谷胱甘肽的抗线粒体脂质过氧化作用

谷胱甘肽是细胞内重要的抗氧化损伤物质之一．以NADH诱导的牛心肌线粒体脂质过氧化体系为模型,研究了谷胱甘肽的抗氧化作用．结果表明,一定浓度的谷胱甘肽能够部分抑制该体系中线粒体的脂质过氧化．保护组的丙二醛含量为损伤组72．5％;线粒体的膨胀度较损伤组降低;细胞色素C氧化酶及ATP酶活力分别较损伤组提高了1．5及2．2倍．     

谷胱甘肽的抗线粒体脂质过氧化作用

谷胱革肽是细胞内重要的抗氧化损伤物质之一,以ＮＡＤＨ诱导的牛心肌线粒体脂质过氧化体系为模型,研究了谷胱甘肽的抗氧化作用。结果表明,一定浓度的谷胱甘肽能够部分抑制该体系中线粒体的脂质过氧化,保护组的丙二醛含量为损伤组７２．５％;线粒体的膨胀度较损伤组降低;细胞色素ｃ氧化酶及ＡＴＰ酶活力分别较损伤组提高了１．５及２．２倍。     

水稻叶片的衰老与超氧物歧化酶活性及脂质过氧化作用的关系

研究了从抽穗开花到籽粒成熟过程中,水稻植株顶部三片叶子的超氧物歧化酶(SOD),脂质过氧化产物丙二醛(MDA)含量及二磷酸核酮糖羧化酶活性的变化。实验结果表明:叶片的衰老伴随着 SOD 活性、RuBP 羧化酶活性及叶绿素含量的降低、丙二醛含量显著增高。分离了三个 SOD 的同工酶,证明为 Cu—Zn SOD。观察了 SOD 同工酶在叶片老化及酶液存放不同时间中的变化。讨论了叶片衰老过程中氧自由基对酶及质膜的损伤影响。     

铁镉互作对水稻脂质过氧化及抗氧化酶活性的影响

利用营养液培养方法,以‘沈农265’为供试品种,研究不同Fe(0、0.1、0.25、0.5mmolFe2+·L-1)、Cd(0、0.1、1.0μmolCd2+·L-1)处理对水稻植株体内脂质过氧化及抗氧化酶活性的影响.结果表明:单独供应Fe显著降低了水稻地上部和根系生物量,同时供应Cd后生物量不再下降;单独供应Cd降低了根系中丙二醛(MDA)和可溶性蛋白含量,而同时供应Fe时这种降低作用消失.Fe处理降低了水稻地上部和根系Cd含量,Cd处理也降低了Fe含量,两者表现出明显的相互抑制作用.高Cd(1.0μmol·L-1)和Fe互作,增加了水稻根系中MDA和可溶性蛋白含量,降低了超氧化物岐化酶(SOD)和过氧化氢酶(CAT)活性.表明在低Cd环境中为水稻提供一定数量的外源Fe能降低植株Cd含量;但高Cd胁迫将降低水稻对Fe的吸收,并导致植株体内产生脂质过氧化.     

铁镉互作对水稻脂质过氧化及抗氧化酶活性的影响

利用营养液培养方法,以‘沈农265’为供试品种,研究不同Fe(0、0.1、0.25、0.5 mmol Fe²⁺·L^-1 )、Cd(0、0.1、1.0 μmol Cd²⁺·L^-1)处理对水稻植株体内脂质过氧化及抗氧化酶活性的影响.结果表明： 单独供应Fe显著降低了水稻地上部和根系生物量,同时供应Cd后生物量不再下降;单独供应Cd降低了根系中丙二醛(MDA)和可溶性蛋白含量,而同时供应Fe时这种降低作用消失.Fe处理降低了水稻地上部和根系Cd含量,Cd处理也降低了Fe含量,两者表现出明显的相互抑制作用.高Cd(1.0 μmol·L^-1)和Fe互作,增加了水稻根系中MDA和可溶性蛋白含量,降低了超氧化物岐化酶(SOD)和过氧化氢酶(CAT)活性.表明在低Cd环境中为水稻提供一定数量的外源Fe能降低植株Cd含量;但高Cd胁迫将降低水稻对Fe的吸收,并导致植株体内产生脂质过氧化.     

黄芪对肠缺血／再灌注时脂质过氧化损伤的防护作用及其机制

目的：探讨黄芪对肠缺血／再灌注（I／R）时脂质过氧化损伤的防护作用及其机制。方法：检测红细胞膜和组织匀浆丙二醛（MDA）含量以及红细胞超氧化物歧化酶（SOD）活性。结果：黄芪可使MDA含量降低,且可防止SOD减少,与1／R组比较均P〈0．01。结论：肠I／R过程中体内脂质过氧化过程加强,黄芪通过抗脂质过氧化作用能稳定细胞膜,减轻组织损伤,延缓I／R损伤的进行性加剧。     

镉致黑斑蛙肝脏氧化损伤与金属硫蛋白含量的变化

为观察镉对黑斑蛙(Rana nigromaculata)肝脏脂质过氧化产物和金属硫蛋白含量的影响,将黑斑蛙暴露于10.0mg·mL-1浓度的镉溶液中30d,分别测定了黑斑蛙在暴露4、10d和30d时肝脏组织中镉(Cd)、还原型谷胱甘肽(GSH)、金属硫蛋白(MT)和过氧化产物丙二醛(MDA)的含量。实验结果表明,黑斑蛙肝脏中镉的积累量、GSH和MT含量均随着镉暴露时间的延长而显著升高,具有明显的时间-效应关系;在镉暴露的第10天,肝MDA含量明显高于对照组。提示镉可对黑斑蛙肝脏造成氧化损伤,而GSH、MT含量的升高则可能是机体抗氧化损伤的机理之一。     

碘乙酸抑制SeGSHPx对RBC膜脂质过氧化速率的影响及硒甲硫氨酸和V_E的保护作用

 本文用碘乙酸抑制SeGSHPx观察其对RBC膜的脂质过氧化速率的影响以及硒甲硫氨酸和V_E的保护作用。结果说明,同一V_E含量的RBC随着SeGSHPx抑制程度的增加脂质过氧化速率增加;同一SeGSHPx抑制状态的RBC随着V_E含量的降低脂质过氧化速率增加,反映了V_E和SeGSHPx在协同地保护细胞免受脂质过氧化损伤,当细胞的抗氧化保护系统处于低能状态时,不论是由于V_E含量降低或SeGSHPx活性降低或二者兼有,补充V_E和应用能提高SeGSHPx活性的含硒制剂,都能有一定的保护作用。     

脂质体过氧化对DNA的损伤研究

研究了以脂质体为材料的脂质过氧化引起的ＥＮＡ损伤,同时检测了脂质过氧化程度与ＤＮＡ受损情况。结果表明：在脂质体过氧化程度中,ＤＮＡ的增色效应,对核酸酶的敏感程度,ＤＮＡ双链百分含量和ＤＮＡ－溴乙锭复合物的荧光强度随着氧化时间的增加而降低。在四种碱基中,鸟嘌呤损伤最严重。多种自由基清除列实验表明：脂质过氧化所产生的羟基自由基和单线态氧可能是引起ＤＮＡ氧化损伤的重要因素。     

氯化钾或谷氨酸对人神经母细胞瘤SH-SY5Y细胞钙离子通透性的影响

用人神经母细胞瘤SH-SY5Y细胞系作为研究对象,通过测定细胞存活率(MTT法)和脂质过氧化代谢产物丙二醛(MDA),探讨了氯化钾(KCl)或谷氨酸分别对入神经母细胞瘤SH-SY5Y细胞的损伤作用。结果发现在含Ca     

Inhibition of zinc absorption by iron depends on their ratio

Previous studies upon zinc-iron interactions gave conflicting results that could come from differences in protocol design or in trace element status of subjects. The present work assessed the influence of zinc : iron ratio and iron deficiency upon zinc absorption. The digestive absorption of zinc sulphate (100 mol Zn/l) in presence of iron gluconate was studied in perfused jejunal loops (n = 6/group) of normal rats (range 0–1000 mol Fe/l) and iron deficient rats (200–750 mol Fe/l). In normal rats no significant iron inhibition on zinc absorption occurred at Fe:Zn ratio below 2:1. At higher ratios zinc uptake and net absorption decreased significantly (p<0.05). Between 2:1 and 5:1 a dose dependent inhibition of zinc absorption occurred and reached a plateau beyond this ratio. In iron deficient animals no changes in zinc uptake, mucosal retention and absorption compared to normal animals occurred at ratio 2:1. At higher ratios differences were observed at every zinc absorption step except for mucosal retention at 7.5:1 ratio.

Iron-zinc interactions depend on their ratio and on previous trace elements status of subjects. Due to the wide and unknown variations that were likely to occur between the subjects of previous human and experimental studies, these results could explain some of the discrepancies between their results.     

Zinc-alleviating effects on iron-induced phytotoxicity in roots of <Emphasis Type="Italic">Triticum aestivum</Emphasis>

The mechanisms of growth inhibition and antioxidative response were investigated in wheat roots exposed to 300 μM iron together with different zinc concentrations (0, 50, and 250 μM). All Zn concentrations decreased Fe content but increased Zn content in the roots and leaves of Fe-treated seedlings. Compared with Fe stress alone, 50 or 250 μM Zn + Fe treatment stimulated root growth, and increased cell viability but decreased malondialdehyde content, which were correlated with the decreases of total and apoplastic hydrogen peroxide and superoxide anion radical (O₂ ^·?) content along with apoplastic hydroxyl radical content. Generation of O₂ ^·? in response to 10 μM diphenylene iodonium suggested that NADPH oxidase activity was lower in Zn + Fe-treated roots than in other roots. In addition, cell wallbound peroxidase, diamine oxidase, and polyamine oxidase in Fe-treated roots were insensitive to Zn addition. Further study showed the stimulation of total superoxide dismutase and glutathione reductase (GR) activities as well as apoplastic catalase, ascorbate peroxidase, and GR in Zn + Fe-stressed roots in comparison with Fe-alone-treated ones. Taken together, Zn could alleviate iron-inhibitory effect on root growth, which might be associated with the decrease of lipid peroxidation, the increase of cell viability and the reductions of reactive oxygen species generation.     

Effects of zinc and/or iron deficiency on rectal temperature in rats

O'Dell et al. reported that rectal temperature was decreased by zinc deficiency in rats. However, it is not known whether a combined deficiency of zinc and iron affects rectal temperature. Forty 4-wk-old male Sprague-Dawley rats were assigned into four dietary treatment groups of 10 rats each for the 4-wk study: zinc-deficient group (4.5 mg Zn and 35 mg Fe/kg diet; −Zn), iron-deficient group (30 mg Zn/kg diet, no supplemental iron; −Fe), zinc/iron-deficient group (4.5 mg Zn/kg diet, no supplemental iron; −Zn−Fe), and control group (AIN-93G; Cont). At d 24–27, the rectal temperature was determined. The rectal temperature of the −Zn group was significantly lower than the Cont group. The rectal temperature of the −Zn−Fe group was similar to that of the Cont group, although thyroid-stimulating hormone and total thyroxin concentrations were the lowest in the −Zn−Fe group among all groups. The pattern of the plasma nitrate/nitrite concentrations across groups was similar to rectal temperature. Although observation of the rectal temperature is not conclusive, the balance between zinc and iron intake seems to determine the body temperature set point. These results suggest that the thermogenic effect of thyroid hormones is not throught to influence the paradoxical maintenance of rectal temperature in combined deficiency of zinc and iron.     

Zinc deficiency decreases plasma erythropoietin concentration in rats

In 1985, Paterson and Bettger found hypoplastic hematopoiesis in severely zinc-deficient rats. Therefore, we investigated plasma erythropoietin concentration in zinc-deficient rats. Forty 4-wk-old male Sprague-Dawley rats were assigned into 4 dietary treatment groups of 10 for the 4-wk study: zinc-deficient group (4.5 mg zinc and 35 mg iron/kg; −Zn), iron-deficient group (30 mg zinc/kg, no supplemental iron; −Fe), zinc/iron-deficient group (4.5 mg zinc/kg, no supplemental iron; −Zn−Fe), and control group (AIN-93G; Cont). Water intake determined at d 19 was similar among all treatment groups. At d 27–28, bioimpedance was measured. The intracellular water/extracellular water ratio was significantly increased in the −Zn group (p<0.05). Compared to the Cont, group, the plasma erythropoietin concentration was increased by iron deficiency and decreased by zinc deficiency (p<0.01). Hematocrit was significantly decreased in both the −Fe and −Zn−Fe groups and was significantly increased in the −Zn group (p<0.01). Transferrin saturation in the −Fe and −Zn−Fe groups was significantly lower than the Cont group (p<0.01), and that of the −Zn group was highest among all groups. The low plasma erythropoietin concentration might account for depressed hematopoiesis associated with zinc deficiency.     

Coexistence of zinc and iron augmented oxidative injuries in the nigrostriatal dopaminergic system of SD rats

Clinical studies have demonstrated an excess of transition metals, including zinc and iron, in the substantia nigra (SN) of Parkinson's patients. In the present study, the neurotoxic effect of zinc was investigated using iron as a positive control. Addition of zinc or iron to brain homogenates increased lipid peroxidation. Zinc was less potent than iron in inducing lipid peroxidation. Coincubation with desferrioxamine prevented zinc- and iron-induced lipid peroxidation. Furthermore, glutathione (GSH), S-nitroso-N-acetylpenicillamine, or melatonin inhibited zinc-induced lipid peroxidation. The oxidative effect of zinc was further investigated in anesthetized rats. Seven days after intranigral infusion of zinc, lipid peroxidation was elevated in the infused SN, and dopamine content and tyrosine hydroxylase-positive axons were decreased in the ipsilateral striatum. Zinc was less potent than iron in inducing neurodegeneration in vivo. L-Buthionine-[S,R]-sulfoximine pretreatment (i.c.v.), which depletes cellular GSH levels, enhanced zinc-induced oxidative injuries in the nigrostriatal dopaminergic system. Moreover, simultaneous infusion of zinc and iron appeared to augment oxidative injuries in rat brain. Taken together, our results demonstrate that intranigral infusion of zinc caused degeneration of the nigrostriatal dopaminergic system in rat brain. Furthermore, coexistence of zinc and iron augmented oxidative injuries in rat brain. These findings indicate that both zinc and iron contribute to the etiology of Parkinsonism.     

Trace element levels in the experimental peritonitis

Electron transfer from iron or copper ions to oxygen is an important example of cellular free radical initiation. Oxygen derived free radicals have been implicated as mediators of cellular injury in several model systems. To evaluate the importance of iron, copper and zinc levels on lipid peroxidation in peritonitis, we measured peritoneum malondialdehyde (MDA) as a marker of lipid peroxidation, zinc, copper, and iron levels during an animal model of intraperitoneal sepsis. Additionally the effects of the free radical scavenger alpha-tocopherol administration was studied. The peritoneum MDA, iron, copper and zinc levels were increased after induction of peritonitis with Escherichia Coli. The treatment with alpha-tocopherol was decreased the peritoneum MDA, iron and copper levels significantly, except the zinc level (p < 0.001, p < 0.001, p < 0.001, respectively). Additionally the alpha-tocopherol treatment for three days prior to injection of E.Coli more decreased MDA, copper and iron levels than that of the treatment with alpha-tocopherol at the time of injection of E. Coli (p < 0.001, p < 0.001, p<0.001, respectively). Our results indicated that copper, iron and zinc had important effects on peroxidation events in E. Coli induced peritonitis, and alpha-tocopherol treatment can improve the oxidant status.     

Lipid Peroxidation and Changes of Trace Elements in Mice Treated with Paradichlorobenzene

Paradichlorobenzene (pDCB) has been used as a space deodorant and moth repellant, as well as an intermediate in the chemical industry. Given its broad applications and high volatility, considerable concern exists regarding the adverse health effects of pDCB in the home and the workplace. In this study, changes in lipid peroxidation, antioxidants, and trace element levels in the liver and kidney of pDCB-treated mice were investigated to determine their roles in toxicity. Mice were orally gavaged once daily for seven consecutive days with pDCB (0 (corn oil control), 450, and 900 mg/kg). The level of malondialdehyde (MDA), an end product of lipid peroxidation, markedly increased in the high-dose pDCB group in both the liver and kidney compared with the control group. Changes in hepatic levels of reduced glutathione (GSH) in the pDCB groups were indistinguishable from the control group, while renal levels of reduced GSH in the high-dose pDCB group were significantly lowered in comparison to the control and the low-dose groups. Superoxide dismutase (SOD) activity in the liver of mice treated with pDCB showed a downward trend, whereas there was no consistent trend associated with changes in SOD activity in the kidney. Additionally, renal iron levels in the high-dose pDCB group were significantly decreased compared with the low-dose group and the controls, whereas hepatic iron content in the low-dose pDCB group was significantly lower compared with the controls. Selenium and zinc levels in the kidney were both significantly decreased in the high-dose pDCB group vs. the control and low-dose groups. There were no treatment-induced changes in copper levels in either the kidney or liver. However, a significant increase was found in the liver zinc/copper ratio in the high-dose pDCB group vs. the controls. In addition, blood zinc levels showed a downward trend with increased pDCB dosage. These results suggest that pDCB toxicity is mediated by oxidative damage and tissue-specific alterations in trace element levels both in the liver and the kidney of mice.     

Antioxidant properties of chromium and zinc: in vivo effects on digestibility,lipid peroxidation,antioxidant vitamins,and some minerals under a low ambient temperature

The effects of chromium (chromium picolinate, CrPic) and zinc (ZnSO(4)H(2)O) supplementation on serum concentrations of malondialdehyde (MDA) (an indicator of lipid peroxidation) and serum status of some antioxidant vitamins and minerals of laying hens (Hy-Line) reared at a low ambient temperature (6.8 degrees C) were evaluated. One hundred twenty laying hens (Hy-Line; 32 wk old) were divided into 4 groups, 30 hens per group. The hens were fed either a basal diet or the basal diet supplemented with either 0.4 mg Cr/kg of diet, 30 mg Zn/kg of diet, or 0.4 mg Cr plus 30 mg Zn/kg of diet. Digestibility of nutrients (dry matter [DM], organic matter [OM], crude protein [CP], and ether extract [EE]) increased by supplementation of chromium and zinc (p < 0.05). Supplemental chromium and zinc increased serum vitamins C and E but decreased MDA concentrations (p < 0.05). Additionally, supplemental chromium and zinc caused an increase in the serum concentrations of Fe, Zn, Mn, and Cr (p < 0.05). The present study showed that low ambient temperature causes detrimental effects on the digestibility of nutrients and antioxidant status and that such detrimental effects caused by low ambient temperature can be alleviated by chromium and zinc supplementation, particularly when Cr and Zn were simultaneously included into the diet. Data obtained in the present study suggest that such supplementation can be considered as a protective management practice in a diet of laying hens for alleviating negative effects of cold stress.     

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。     

Effect of magnesium deficiency on enterocyte Ca, Fe, Cu, Zn, Mn and Se content

In previous studies based on indirect procedures, we reported that Mg deficit increased the bioavailability of a number of elements such as calcium, zinc, iron, copper, manganese and decreased selenium absorption. The present study was designed to verify these findings by direct methods. We investigated the effect of dietary magnesium deficiency on enterocyte Ca, Fe, Zn, Cu, Mn and Se concentrations. Male Wistar rats were fed a Mg-deficient diet (129 mg Mg/kg food) for 70 days. Whole enterocytes from the upper jejunum were isolated and Ca, Fe, Zn, Cu, Mn and Se were determined. The results were compared with findings in a control group that was pair-fed with an identical diet except that it covered this species's nutritional requirements for Mg (480 mg Mg/kg food). The Mg-deficient diet significantly increased enterocyte content of Ca, Fe, Zn, Cu and Mn; however, we found no significant changes in the Se content of these cells. These data support the results obtained by indirect methods.