Effect of polyethylene glycol on lipid peroxidation in cold-stored rat hepatocytes

A mechanism suggested to cause injury to preserved organs is the generation of oxygen free radicals either during the cold-storage period or after transplantation (reperfusion). Oxygen free radicals can cause peroxidation of lipids and alter the structural and functional properties of the cell membranes. Methods to suppress generation of oxygen free radicals of suppression of lipid peroxidation may lead to improved methods of organ preservation. In this study we determined how cold storage of rat hepatocytes affected lipid peroxidation by measuring thiobarbituric acid reactive products (malondialdehyde, MDA). Hepatocytes were stored in the UW solution +/- glutathione (GSH) or +/- polyethylene glycol (PEG) for up to 96 h and rewarmed (resuspended in a physiologically balanced saline solution and incubated at 37 degrees C under an atmosphere of oxygen) after each day of storage. Hepatocytes rewarmed after storage in the UW solution not containing PEG or GSH showed a nearly linear increase in MDA production with time of storage and contained 1.618 +/- 0.731 nmol MDA/mg protein after 96 h. When the storage solution contained PEG and GSH there was no significant increase in MDA production after up to 72 h of storage and at 96 h MDA was 0.827 +/- 0.564 nmol/mg protein. When freshly isolated hepatocytes were incubated (37 degrees C) in the presence of iron (160 microM) MDA formation was maximally stimulated (3.314 +/- 0.941 nmol/mg protein). When hepatocytes were stored in the presence of PEG there was a decrease in the capability of iron to maximally stimulate lipid peroxidation. The decrease in iron-stimulated MDA production was dependent upon the time of storage in PEG (1.773 nmol/mg protein at 24 h and 0.752 nmol/mg protein at 48 h).(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparing beta-carotene,vitamin E and nitric oxide as membrane antioxidants

Singlet oxygen initiates lipid peroxidation via a nonfree radical mechanism by reacting directly with unsaturated lipids to form lipid hydroperoxides (LOOHs). These LOOHs can initiate free radical chain reactions leading to membrane leakage and cell death. Here we compare the ability and mechanism by which three small-molecule membrane antioxidants (beta-carotene, alpha-tocopherol and nitric oxide) inhibit lipid peroxidation in membranes. We demonstrate that beta-carotene provides protection against singlet oxygen-mediated lipid peroxidation, but does not slow free radical-mediated lipid peroxidation. Alpha-Tocopherol does not protect cells from singlet oxygen, but does inhibit free radical formation in cell membranes. Nitric oxide provides no direct protection against singlet oxygen exposure, but is an exceptional chain-breaking antioxidant as evident from its ability to blunt oxygen consumption during free radical-mediated lipid peroxidation. These three small-molecule antioxidants appear to have complementary mechanisms for the protection of cell membranes from detrimental oxidations.     

Effect of aluminium on lipid peroxidation, superoxide dismutase, catalase, and peroxidase activities in root tips of soybean (Glycine max)

Inhibition of root elongation and modification of membrane properties are sensitive responses of plants to aluminium. The present paper reports on the effect of AI on lipid peroxidation and activities of enzymes related to production of activated oxygen species. Soybean seedlings (Glycine max L. cv. Sito) were precultured in solution culture for 3–5 days and then treated for 1–72 h with Al (AICI₃) concentrations ranging from 10 to 75 μM at a constant pH of 4.1. In response to Al supply, lipid peroxidation in the root tips (< 2 cm) was enhanced only after longer durations of treatment. Aluminium-dependent increase in lipid peroxidation was intensified by Fe²⁺ (FeSO₄). A close relationship existed between lipid peroxidation and inhibition of root-elongation rate induced by Al and/or Fe toxicity and/or Ca deficiency. Besides enhancement of lipid peroxidation in the crude extracts of root tips due to Al, the activities of superoxide dismutase (EC 1.15.1.1) and peroxidase (EC 1.11.1.7) increased, whereas catalase (EC 1.11.1.6) activity decreased. This indicates a greater generation of oxygen free radicals and related tissue damage. The results suggest that lipid peroxidation is part of the overall expression of Al toxicity in roots and that enhanced lipid peroxidation by oxygen free radicals is a consequence of primary effects of Al on membrane structure.     

Free radicals, lipid peroxidation and muscular ischemia]

The role of oxygen free radicals in ischemia and reperfusion injury of skeletal muscle has not been well defined, partly because of the relative resistance of this tissue to normothermic ischemia. Under normal conditions small quantities of oxygen free radicals are produced but they are quenched by intracellular free radical scavenging enzymes (superoxide dismutase, catalase and glutathione peroxidase) or alpha-tocopherol. The increase in malondialdehyde suggests increased lipid peroxidation initiated by free radical reactions. Lipid peroxidation is potentially a very damaging process to the organized structure and function of membranes. The results of recent studies indicate that: a) oxygen free-radicals mediates, at least in part, the increased microvascular permeability produced by reoxygenation, b) free radical scavengers can reduce skeletal muscle necrosis occurring after prolonged ischemia. Additional evidence support the hypothesis of the interrelationship between ischemic tissue and inflammatory cells. So capillary plugging by granulocytes and oxygen free radical formation may contribute to the ischemic injury.     

间歇升温和热处理对‘紫李’果实采后生理的影响

以美国‘紫李’为试材,测定经间歇升温和热处理后果实的褐变度、抗氧化酶活性、抗氧化剂含量、膜质过氧化水平、总酚和可滴定酸含量的变化。结果表明:间歇升温和热处理可适当恢复因冷害而降低的细胞抗氧化活性,清除活性氧自由基,减少膜脂过氧化产物丙二醛的积累,抑制多酚氧化酶和过氧化物酶活性升高,强化抗低温防御系统,阻止多酚逆境代谢发生,使冷害和褐变症状得以延缓和减轻;同时,还可抑制可滴定酸含量的减少和固酸比的上升,延缓后熟衰老。间歇升温处理,李贮藏两个月果实品质良好。初步认为,-0.5～0℃贮藏,每15 d加温至18～20℃并保持l d,是贮藏美国‘紫李’适宜的变温模式。     

Oxygen free radical producing activity of polymorphonuclear leukocytes in patients with Parkinson's disease

Oxygen free radicals (OFRs) have been suggested in the pathogenesis of Parkinson's disease (PD). These free radicals exert their cytotoxic effect by peroxidation of lipid membrane resulting in the formation of malondialdehyde (MDA). Polymorphonuclear (PMN) leukocyte is one of the major sources of OFR. However, the oxygen free radical producing activity of PMN leukocytes in patients with PD is not known. We therefore studied the oxygen free radical producing activity of polymorphonuclear leukocytes and MDA levels in the serum of healthy subjects and in patients with Parkinson's disease. The oxygen free radical producing activity of PMN leukocytes in blood and the MDA content in serum were significantly higher in patients with Parkinson's disease than in healthy subjects. These results indicate a possible role of oxygen free radicals in the pathogenesis of Parkinson's disease.     

Lipid peroxidation induced by cercosporin as a possible determinant of its toxicity

The photodynamic action of cercosporin was assayed in various kinds of natural and artificial membranes. Cerosporin induces lipoperoxidation of liposomes, rat liver and pea internode mitochondria and microsomes, estimated both as malondialdehyde (MDA) formation and O2 consumption. Cercosporin-induced lipoperoxidation is inhibited by either singlet oxygen quenchers, free radical trapping agents or EDTA. Superoxide anion (O2-), hydrogen peroxide and hydroxyl radicals (.OH) are not involved in the activity of cercosporin. In addition cercosporin, by chelating iron, lowers the lipoperoxidation induced by such a metal. Therefore cercosporin stimulates, through singlet oxygen production, the hydroperoxide formation but, at the same time, it inhibits the continuation of the iron-mediated free radical chain. The present results suggest that cellular lipid peroxidation has a certain relevance to toxic activity of cercosporin.     

Effect of cisplatin, carboplatin and stobadine on lipid peroxidation of kidney homogenate and phosphatidylcholine liposomes.

The effects of the nephrotoxic, anticancer agents cisplatin (CDDP) and carboplatin (CBDCA), and the free radical scavenger, stobadine, were investigated on lipid peroxidation (LPO) of rat kidney homogenates and phosphatidylcholine (PC) liposomes. Kidney homogenates were incubated in air at 37 degrees C for 6-48 h and lipid peroxidation was detected spectroscopically as absorbance (533 nm) of the thiobarbituric acid-malondialdehyde (TBA-MDA) complex. CDDP (0.3-10 mmol.l-1) increased LPO of the homogenate. CBDCA decreased the TBA-MDA absorbance, yet was found to interfere with MDA, TBA and/or with the TBA-MDA complex. Thus when CBDCA is involved, the TBA-MDA method for detection of LPO is not suitable. Stobadine (0.1 mmol.l-1 and 1 mmol.l-1) inhibited LPO either in the control homogenate and in the homogenate where peroxidation was increased by CDDP. The effect of CDDP and CBDCA on peroxidation of PC liposomes was monitored as oxygen consumption using a Clark-type oxygen electrode. CDDP increased but CBDCA decreased the rate of oxygen consumption during the peroxidation of liposomes induced by FeSO4. The results suggest that the effects of CDDP and CBDCA on LPO may be linked with their nephrotoxicity.     

5-methoxytryptophol preserves hepatic microsomal membrane fluidity during oxidative stress

Lipid peroxidation is a degenerative chain reaction in biological membranes that may be initiated by exposure to free radicals. This process is associated with changes in the membrane fluidity and loss of several cell membrane-dependent functions. 5-methoxytryptophol (ML) is an indole isolated from the mammalian pineal gland. The purpose of this study was to investigate the effects of ML (0. 01mM-10mM) on membrane fluidity modulated by lipid peroxidation. Hepatic microsomes obtained from rats were incubated with or without ML (0.01-10 mM). Then lipid peroxidation was induced by FeCl(3), ADP, and NADPH. Membrane fluidity was determined using fluorescence spectroscopy. Malonaldehyde (MDA) +4-hydroxyalkenals (4-HDA) concentrations were estimated as an indicator of the degree of lipid peroxidation. With oxidative stress, membrane fluidity decreased and MDA+4-HDA levels increased. ML (0.01-3 mM) reduced membrane rigidity and the rise in MDA+4-HDA formation in a concentration-dependent manner. 10 mM ML protected against lipid peroxidation but failed to prevent the membrane rigidity. In the absence of oxidative reagents, ML (0.3-10 mM) decreased membrane fluidity whereas MDA+4-HDA levels remained unchanged. This indicates that ML may interact with membrane lipids. The results presented here suggest that ML may be another pineal indoleamine (in addition to melatonin) that resists membrane rigidity due to lipid peroxidation.     

The effect of oxygen radicals on rat thymocyte glucose transport is independent of the site of their generation

We studied the relationship between the site of production of oxygen radicals and their effect on a rat thymocyte functional activity, the glucose transport, measured using a radioactive analogue of glucose, 2-deoxy-glucose. We compared the effects of a hydrophilic thermolabile azo compound, mimicking a radical attack outside the cell, with the lipid-soluble cumene hydroperoxide, which initiates lipid peroxidation in cell membranes. Our results show that a low grade oxidative stress stimulated glucose uptake rapidly, independently of the site of radical generation. In the presence of the azocompound, glucose uptake increased smoothly, attaining its maximum extent within 1 h. In thymocytes treated with cumene hydroperoxide the rate of glucose transport increased suddenly and remained constant over 1 h. The effects of the radical donors on TBARS production and protein sulfhydryl groups content were also evaluated. In thymocytes treated with the azo derivative no lipid peroxidation was observed, but a slow decrease of protein thiol groups occurred; after the addition of cumene hydroperoxide sulfhydryl groups did not change and TBARS increased significantly. The water-soluble antioxidant Trolox was able to remove the glucose uptake increase induced by the hydrophilic initiator and to delay the loss of membrane integrity.     

Measurement of doxorubicin-induced lipid peroxidation under the conditions that determine cytotoxicity in cultured tumor cells.

We have investigated doxorubicin-induced lipid peroxidation by the measure of malondialdehyde (MDA) formation in rat glioblastoma cells and human breast carcinoma cells in culture. There was a significant production of MDA when the cells were incubated with pharmacologically relevant doxorubicin concentrations, i.e., concentrations that produce a significant cytotoxicity (0.1 micrograms/ml). At equitoxic doses, vincristine provided no lipid peroxidation, indicating that MDA formation is not a consequence of cell death. Doxorubicin-induced lipid peroxidation was maximal 24 h after incubation of the cells with doxorubicin, indicating that a delay was necessary for the free radical-mediated membrane damage induced by doxorubicin. In the presence of alpha-tocopherol in the culture medium, the doxorubicin-induced MDA formation was inhibited. The development of this method will help in defining the role of free radicals and lipid peroxidation in the cytotoxicity of doxorubicin.     

Evidence for Oxidative Stress in the Subthalamic Nucleus in Progressive Supranuclear Palsy

Increased free radical production and oxidative stress have been proposed as pathogenic mechanisms in several neurodegenerative disorders. Free radicals interact with biological macromolecules, such as lipids, which can lead to lipid peroxidation. A well-established marker of oxidative damage to lipids is malondialdehyde (MDA). We measured tissue MDA levels in the subthalamic nucleus (STN) and cerebellum from 11 progressive supranuclear palsy (PSP) cases and 11 age-matched control cases using sensitive HPLC techniques. In PSP, a significant increase in tissue MDA levels was observed in the STN when compared with the age-matched control group. By contrast, no significant difference between tissue MDA content was observed in cerebellar tissue from the same PSP and age-matched control cases. These results indicate that lipid peroxidation may play a role in the pathogenesis of PSP.     

Acidic pH amplifies iron-mediated lipid peroxidation in cells

The goal of our study was to investigate the mechanism by which changes in extracellular pH influence lipid peroxidation processes. Ferrous iron can react with hydroperoxides, via a Fenton-type reaction, to initiate free radical chain processes. Iron is more soluble at lower pH values, therefore we hypothesized that decreasing the environmental pH would lead to increased iron-mediated lipid peroxidation. We used Photofrin, a photosensitizer that produces singlet oxygen, to introduce lipid hydroperoxides into leukemia cells (HL-60, K-562, and L1210). Singlet oxygen reacts with the PUFA of cells producing lipid hydroperoxides. Using EPR spin trapping with POBN, free radical formation from HL-60 cells was only detected when Photofrin, light, and ferrous iron were present. Free radical formation increased with increasing iron concentration; in the absence of extracellular iron, radical formation was below the limit of detection and lipid hydroperoxides accumulated in the membrane. In the presence of iron, lipid-derived radical formation in cells is pH dependent; the lower the extracellular pH (7.5-5.5), the higher the free radical flux; the lower the pH, the greater the membrane permeability induced in K-562 cells, as determined by trypan blue dye exclusion. These data demonstrate that lipid peroxidation processes, mediated by iron, are enhanced with decreasing extracellular pH. Thus, acidic pH not only releases iron from "safe" sites, but this iron will also be more damaging.     

Iron-induced peroxidative injury to isolated rat hepatic mitochondria

Peroxidative injury to the mitochondrial inner membrane with resultant defects in oxidative metabolism may be partially responsible for hepatocellular injury in iron overload. We examined the effects of iron-induced lipid peroxidation in vitro on hepatic mitochondrial morphology and function and determined if various inhibitors of free-radical-mediated injury could be protective. Normal rat liver mitochondria were prepared by differential centrifugation and were incubated with 1, 2, and 3 μM Fe²⁺, NADPH, and with and without oxygen radical scavengers, iron chelators, and antioxidants. There was a direct linear relationship between the concentration of added iron and the degree of lipid peroxidation as measured by malondialdehyde (MDA) production (r =.85). With 3 μM Fe²⁺ there was a decrease in the respiratory control ratio (RCR) for all four substrates tested; this decrease in RCR was due to a decrease in the state 3 respiratory rate for all substrates, with no changes in the state 4 respiratory rate for glutamate, β-hydroxybutyrate, or succinate. Oxygen radical scavengers failed to prevent iron-induced lipid peroxidation or to protect against associated mitochondrial dysfunction. Iron chelators and antioxidants prevented MDA formation and mitochondrial function was maintained. Iron-induced lipid peroxidation in vitro produces an irreversible inhibitory defect in mitochondrial electron transport that may be specific at complex IV (cytochrome oxidase).     

Cadmium-induced excretion of urinary lipid metabolites,DNA damage,glutathione depletion,and hepatic lipid peroxidation in sprague-dawley rats

Recent studies have described lipid peroxidation to be an early and sensitive consequence of cadmium exposure, and free radical scavengers and antioxidants have been reported to attenuate cadmium-induced toxicity. These observations suggest that cadmium produces reactive oxygen species that may mediate many of the untoward effects of cadmium. Therefore, the effects of cadmium (II) chloride on reactive oxygen species production were examined following a single oral exposure (0.50 LD₅₀) by assessing hepatic mitochondrial and microsomal lipid peroxidation, glutathione content in the liver, excretion of urinary lipid metabolites, and the incidence of hepatic nuclear DNA damage. Increases in lipid peroxidation of 4.0- and 4.2-fold occurred in hepatic mitochondria and microsomes, respectively, 48 h after the oral administration of 44 mg cadmium (II) chloride/kg, while a 65% decrease in glutathione content was observed in the liver. The urinary excretion of malondialdehyde (MDA), formaldehyde (FA), acetaldehyde (ACT), and acetone (ACON) were determined at 0–96 h after Cd administration. Between 48 and 72 h posttreatment maximal excretion of the four urinary lipid metabolites was observed with increases of 2.2- to 3.6-fold in cadmium (II) chloride-treated rats. Increases in DNA single-strand breaks of 1.7-fold were observed 48 h after administration of cadmium. These results support the hypothesis that cadmium induces production of reactive oxygen species, which may contribute to the tissue-damaging effects of this metal ion.     

Effect of bacterial lipopolysaccharide on the content of lipid peroxidation products in lungs and other organs of mice

The influence of lipopolysaccharide fromEscherichia coli (LPS, 17 mg/kg body weight) on the lipid peroxidation process in organs of mice was studied. The content of conjugated dienes (CD), lipid peroxides (LP), malondialdehyde (MDA) (all three lipid peroxidation by-products), peroxidase (PO) activity and wet-to-dry weight ratio in lungs, heart, spleen, kidneys and liver were determined 1.5 h after intravenous injection of LPS. Animals observed at this time-point had reduced activity and decreased body temperature by about 2°C, however, all analysed organs did not reveal any changes of wet-to-dry weight ratio comparing to organs from mice injected with sterile, pyrogen free 0,9% NaCl. Only extracts from heart and lungs showed significant increase in the tissue level of at least two lipid peroxidation products. The heart content of CD, MDA, and LP was about 1.5-, 1.3-, and 2.4-fold higher than in control group. In lungs CD and MDA increased 3.3- and 1.3-times but in spleen only content of LP was elevated. In these organs the suppression of PO activity was also observed. Liver and kidneys did not reveal any convincing enhancement of lipid peroxidation process and alterations of PO activity. Since free radical reactions are involved in lipid peroxidation process and inactivation of PO these results suggest that heart, lungs and spleen are the organs mostly exposed to oxidative stress during the first 1.5 h after single injection of LPS in mice.Abbreviations CD conjugated dienes - LP lipid peroxides - LPS lipopolysaccharide - MDA malondialdehyde - PMNL polymorphonuclear leukocytes - PO peroxidase - TBA thiobarbituric acid     

冷藏条件下白沙枇杷与红沙枇杷果皮活性氧代谢研究

为探讨红沙枇杷与白沙枇杷冷藏耐储性差异的原因,为枇杷采后生理和保鲜技术研究提供参考,以白沙枇杷"白玉"和红沙枇杷"鸡蛋红"为材料,在6℃的冷藏条件下,测定了果皮中氧自由基产生速率(oxygenfree radical production rate, SPR)、超氧化物歧化酶(SOD)、过氧化物酶(POD)和过氧化氢酶(CAT)等保护酶活性,以及膜脂过氧化伤害产物(MDA)的含量等活性氧(reactive oxygen species, ROS)代谢相关指标的变化规律。表明,随着冷藏的进程,冷藏的前10 d,红沙枇杷果皮SPR高于白沙枇杷,10 d后红沙枇杷果皮SPR有所下降而白沙枇杷果皮则大幅上升,导致10 d后红沙枇杷果皮SPR低于白沙枇杷;冷藏后红沙枇杷果皮ROS相关酶(SOD, POD和CAT)活性高于白沙枇杷果皮,即其ROS清除能力高于白沙枇杷果皮;在冷藏5 d后白沙枇杷果皮膜脂过氧化伤害产物MDA含量持续上升,而红沙枇杷果皮则维持在较低水平并低于白沙枇杷果皮,说明白沙枇杷果皮膜脂过氧化程度较高。分析认为冷藏初期红沙枇杷果皮较高的氧自由基产生速率激活了ROS清除系统,导致红沙枇杷果皮具有更高的ROS清除能力;冷藏后期白沙枇杷果皮则出现了氧自由基和MDA的积累,暗示其膜脂过氧化的发生和果实内外环境的恶化。红沙枇杷和白沙枇杷果皮ROS代谢的差异与冷藏耐储性相关。     

Intestinal mucosal lipid peroxidation and absorptive function In Salmonella typhimurium mediated intestinal infection

S. typhimurium infection is associated with neutrophil infiltration within the intestinal mucosa. Neutrophil activation provides a major source of reactive oxygen species (ROS). The mucosal pathology of S. typhimurium infection may be in part due to the excessive production of these reactive species. This study was carried out to investigate if ROS play a role in mediating the changes in the structural components and functional properties of brush border membrane (BBM) in rats during S. typhimurium infection. This was done by determining the changes in the BBM extent of lipid peroxidation and absorptive function. A significant increase in the extent of lipid peroxidation of BBM during S. typhimurium infection was observed as judged by malondialdehyde (MDA) and conjugated diene formation and depletion of -tocopherol and protein associated thiol groups. A significant decrease in the BBMV (brush border membrane vesicle) transport of amino acids was also observed. However there was no change in the transport of D-glucose. The decrease in amino acid transport further led to a significant decrease in the enterocyte level of protein synthesis. Exposure of BBMV to a free radical donor, cumene hydroperoxide, also led to an increase in the extent of lipid peroxidation and a decrease in the amino acid transport. Possibly ROS might play a significant role in mediating the mucosal damage during S. typhimurium infection.     

Maintenance of left ventricular function (90%) after twenty-four-hour heart preservation with deferoxamine.

During 24-h in vitro heart preservation and reperfusion, irreversible tissue damage occurs caused by reactive oxygen intermediates, such as superoxide radicals, singlet oxygen, hydrogen peroxide, hydroperoxyl, hydroxyl radicals, as well as the peroxynitrite radical. Reduction of the related oxidative damage of reperfused ischemic tissue by free radical scavengers and metal chelators is of primary importance in maintaining heart function. We assessed whether deferoxamine (DFR) added to a cardioplegia solution decreased free radical formation during 24-h cold (5 degrees C) heart preservation and normothermic reperfusion (37 degrees C) in the Langendorff isolated perfused rat heart. The deferoxamine treated hearts were significantly (p less than .001) better preserved than the control hearts after 24 h of preservation with regard to recovery of left ventricular diastolic pressure, contractility (+dP/dt), relaxation (-dP/dt), creatine kinase release, and lipid peroxidation. DFR preserved cell membrane integrity and maintained 93% of left ventricular contractility. The evidence suggests that DFR reduces lipid peroxidation damage by reducing free radical formation and thereby maintaining normal coronary perfusion flow and myocardial function.     

海滨沙滩单叶蔓荆对沙埋的生理响应特征

海滨沙滩单叶蔓荆(Vitex trifolia L.var.simplicifolia)是优良的抗沙埋地被植物.以烟台海岸沙地单叶蔓荆为材料,通过不同厚度沙埋过程中沙上和沙下叶片抗逆生理指标的测定以揭示其抗沙埋生理调控机制.结果表明,轻度和中度沙埋5d,成株和幼株整株叶片细胞膜透性增大、POD和SOD活力增高、MDA和脯氨酸含量和叶片相对含水量(RWC)增加、可溶性糖含量下降.但同株沙上叶片细胞膜透性、MDA含量、SOD和POD活力和可溶性糖含量均高于沙下,而沙上叶片脯氨酸含量低于沙下叶片.在轻度和中度沙埋lOd,沙上叶片细胞膜透性、MDA和可溶性糖含量、叶片POD活力降低,叶片SOD活力仍有小幅度增高,但脯氨酸含量增加,沙上叶片生长旺盛.研究表明,沙埋下叶片抗氧化酶活力和脯氨酸含量与细胞膜透性和膜脂过氧化成正相关.沙埋使植株上部叶片接近沙表面而经受干旱和地面热辐射胁迫引起细胞膜脂过氧化加剧和细胞膜透性加大.同时沙埋也使沙下叶片遭遇黑暗和缺氧胁迫诱导细胞内膜脂过氧化,但也激活了叶片抗氧化酶保护系统和叶片脯氨酸的积累抑制细胞膜脂过氧化维护细胞膜的稳定.因此在沙埋过程中,叶片快速响应沙埋胁迫激活叶片抗氧化酶系统抑制膜脂过氧化作用维持氧自由基和抗氧化酶系统的动态平衡在单叶蔓荆适应轻度和中度沙埋,维护沙上叶片旺盛生长中起重要作用,也是重度全埋下沙下植株茎顶端能快速延伸弯曲生长最后顶出沙面再生的主要生理保护原因.