its physiological role in modulating the oxygen affinity and cooperativity.     

过氧化钙的净水增氧效果评估

过氧化钙作为一种新型净水剂,其净水和增氧效果尚未确定.通过研究过氧化钙对海水的化学需氧量、pH值以及氨氮的影响,从水化学的角度确定过氧化钙用量与主要水质指标变化的关系;通过过氧化钙对卤虫孵化和细菌计数,来确定过氧化钙用于净化水质的安全浓度和有效浓度,从而指导水产养殖实践中的实际用量.实验结果表明,施加0.1%的过氧化钙既可以显著降低海水中的化学需氧量和氨氮含量,提高溶解氧和pH值,同时可有效抑制细菌的繁殖,而且对卤虫孵化也是安全的.     

阴离子通道参与了harpin_(Pss)诱导的烟草细胞早期防卫反应的信号传导

无论在harpin_(Pss)之前、同时、还是之后向烟草植株或悬浮培养系加阴离子通道的抑制剂DIDS(4,4’-diisothiocyanatostilbene-2,2’-disulfonic acid)或AgC(anthracene-9-carboxylic acid),都可以抑制harpin_(Pss)诱导的烟草植株过敏反应和悬浮细胞的活性氧的释放及胞外碱性化。DIDS和A9C还可以抑制harpin_(Pss)诱导的Ca~(2 )内流。而且DIDS的抑制效率比A9C高。推测质膜上的阴离子通道对钙离子通道有着正调节作用,harpin_(Pss)通过阴离子通道和钙离子通道介导的信号传导途径,调节胞内Ca~(2 )浓度,从而启动这些防卫反应。