Dietary Modulation of Plasma Bilirubin and of Hepatic Microsomal Lipid Peroxidation in the Gunn Rat

An in vitro assay for the simultaneous measurement of lipid peroxidation (LPO) and bilirubin degradation BRD) activities in rat liver microsomes has been developed; a good correlation between the 2 activities was observed (r = 0.78). In the Gunn rat a lipid free diet caused an increase in plasma bilirubin (62.4 ± 25.8%, n = 6) and a concomitant decrease in both hepatic microsomal LPO and BRD to zero. In contrast, on a 25% lipid diet there was a decrease in plasma bilirubin (46.1 ± 3.6%; n = 8) associated with an increase in LPO (1.26 ± 0.11 nmol/min/mg protein, and BRD (0.21 ± 0.6 nmol/min/mg protein). Therefore, in the absence of bilirubin glucuronidation, dietary modulation of plasma bilirubin and lipid peroxidation appear to be closely associated.     

The Effect of Lipid Peroxide on the Lipid and Carbohydrate Metabolism in Rat Liver

Feeding tests were carried out on rats to clarify the mechanisms of fatty liver formation induced by autoxidized methyl linoleate. Lipid peroxides prepared by autoxidation of highly purified methyl linoleate were given orally to rats. Triglyceride and glycogen contents in liver were determined and enzyme activities including triglyceride synthetase and α-glycerophosphate dehydrogenase were also examined. The following results were obtained. 1. Triglyceride accumulation in rat liver fed autoxidized methyl linoleate was observed. 2. Increase in triglyceride content in rat liver was soon followed by the decrease of hepatic glycogen. 3. When rats were starved prior to introduction of autoxidized methyl linoleate, hepatic triglyceride accumulation did not occur. 4. The activities of α-glycerophosphate dehydrogenase and triglyceride synthetase in liver, and those of glutamic oxalacetic transaminase and leucine aminopeptidase in plasma were practically similar among the rats of test groups fed fresh or autoxidized methyl linoleate and the control fed diet without methyl linoleate. 5. The addition of l-carnitine which is a stimulator of fatty acid oxidation retarded the accumulation of the hepatic triglyceride mentioned above.     

Inhibition of Lipid Peroxidation by S -nitrosoglutathione and Copper

The antioxidant properties of S -nitrosoglutathione, a nitric oxide-derived product were studied in different experimental systems. By using the crocin bleaching test, S -nitrosoglutathione, in the presence of copper ions, shows an antioxidant capacity about six times higher than that of Trolox c and referable to the interception of peroxyl radicals by nitric oxide. Copper alone shows a modest inhibitory action, which is about seven times lower than that of Trolox c. S -nitrosoglutathione prevents lipid peroxidation induced by the well-known Fe 2+ /ascorbate system (IC 50 =450 &#119 M) and the inhibitory effect is strongly reinforced by the presence of copper ions (IC 50 =6.5 &#119 M). In addition, cumene hydroperoxide-induced lipid peroxidation is markedly decreased by S -nitrosoglutathione, provided that copper ions, maintained reduced by ascorbate, are present. Decomposition of S -nitrosoglutathione through metal catalysis and/or the presence of reducing agents and the consequent release of nitric oxide are of crucial importance for eliciting the antioxidant power. In this way, copper ions and/or reducing species with low antioxidant potency are able to promote the formation of an extremely strong antioxidant species such as nitric oxide.     

Influence of Dietary Copper Proteinate on Performance,Selected Biochemical Parameters,Lipid Peroxidation,Liver, and Egg Copper Content in Laying Hens

This study was performed to determine the effects of copper proteinate on performance, blood chemistry, lipid peroxidation status, and organs as well as copper deposition in the liver and eggs of laying hens. Seventy-two 30-week-old Bovans laying hens were distributed into four groups with three replicates. Animals were fed basal diet containing at least 17% crude protein and 2,800 kcal/kg metabolizable energy supplemented with either 0, 150, 300, or 450 mg/kg copper as copper proteinate. Supplementation of 150 and 300 mg/kg copper increased egg production, whereas 450 mg/kg copper decreased (p < 0.001). Liver copper levels were elevated in 300 and 450 mg/kg copper-supplemented groups (p < 0.001). Egg copper contents increased in all treatment groups (p < 0.01). An increase in glucose (p < 0.001) and decreases in albumin (p < 0.01) and total cholesterol (p < 0.05) levels were determined with 300 and 450 mg/kg copper. Supplementation of 450 mg/kg copper increased alkaline phosphatase and gamma glutamyl transpeptidase activities (p < 0.05), malondialdehyde, and high-density lipoprotein levels (p < 0.01) but decreased alanine aminotransferase and lactate dehydrogenase activities (p < 0.01). No gross and microscopic changes were observed in the liver and kidneys. These results indicated that 150 and 300 mg/kg copper increased egg production without having marked adverse effects, but 450 mg/kg copper altered some blood chemistry variables and reduced egg production in laying hens.     

Inhibitory Effects of Ebselen on Lipid Peroxidation in Rat Liver Microsomes

The effects of ebselen(2-pheny1-1,2-benzoisoselenazol-3(2H)-one), a synthetic seleno-organic compound with glutathione peroxidase-like activity were investigated on lipid peroxidation in rat liver microsomes. Ebselen inhibited malondialdehyde production coupled to the lipid peroxidation stimulated by either ADP-iron-ascorbate or CC1₄. The inhibitory activity of ebselen on each system was strongly increased by a 5-min preincubation with liver microsomes; the IC₅₀ values against ADP-Fe-ascorbate-stimulated and CC1₄-stimulated lipid peroxidation were 1.6/jM and 70 μM respectively. Ebselen also inhibited the endogenous lipid peroxidation with a NADPH-generating system, but it slightly stimulated the endogenous activity of ADP-Fe-ascorbate-stimulated lipid peroxidation (without a NADPH-generating system). Furthermore, ebselen inhibited oxygen uptake coupled to the lipid peroxidation by ADP-Fe-ascorbate and NADPH-ADP-iron; the IC₅₀ values were 2.5μM AND 20.3 μM respectively. Ebselen also prolonged the lag-time of onset of ADP-Fe-ascorbate-stimulated lipid peroxidation significantly, but not that observed with NADPH-ADP-Fe-stimulated lipid peroxidation.     

The Influence of Nutrigenetics on the Lipid Profile: Interaction Between Genes and Dietary Habits

Nutrigenetics is a new field with few studies in Latin America. Our aim is to investigate the way in which different genes related to the lipid profile influence the response to specific dietary habits. Eight polymorphisms on seven genes were investigated in a sample (n = 567) from Porto Alegre, RS, Brazil. All the volunteers completed a food diary that was then assessed and classified into nine food groups. A number of nutrigenetic interactions were detected primarily related to the apolipoprotein E (apoE) gene. For example, frequent consumption of foods rich in polyunsaturated fat resulted in the beneficial effect of increasing HDL-C only in individuals who were not carriers of the E*4 allele of the APOE gene, whereas variations in eating habits of E*4 carriers did not affect their HDL-C (P = 0.018). Our data demonstrate for the first time nutrigenetic interactions in a Brazilian population.     

Tenoxicam Modulates Antioxidant Redox System and Lipid Peroxidation in Rat Brain

We investigated effects of two doses of Tenoxicam, a type 2 cyclooxygenase inhibitor, administration on lipid peroxidation and antioxidant redox system in cortex of the brain in rats. Twenty-two male Wistar rats were randomly divided into three groups. First group was used as control. 10 and 20 mg/kg body weight Tenoxicam were intramuscularly administrated to rats constituting the second and third groups for 10 days, respectively. Both dose of Tenoxicam administration resulted in significant increase in the glutathione peroxidase activity, reduced glutathione and vitamins C and E of cortex of the brain. The lipid peroxidation levels in the cortex of the brain were significantly decreased by the administration. Vitamin A and β-carotene concentration was not affected by the administration. There was no statistical difference in all values between 10 and 20 mg Tenoxicam administrated groups. In conclusion, treatment of brain with 10 and 20 mg Tenoxicam has protective effects on the oxidative stress by inhibiting free radical and supporting antioxidant redox system.     

Increased Hepatic Lipid Peroxidation with Methionine Toxicity in the Rat

Consumption of excess methionine by rats is known to cause membrane damage, liver enlargement and accumulation of iron in the spleen. In this study two groups (n = 5) of male, Wistar rats were pair-fed either a methionine supplemented (20.0 g/kg) or control (2.0 g/kg) diet for 7 weeks. Hepatic and erythrocyte copper-zinc superoxide dismutase activities were significantly reduced (P < 0.05 and P < 0.001 respectively) by methionine supplementation while the activities of catalase (P < 0.01 and 0.05) and glutathione peroxidase (P < 0.05) were significantly increased. Methionine supplementation also increased hepatic lipid peroxidation (P < 0.01), as measured by the level of thiobarbituric acid reactive substances, and iron (P < 0.001) concentrations. These changes are indicative of increased oxidative stress resulting from methionine toxicity.     

Iron-Melanin Interaction and Lipid Peroxidation: Implications for Parkinson''s Disease

The vulnerability of substantia nigral (SN) melaninized dopamine neurons to neurodegeneration in Parkinson's disease and the selective increases of iron and basal lipid peroxidation in SN indicate that iron-melanin interaction could be crucial to the pathogenesis of this disease. The present study describes, for the first time, the identification and characterization of a high-affinity (KD = 13 nM) and a lower affinity (KD = 200 nM) binding site for iron on dopamine melanin. The binding of iron to melanin is dependent on pH and the concentration of melanin. Iron chelators, U74500A, desferrioxamine, and to less extent 1,10-phenanthroline and chlorpromazine, but not the Parkinson-inducing neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, can inhibit the binding of iron to melanin and iron-induced lipid peroxidation. Although melanin alone diminishes basal lipid peroxidation in rat cortical homogenates, it can also potentiate that initiated by iron, a reaction inhibited by desferrioxamine. In the absence of an identifiable exogenous or endogenous neurotoxin in idiopathic Parkinson's disease, iron-melanin interaction in pars compacta of SN may be a strong candidate for the cytotoxic component of oxygen radical-induced neurodegeneration of melaninized dopamine neurons.     

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.     

The Effects of Electromagnetic Radiation on Lipid Peroxidation and Antioxidant Status in Rat Blood

Biophysics - Abstract—The aim of this study was an evaluation of the effect of an electromagnetic field at a frequency of 460 MHz on lipid peroxidation and total antioxidant capacity in rat...     

丁基苯酞对大鼠心肌损伤及脂质过氧化的作用

目的:大量的临床以及动物实验表明丁基苯酞对缺血性脑损害具有明确的保护作用,但其对于相似发病机理的心肌损伤国内外尚无研究。本课题探讨丁基苯酞对异丙肾上腺素诱导大鼠心肌损伤保护作用及机制。方法:SD大鼠48只,随机分为对照组(n=12),异丙肾上腺素组(n=12),异丙肾上腺素+Tween-80(丁苯酞溶媒)组(n=12),异丙肾上腺素+丁苯酞组(n=12)。7天后处死大鼠,测定左心室血流动力学、血清SOD活性、组织MDA含量及组织病理学观察。结果:ISO组成功的制备了心肌损伤模型,与Control组相比,ISO组左室舒张末期压(LVEDP)明显升高(P0.01),+dp/dtmax显著下降(P0.01),SOD活性下降,MDA含量增加,心肌坏死病理积分明显增加。丁基苯酞(NBP)能显著减轻异丙肾上腺素导致的心肌损害。与ISO组相比,ISO+NBP组LVEDP明显下降,SOD活性提高,MDA含量减少,心肌坏死病理积分明显减少。结论:丁基苯酞对异丙肾上腺素引起的大鼠缺血损伤心肌具有保护作用,其机制可能与其抗脂质过氧化有关。本研究发现一种新的具有心脏保护作用的药物,可能为心肌缺血损伤疾病的预防和治疗提供新的选择。     

Antioxidant Properties of New Chalcogenides Against Lipid Peroxidation in Rat Brain

Ebselen (2-phenyl- 1,2-benzisoselenazole-3 (2H)-one) is a seleno-organic compound with antioxidant properties, and anti-inflammatory actions. Recently, ebselen improved the outcome of acute ischemic stroke in humans. In the present study, the potential antioxidant capacity of organochalcogenide compounds diphenyl diselenide (PhSe)₂, diphenyl ditelluride (PhTe)₂, diphenyl disulfide (PhS)₂, p-Cl-diphenyl diselenide (pCl-PhSe)₂, bis-[S-4-isopropyl 2-phenyl oxazoline] diselenide (AA-Se)₂, bis-[S-4-isopropyl 2-phenyl oxazoline] ditelluride (AA-Te)₂ and bis-[S-4-isopropyl 2-phenyl oxazoline] disulfide (AA-S)₂ was compared with that of ebselen (a classical antioxidant). Spontaneous and quinolinic acid (QA)- (2 mM) and sodium nitroprusside (SNP)- (5 M)-induced thiobarbituric reactive species (TBARS) production by rat brain homogenates was determined colorimetrically. TBARS formation was reduced by ebselen, (PhSe)₂, (PhTe)₂, (AA-Se)₂, (AA-S)₂ and (pCl- PhSe)₂ to basal rates. The concentrations of these compounds needed to inhibit TBARS formation by 50% (lC₅₀) are 1.71 M, 3.73 M, 1.63 M, 9.85 M, > 33.3 M, 23.2 M and 4.83 M, respectively for QA. For TBARS production induced by SNP the lC₅₀ was 2.02 M, 12.5 M, 2.80 M, > 33.3 M, 24.5 M and 7.55 M, respectively. The compounds (AA-Te)₂ and (PhS)₂ have no antioxidant activity and pro-oxidant activity, respectively. These results suggest that (AA-Se)₂ and (AA-S)₂ can be considered as potential pharmaceutical antioxidant agents.     

Estrogen Hormones Reduce Lipid Peroxidation in Cells and Tissues of the Central Nervous System

Effects of estrogen hormones on lipid peroxidation (LPO) were examined in rat brain homogenates (RBHs), hippocampal HT 22 cells, rat primary neocortical cultures, and human brain homogenates (HBHs). Dose-response curves indicated half-maximal effective concentrations (EC50) of 5.5 and 5.6 mM for iron-induced LPO in RBHs and HT 22 homogenates. Incubation of living rat primary neocortical cultures with iron resulted in an EC50 of 0.5 mM, whereas culture homogenates showed an EC50 of 1.2 mM. Estrogen hormones reduced LPO in all systems: In RBHs, estrone inhibited iron-induced LPO to 74.1 +/- 5.8% of control levels (17beta-estradiol: 71.3 +/- 0.1%) at a concentration of 10 microM. In hippocampal HT 22 cell homogenates, levels of LPO were reduced to 74.8 +/- 5.5% by estrone and to 47.8 +/- 6.2% by 17beta-estradiol. In living neocortical cultures, 17beta-estradiol decreased iron-induced LPO to 79.2 +/- 4.8% and increased the survival of cultured neuronal cells. Of the other steroid compounds tested (corticosterone, progesterone, testosterone), only progesterone decreased LPO in HT 22 cell homogenates. In HBHs, LPO was dose-dependently increased by iron concentrations from 2.7 to 6.0 mM. Incubation with estrogens resulted in a dose-dependent inhibition of LPO to 53.8 +/- 8.6% with 10 microM 17beta-estradiol, whereas estrone failed to affect iron-induced LPO to a significant extent. Nonestrogenic steroids, including hydrocortisol, did not show significant effects on LPO in HBHs.     

Hypoxia-Induced Lipid Peroxidation in Rat Brain and Protective Effect of Carnitine and Phosphocreatine

The exposure to hypobaric hypoxia increased lipid peroxidation (as indicated by thiobarbituric acid-reactive substances [TBARS] in rat brain. Plasma lactate/pyruvate ratio was used as a marker of hypoxia. We compared the protective effect of -tocopherol with the effect of l-carnitine or phosphocreatine. Rats pretreated with -tocopherol, l-carnitine, or phosphocreatine had lower TBARS levels after the exposure to hypobaric hypoxia. However, lactate/pyruvate ratio was improved only in rats pretreated with l-carnitine or phosphocreatine. We conclude from our data that, contrary to -tocopherol, protective effects of l-carnitine and phosphocreatine administrations are due to their regulation of metabolic reactions during hypobaric hypoxia rather than to their scavenger activity.     

Influences of Different Stress Models on the Antioxidant Status and Lipid Peroxidation in Rat Erythrocytes

The aim of this study was to investigate the influences of different stress models on the antioxidant status and lipid peroxidation (LPO) in erythrocytes of rats. Swiss-Albino female rats (3 months old) were used in this study. Rats were randomly divided into the following four groups; control group (C), cold stress group (CS), immobilization stress group (IS) and cold+immobilization stress group (CS+IS). Control group was kept in an animal laboratory (22 &#45 2°C). Rats in CS group were placed in cold room (5°C) for 15 min/day for 15 days. Rats in IS group were immobilized for 180 min/day for 15 days. Rats in CS+IS group were exposed to both cold and immobilization stresses for 15 days. At the end of experimental periods, the activities of glucose-6-phosphate dehydrogenase (G-6-PD), Cu,Zn-superoxide dismutase (Cu,Zn-SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), and concentration of reduced glutathione (GSH) were measured. LPO was determined by measuring the contents of thiobarbituric acid-reactive substances (TBARS). Cu,Zn-SOD activity and TBARS concentration were increased after cold and immobilization stresses, but CAT and GSH-Px activities and GSH levels were decreased. Immobilization stress decreased the activity of G-6-PD. The activities of G-6-PD, CAT and GSH-Px, and the level of GSH were lower in CS+IS group than in the control group. Cu,Zn-SOD activity and TBARS levels were increased in CS+IS group when compared with the control group. From these findings, three stress models are thought to cause oxidative stress.     

Allyl Chloride-Induced Time Dependent Changes of Lipid Peroxidation in Rat Nerve Tissue

To accurately know the time-dependent changes of the lipid peroxidation and antioxidative status for elucidating the mechanism of neuropathy induced by allyl chloride (AC), the malondialdehyde (MDA), anti-reactive oxygen species (anti-ROS), glutathione (GSH), catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD) were investigated in cerebrum, spinal cord and sciatic nerve of rats after 0, 3, 6, 9, 12 weeks of␣AC administration. AC was administrated to Wistar rats by gavage at a single dosage of 200 mg/kg/per dose (three times per week). Rats were sacrificed after 0, 3, 6, 9, 12 weeks of treatment, and cerebrum, spinal cord, sciatic nerves were dissected, homogenized and used for the determination of lipid peroxidation and antioxidative status. The results showed that MDA in cerebrum (112.4%) and sciatic nerve (113.1%) significantly increased (P < 0.05) on third week of AC treatment and at gait score of 2, and further changes of MDA were observed after 6, 9, 12 weeks and at gait score of 3, 4. While a decrease (P < 0.05) in the activities of GSH, CAT, GPx and SOD after 6, 9, 12 weeks intoxication and at gait score of 2, 3, 4 were observed in cerebrum, spinal cord and sciatic nerve. Anti-ROS activities also decreased in all three nerve tissues after 3, 6, 9, 12 weeks intoxication and at gait score of 2, 3, 4. Thus, AC intoxication was associated with elevation of lipid peroxidation and reduction of antioxidative status, and the time-dependent changes of these indexes in Wistar rats nerve tissues occurred. Sciatic nerve was the main target tissue and MDA was most sensitive among all indexes. The changes of lipid peroxidation and antioxidative status might be related to the degradation of nerve fiber and served as one of mechanisms of toxic neuropathy induced by AC.     

Lipid Peroxidation In Vivo Induced by Reversible Global Ischemia in Rat Brain

It has been hypothesized that ischemia, followed by reperfusion, facilitates peroxidative free-radical chain processes in brain. To resolve this question, rats were subjected to reversible global ischemia. From coronal sections of brains frozen in situ, small (ca. 2 mg) amounts of tissue were sampled from neocortex, hippocampus, and thalamus of both cerebral hemispheres of four groups of rats exposed to 30 min cerebral ischemia followed by 0, 30, 60, and 240 min of reperfusion, and from a control group subjected to the same operative procedures, except for the induction of ischemia. Heptane-solubilized total lipid extracts from these samples were analyzed spectroscopically in the 190-330 nm range for content of isolated (nonconjugated) double bonds and of conjugated diene structures; the latter are formed from isolated double bonds during peroxidation of unsaturated fatty acids. Spectra derived from tissue regions of rats subjected to ischemia, or ischemia followed by reperfusion, were compared to averaged, region-specific control spectra and were normalized to the original content of isolated double bonds in the peroxidized samples. The resultant difference spectra were analyzed in terms of ratios of conjugated diene concentration to the concentration of isolated double bonds originally at risk in the specific tissue zones considered. The peak representing conjugated diene formation was centered at 238 +/- 1 nm and was usually well resolved when the molar ratio [conjugated diene]/[isolated double bonds], expressed as a percentage [( CD]/[IDB]), was greater than 0.25%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of Vitamin A and Its Analogs on Nonenzymatic Lipid Peroxidation in Rat Brain Mitochondria

Vitamin A (retinol) and some of its analogs exhibited varying degrees of inhibition on induced iron and ascorbic acid lipid peroxidation of rat brain mitochondria. Malonyldialdehyde production was used as an index of the extent of in vitro lipid peroxidation. The fat-soluble vitamins retinol, retinol acetate, retinoic acid, retinol palmitate, and retinal at concentrations between 0.1 and 10.0 mmol/L inhibited brain lipid peroxidation. Retinol and retinol acetate were the most effective inhibitors. It is concluded from this study that retinol and its analogs can be considered as potential antioxidant factors, more potent than some of the well-known antioxidants such as alpha-tocopherol and butylated hydroxytoluene.     

异丙酚和氯胺酮对大鼠离体缺血再灌注损伤心肌脂质过氧化的影响

目的：比较异丙酚和氯胺酮对大鼠离体缺血再灌注损伤心肌脂质过氧化的影响。方法：成年Wistar大鼠18只,雌雄不拘。体重240-300g,随机分为3组（T1=6）：心肌缺血再灌注损伤组（I／R组）,异丙酚组（P组）,氯胺酮组（K组）。采用Langendorff灌装置建立离体心脏缺血再灌注模型,将心脏连接至Langendorff逆灌装置,3组均以K-H液平衡灌注10min后,再分别以K．H液、含30μmol/L。异丙酚的K-H液、含10μmol-L-1氯胺酮的K-H液灌注10min,然后全心停灌25min,再分别以停灌前相同的灌注液恢复灌注30min。留取冠脉流出液测定总LDH活性;灌注末取左室心肌组织置于2．5％的戊二醛固定,观察心肌的超微结构;心尖部心肌组织留待检测8-异前列腺素和SOD活性。结果：与I／R组比较,P组8-异前列腺素含量降低,SOD活性升高,LDH活性降低（P〈0．05）;K组8-异前列腺素含量,SOD及LDH活性均无统计学意义（P〉0．05）;与P组比较,K组8-异前列腺素含量升高,SOD及LDH活性降低（P〈0．05）;P组心肌超微结构损伤较m组和K组也明显改善。结论：异丙酚可显著减轻心肌缺血再灌注损伤大鼠的脂质过氧化和心肌缺血再灌注损伤,而氯胺酮没有抗心肌缺血再灌注损伤心肌脂质过氧化的作用。