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1.
The aim of this study was to determine the effects of alpha-tocopherol on lipid peroxidation and total antioxidant status of spontaneously hypertensive rats (SHR), comparing them with normal Wistar-Kyoto (WKY) rats. SHR were divided into three groups and treated with different doses of alpha-tocopherol (alpha1, 17 mg/kg diet; alpha2, 34 mg/kg diet; and alpha3, 170 mg/kg diet). Normal WKY and untreated SHR were used as normal (N) and hypertensive control (HC). Blood pressures were recorded every 10 days for 3 months. At the end of the trial, animals were killed and measurement of plasma total antioxidant status, plasma superoxide dismutase (SOD) activity, and lipid peroxide levels in plasma and blood vessels was carried out following well-established methods. From our study it was found that lipid peroxides in thoracic aorta (N, 0.47 +/- 0.17; H, 0.96 +/- 0.37; P < .0001) and plasma (N, 0.06 +/- 0.01; H, 0.13 +/- 0.01) were significantly higher in hypertensives than in normal rats. SOD activity was significantly lower in hypertensive than normal rats (N, 172.93 +/- 46.91; H, 110.08 +/- 14.38; P < .005). Total antioxidant status was significantly higher in normal than hypertensive rats (N, 0.88 +/- 0.05; H, 0.83 +/- 0.02; P < .05). After the antioxidant trial, it was found that in the treated groups rise of blood pressure was prevented significantly (P < .001) and lipid peroxides in blood vessels were significantly reduced more than in the controls (P < .001). For plasma lipid peroxide it was only significant for groups alpha2 (P < .001) and alpha3 (P < .05). Although all three treated groups showed improved total antioxidant status, only groups alpha2 (0.87 +/- 0.04, P < .005) and alpha3 (1.20 +/- 0.18, P < .001) were statistically significant. All the three groups showed significant increases in their SOD activity (P < .001). Correlation studies showed that total antioxidant status and SOD were significantly negatively correlated with blood pressure in normal rats (P = .007; P = .008). Lipid peroxides in both blood vessel and plasma showed a positive correlation. In the treated groups, lipid peroxides in blood vessels maintained a significant positive correlation with blood pressure in all groups (alpha1, P = .021; alpha2, P = .019; alpha3, P = .002), whereas for plasma lipid peroxides the correlation was in groups alpha1 (P = .005) and alpha2 (P = .009). For SOD activity, significant negative correlations were found with blood pressure in the alpha2 (P = .017) and alpha3 (P = .025) groups. Total antioxidant status maintained a significant negative correlation with blood pressure in all three groups (alpha1, P = .012; alpha2, P = .044; alpha3, P = .014). In conclusion it was found that supplement of alpha-tocopherol may prevent development of increased blood pressure, reduce lipid peroxides in plasma and blood vessels, and enhance the total antioxidant status, including SOD activity. 相似文献
2.
Photodynamic-induced cytotoxicity by hypericin (HYP) was studied on three human melanoma cell lines: one pigmented cell line (G361) and two amelanotic cell lines (M18 and M6). No significant variation in the rate of uptake and in the maximum level of HYP incorporation for the different cells was observed. In the dark, no cytotoxicity was observed in the range 0-10-6 M HYP for the three cell lines. Amelanotic cells were found to be more sensitive than pigmented cells to irradiation of HYP with visible light (lambda > 590 nm). In addition, for the three cell lines HYP-induced photocytotoxicity was found to be drug-dose and light-dose dependent. Under the conditions used, thiobarbituric acid-reacting substances (TBARs) were significantly increased in amelanotic cells after irradiation (P < 0.0001). By contrast, the amount of TBARS remained unchanged in pigmented cells. Antioxidant defenses including enzymes and glutathione (GSH) were assayed before and after HYP photosensitization. Significantly increased total SOD activity was observed after photosensitizaton for amelanotic cells (P < 0.05), while glutathione peroxidase (GSHPx) and catalase (Cat) activities but also GSH levels were significantly decreased (P < 0.01). In pigmented cells a significantly increased Cat activity was found (P < 0.05), whereas GSHPx was unaffected after irradiation. It can be inferred that (a) HYP may be an effective PDT agent for melanoma and (b) there is a relationship between melanin content and sensitivity to HYP phototoxicity in human melanoma cells. 相似文献
3.
RJ Lemarié G Hosgood J VanSteenhouse EC Hodgin BL Tedford GM Strain 《Canadian Metallurgical Quarterly》1998,59(7):913-917
OBJECTIVE: To document that free skin grafts treated with hyperbaric oxygen (HBO) are at greater risk for reperfusion injury, resulting in lipid peroxidation, than are free skin grafts without HBO treatment. ANIMALS: 40 Sprague-Dawley rats. PROCEDURE: Free skin grafting was performed bilaterally on each rat. The HBO-treated rats received HBO twice daily for 90 minutes at 2 ATA. Biopsy specimens were taken from each rat at the time of grafting and on days 2, 4, 7, 10, 14, 21, and 28, then were processed for tissue concentration of total glutathione (GSHt), glutathione peroxidase activity (GPx), and presence of thiobarbituric acid-reactive substances (TBARS). RESULTS: Both groups had a similar pattern of change in TBARS and GPx values--initial increase, returning to preoperative values at days 21 (control) and 28 (HBO). The GPx activity peaked later than did TBARS concentration (day 7 vs day 4). The pattern was significantly more pronounced in HBO-treated than in control rats. Both groups had a similar pattern of change in GSHt values-significant decrease from preoperative concentration at day 2, return to preoperative concentration by days 4 (HBO) and 7 (control), increase above preoperative concentration by day 21, and return to preoperative concentration by day 28. Obvious visual or histologic differences in the grafts were not detected between groups. CONCLUSIONS: Cellular effects of oxidative stress were apparent in both groups of rats; however, the degree of these effects was exacerbated by HBO. In the face of enhanced cellular lipid peroxidation, use of HBO for the treatment of free skin grafts must be questioned. 相似文献
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Recent years have witnessed a renewed interest in plants as pharmaceuticals in the Western world. This interest is channeled into the discovery of new biologically-active molecules by the pharmaceutical industry and into the adoption of crude extracts of plants for self-medication by the general public. In both of these areas some attention is being paid to the investigation and use of ethnopharmacology, the traditional use of plants for medicinal purposes by particular cultural groups. Ethnopharmacologic leads have resulted in the introduction of new single molecule drugs but have a greater role to play if crude extracts are accepted for clinical use in the West. The problems confronting such usage are discussed. Considerable benefits for developing countries are possible when the local medicinal plants are subjected to scientific methods of validation of traditional use and quality control. This approach has met with success in some parts of the world but is not always appreciated by national governments and international agencies. Related areas of concern such as conservation of ecology and culture must be integrated with any such program. Plants used in traditional medicine therefore have an important role to play in the maintenance of health in all parts of the world and in the introduction of new treatments. 相似文献
6.
Nephropathy is common among the diabetic population. However, the molecular mechanisms by which hyperglycemia can cause alteration in kidney structure and function is not known. In this study, we examined the effect of high glucose levels on cellular growth and membrane lipid peroxidation in Vero cells, an African green monkey kidney cell line. Cell growth was assessed by a tetrazolium salt reduction test (MTT); and lipid peroxidation was measured by thiobarbituric acid reactivity. Our results show that elevated levels of glucose (25, 50 and 100 mM) can cause up to 50% reduction in cell growth in cultured Vero cells as compared with controls (8 mM). Also, we observed a significant increase in the amount of oxidative damage in Vero cells cultured with elevated glucose concentrations. This study demonstrates that hyperglycemia can cause increased lipid peroxidation and affect the cellular proliferation in a monkey kidney cell line. 相似文献
7.
P Dandona K Thusu R Hafeez E Abdel-Rahman A Chaudhuri 《Canadian Metallurgical Quarterly》1998,47(7):788-791
Corticosteroids are known to exert antiinflammatory and immunosuppressive effects. Since reactive oxygen species (ROS) induce tissue damage and inflammation and since mononuclear cells (MNCs) generate ROS, we investigated whether corticosteroids inhibit ROS generation by MNCs when given systemically. A single dose of either 300 mg (n = 8) or 100 mg (n = 6) of hydrocortisone (HC) was injected intravenously into eight and six subjects, respectively. Blood samples were obtained before and sequentially after the injection. Following 300 mg HC, N-formylmethionyl leucyl phenylalanine (fMLP)-induced ROS generation, assayed by measuring chemiluminescence with luminol, decreased significantly at 0.5 hours and reached a nadir at 2 hours (8% of basal, P < .001); thereafter, it gradually recovered, but was still below baseline at 24 hours. Following the dose of 100 mg HC, ROS generation decreased significantly at 1 hour (nadir, 30% of basal; P < .01) and gradually recovered to near basal level at 8 hours. Serum cortisol concentrations were markedly elevated over basal and remained elevated throughout the first 8 hours of the experiment, returning to baseline at 24 hours. This inhibition of ROS generation by HC (and other glucocorticoids) may have a role to play in mediating the antiinflammatory action of corticosteroids. 相似文献
8.
D Miyamoto N Endo N Oku Y Arima T Suzuki Y Suzuki 《Canadian Metallurgical Quarterly》1998,21(12):1258-1262
The cytotoxic effects of beta-thujaplicin and five kinds of metal chelates were examined on mouse melanoma B16BL6 cells by cell viability and lactate dehydrogenase (LDH) release assay. Beta-thujaplicin-zinc chelate and beta-thujaplicin-copper chelate had higher cytotoxic effects than beta-thujaplicin, and the 50% effective doses (ED50) of these metal chelates were 12.5 and 25 microM, respectively. In addition, the zinc chelate induced DNA ladder formation in B16BL6 cells, as shown by the DNA fragmentation assay, suggesting that cell death induced by the zinc chelate is apoptosis. The zinc chelate also had a cytotoxic effect and induced DNA fragmentation on other tumor cell lines: HeLa, Meth A, and B16F1 cells, but not on normal human diploid fibroblasts FS-4. These results suggest that beta-thujaplicin-zinc chelate induces apoptotic cell death in various tumor cell lines and is a potent antitumor agent for tumor cells including malignant melanomas. 相似文献
9.
Tanshinone II-A (TSII-A) isolated from the root of Salvia miltorrhiza Bunge, a traditional medicine in China, is a derivative of phenanthrenequinone, which is known to have antioxidant properties. In the present study, effects of TSII-A on DNA damage by lipid peroxidation were investigated using liver cells, labeled with [3H] arachidonic acid, in the presence of FeCl2-DTPA. The results show that the nuclear DNA isolated from treated cells had higher radioactivity compared to controls and the radioactivity increased with longer incubation times. Purified lipid-DNA adducts had a characteristic fluorescent spectra and showed a decrease of hyperchromicity and melting point. TSII-A could inhibit the association of peroxidation products with DNA in liver cells and prevent a decrease in cell viability and in the the activity of O6-methylguanine acceptor protein with increasing incubation time. Compared with other antioxidants, TSII-A had a higher inhibitory ratio, which was similar to vitamin E and butylated hydroxy-toluene (BHT), but markedly stronger than NaN3, mannatol, and superoxide dismutase (SOD). These data suggest that TSII-A represents a new and effective antioxidant that inhibits the association of lipid peroxidation products with DNA. Its protective effect may be through breaking the chain reactions of peroxidation by scavenging lipid free radicals, thereby decreasing their cytotoxicity. 相似文献
10.
OBJECTIVE: Oxygen free radical-mediated lipid peroxidation has been proposed to be one of the major mechanisms of secondary damage in traumatic brain injury. The first purpose of this study was to establish the time-level relationship for lipid peroxidation in injured brain tissue. The second purpose was to examine the protective effect of alpha-tocopherol against lipid peroxidation. METHODS: For this study, 65 guinea pigs in five groups were studied. Five of the animals were identified as a control group, and the remaining 60 animals were divided equally into four groups (Groups A, B, C, and D). Mild injury (200 g x cm) (Groups A and C) and severe injury (1000 g x cm) (Groups B and D) were produced by the method of Feeney et al. Alpha-tocopherol (100 mg/kg) was administered intraperitoneally before brain injury in Groups C and D. Five animals from each group were killed immediately after trauma, five after 1 hour, and the remaining five animals after 36 hours. Lipid peroxidation in traumatized brain tissues was assessed using the thiobarbituric acid method. RESULTS: In all groups with traumatic brain injuries, levels of malondialdehyde, a lipid peroxidation product, were higher than in the control group. The amount of lipid peroxidation was increased by the severity of the trauma. Alpha-tocopherol significantly suppressed the rise in lipid peroxide levels in traumatized brain tissues. CONCLUSION: This study demonstrates that lipid peroxidation is increased by the severity of trauma and that alpha-tocopherol has a protective effect against oxygen free radical-mediated lipid peroxidation in mild and severe brain injury. 相似文献
11.
K Fukuzawa Y Inokami A Tokumura J Terao A Suzuki 《Canadian Metallurgical Quarterly》1998,33(8):751-756
BACKGROUND: Familial juvenile polyposis (JP) is an autosomal dominant condition in which affected individuals develop upper or lower gastrointestinal (GI) juvenile polyps, or both, and have a predisposition to cancer of the gastrointestinal tract. The risk of GI cancer has not been well defined because of the small number of these families and the lack of follow-up. The objective of this study was to determine the prevalence and age at diagnosis of GI polyposis and cancer in a large JP kindred. METHODS: Medical records were reviewed, patients were interviewed, and histories were taken. Pathology reports and slides were reviewed by our pathologists. A database was created for analysis of clinical and pathologic factors. RESULTS: This kindred contains 117 members, 29 of whom have had upper or lower GI polyps or cancer, or both. All those affected have had colonic juvenile polyps or cancer, except for two who died of advanced gastric cancer and never had colonic evaluation. Nine individuals have had both upper and lower GI polyps or cancer. Sixteen of 29 (55%) affected patients have developed gastrointestinal cancer. Eleven (38%) have had colon cancer, and six (21%) have had upper GI cancers. CONCLUSIONS: The risk of gastrointestinal malignancy in affected members of this JP kindred exceeds 50%. The high risk of GI cancer warrants frequent endoscopic screening of both affected and at-risk family members. Screening will soon be facilitated by presymptomatic genetic testing for the identification of gene carriers. 相似文献
12.
Recent studies have suggested that free radical scavenger administration reduces the rate of development of diaphragm fatigue. Much of this work has been done, however, using in vitro muscle preparations; the purpose of the present study was to assess the effect of scavengers on in vivo diaphragm contractile function. To accomplish this, we compared the rate of development of fatigue of the electrically stimulated diaphragm in four groups of dogs: (1) animals given intravenous polyethylene glycol adsorbed superoxide dismutase (PEG-SOD, 2,000 units/kg) 1 h before a fatigue trial; (2) a group given intravenous dimethylsulfoxide (DMSO, 0.5 ml/kg of a 50% solution) before fatigue; (3) a group given saline before fatigue; and (4) a group treated with denatured PEG-SOD (2,000 units/kg) before fatigue. We measured diaphragmatic concentrations of thiobarbituric acid reactive substances (TBAR), a marker of free radical-mediated lipid peroxidation, on muscle samples taken at the conclusion of fatigue trials. As a control, we also measured TBAR concentrations for muscle samples taken from nonfatigued diaphragm. We found that the rate of development of diaphragm fatigue was much greater in saline and denatured PEG-SOD-treated groups than for animals pretreated with either PEG-SOD or DMSO, with force falling to 23 +/- 4, 21 +/- 4, 50 +/- 7, and 47 +/- 6% of its initial value, respectively, over a 2-h period of electrophrenic stimulation in these four groups of animals (p < 0.01). TBAR concentrations in fatigued diaphragm from saline and denatured PEG-SOD-treated animals were significantly higher than levels for either nonfatigued fresh diaphragm or fatigued diaphragm taken from PEG-SOD- or DMSO-treated animals (p < 0.01). These data suggest that diaphragm fatigue resulting from repetitive low-frequency stimulation is associated with lipid peroxidation within this muscle and that pretreatment with free radical scavengers prevents lipid peroxidation and reduces the rate of development of fatigue. 相似文献
13.
A Guerrero R Pamplona M Portero-Otín G Barja M López-Torres 《Canadian Metallurgical Quarterly》1999,26(1-2):73-80
In order to analyze the possible relationship between metabolic rate and oxidative stress, OF1 female mice were rendered hyper- or hypothyroid for 4-5 weeks by administration of 0.0012% L-thyroxine (T4) or 0.05% 6-n-propyl-2-thiouracil (PTU), respectively, in their drinking water. Treatment with T4 resulted in increased basal metabolic rate measured by oxygen consumption and liver cytochrome oxidase activity without altering the glutathione redox system. Endogenous lipid peroxidation, sensitivity to lipid peroxidation and fatty acid unsaturation were decreased in the hyperthyroid group. Hypothyroidism also decreased phosphatidylcholine and cardiolipin fatty acid unsaturation but not in total lipids, and thus lipid peroxidation was not altered. Cardiolipin, a mainly mitochondrial lipid, was the most profoundly altered fraction by both hyper- and hypothyroidism. It is suggested that the lipid changes observed in hyperthyroid animals can protect them against an increased oxidative attack to tissue lipids due to their increased mitochondrial activities. 相似文献
14.
P Ljubuncic B Fuhrman J Oiknine M Aviram A Bomzon 《Canadian Metallurgical Quarterly》1996,39(3):475-478
BACKGROUND: Kupffer cells are essential for normal hepatic homeostasis and when stimulated, they secrete reactive oxygen species, nitric oxide, eicosanoids, and cytokines. Some of these products are cytotoxic and attack nucleic acids, thiol proteins, or membrane lipids causing lipid peroxidation. Hydrophobic bile acids, such as deoxycholic acid (DCA), can damage hepatocytes by solubilising membranes and impairing mitochondrial function, as well as increasing the generation of reactive oxygen species. OBJECTIVES: The hypothesis that hydrophobic bile acids could stimulate Kupffer cells to increase their capacity to generate reactive oxygen species by measuring cellular lipid peroxidation was tested. Because the hydrophilic bile acid, ursodeoxycholic acid (UDCA) can block hydrophobic bile acid induced cellular phenomena, it was also hypothesised that UDCA could antagonise macrophage activation by hydrophobic bile acids to blunt their capacity to generate reactive oxygen species. METHODS: J-774A.1 murine macrophages were incubated for 24 hours with either 10(-5) M and 10(-4) M (final concentration) DCA alone, or 10(-4) M UDCA alone, or a mixture of 10(-4) M 1:1 molar ratio of DCA and UDCA. At the end of the incubation period, the culture medium was collected for determination of cellular lipid peroxidation by measuring the malondialdehyde (MDA) content in the medium with the thiobarbituric acid reactive substances assay. RESULTS: 10(-5) M and 10(-4) M DCA increased MDA generation by cultured macrophages. 10(-4) M UDCA alone did not increase MDA generation but blocked the peroxidative actions of DCA. CONCLUSIONS: Hydrophobic bile acids, after their hepatic retention, can oxidatively activate Kupffer cells to generate reactive oxygen species. Because UDCA can block this action, the beneficial effect of UDCA is, in part, related to its ability to act as an antioxidant. 相似文献
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The experimental metastatic potential (lung-colonizing ability) of B16BL6 melanoma cells was examined in C57BL/6 mice after exposure to ethanol in vitro and in vivo. In vitro, tumor cells were cultured with ethanol (0.3% v/v), or medium alone, for three passages at 5-day intervals. In vivo, B16BL6 melanoma was exposed to ethanol by administering ethanol (10% or 20% w/v) to mice following subcutaneous inoculation of tumor cells into the dorsal hip. All tumor cells were subsequently inoculated intravenously into the lateral tail vein of water-drinking mice to assess changes in metastatic phenotype. Tumor cells cocultured in vivo with ethanol produced significantly higher numbers of superficial lung colonies, compared with tumor cells cultured in control medium. Experimental metastasis of tumor cells obtained from 20% w/v ethanol-consuming mice was also significantly increased, compared with cells obtained from water-drinking mice. Metastasis of B16BL6 melanoma cells previously obtained from mice consuming 10% w/v ethanol did not differ from controls. In other experiments, water-drinking and ethanol-consuming (2.5%, 10%, and 20% w/v) mice were inoculated subcutaneously into the dorsal hip with B16BL6 melanoma cells, and monitored for tumor growth rate and survival time. In these experiments, survival times were significantly shorter in mice consuming 20% ethanol, compared with all other groups. Subcutaneous tumor growth rate was unaffected by ethanol consumption. Lung metastasis resulting from subcutaneous tumor implantation of B16BL6 melanoma was respectively inhibited, or absent, in 10% and 20% ethanol-consuming groups. Thus, tumor growth rate and incidence of lung metastases were not apparent determinants of decreased survival in 20% ethanol-consuming mice. The results of this study indicate that the experimental metastatic potential of B16BL6 melanoma is increased during exposure to ethanol; however, metastasis from subcutaneous tumor-bearing mice is suppressed. This latter finding is consistent with previous results in which spontaneous metastasis was also suppressed after inoculation of the tumor into the pinna of the ear. Although ethanol increases the ability of B16BL6 melanoma to colonize the lung after intravenous inoculation, this effect is abated in the presence of host factors in ethanol-consuming mice. 相似文献
17.
ES Dierenfeld PP Hoppe MH Woodford NP Krilov VV Klimov NI Yasinetskaya 《Canadian Metallurgical Quarterly》1997,28(2):144-147
To describe the features of railway-related deaths in Cape Town, South Africa, we reviewed demographic, autopsy, and accident report data on all such deaths between 1 April 1992 and 30 September 1994. Of the 379 railway-related deaths, 27 were among pedestrians or commuters who were hit by a train while crossing the track, 38 were among commuters who fell from moving trains, 32 were suicides, 43 were the result of criminal violence on trains or at railway stations, and 38 were due to other causes. Most railway fatalities were among men between the ages of 25 and 44 years. About half of all railway fatalities occurred at peak commuting times, with high levels of violence (often robbery related) recorded during the evening peak. A blood alcohol concentration > 0.1 g/100 ml was found in 35% of the people who died from crossing the track or falling from moving trains. Fatal railway injury is characterized by extensive disruption of more than one body region. The high levels of fatal railway injury make a strong case for a range of injury control interventions, including ticket control, surveillance, law enforcement, and safety engineering. 相似文献
18.
VIu Kulikov VP Kaznacheev NG Kolosova LV Molchanova 《Canadian Metallurgical Quarterly》1976,82(9):1086-1088
Physiological concentration (10 units/ml) of heparin activates ascorbate-dependent lipid peroxidation of erythrocytes and reduces their stability in the citrate-phosphate buffer (pH 3.0). In a concentration of 100 units/ml heparin does not influence the thermal (62 degrees) oxidation of methyloleate. It follows that heparin is not direct prooxidant. 相似文献
19.
Y Morita T Yoshikawa S Takeda K Matsuyama S Takahashi N Yoshida MG Clemens M Kondo 《Canadian Metallurgical Quarterly》1998,17(4):383-389
Ophthalmologists play a relatively peripheral role in medical student and resident education. A review of the evolution, funding, and administration of medical education in the United States lends insight into why this is so. The author reviews the current status of education in ophthalmology for medical students and residents; the development of an ophthalmology curriculum; alternatives to the traditional medical school curriculum and how these have been incorporated into ophthalmic education; and the effect of new trends in medical education and pressures created by health care reform on the education of medical students and residents. The role of ophthalmologists in the general practice of medicine and in teaching doctors about the eye is discussed. Finally, the opportunity that the current climate presents for ophthalmologists to define their role in health care through education is considered. 相似文献
20.
Oxidation of alpha-tocopherol during the peroxidation of dilinoleoylphosphatidylcholine in liposomes
Liposomal suspensions of dilinoleoylphosphatidylcholine (DLPC) containing alpha-tocopherol (0.1 mol%, based on DLPC were oxidized at 37 degrees C. The oxidation was initiated by a lipid-soluble or water-soluble free radical initiator, or by the addition of CuSO4 and fructose. In all the oxidation systems, alpha-tocopherol suppressed the formation of DLPC hydroperoxides until all the alpha-tocopherol had been depleted. The oxidation products of alpha-tocopherol were 8a-alkyldioxy-alpha-tocopherones, 5,6-epoxy-alpha-tocopherylquinone, 2,3-epoxy-alpha-tocopherylquinone, and alpha-tocopherylquinone. The 8a-alkyldioxy-alpha-tocopherones were decomposed in the liposomes primarily by being hydrolyzed to produce alpha-tocopherylquinone. The results indicate that alpha-tocopherol can trap peroxyl radical to form 8a-alkyldioxy-alpha-tocopherones which are hydrolyzed to alpha-tocopherylquinone in phospholipid bilayers. In another oxidation pathway, alpha-tocopherol may be oxidized by peroxyl radicals to form isomeric epoxy-alpha-tocopherylquinones. 相似文献