Hepatoprotective effects of Nigella sativa L and Urtica dioica L on lipid peroxidation, antioxidant enzyme systems and liver enzymes in carbon tetrachloride-treated rats

AIM: To investigate the effects of Nigella sativa L (NS) and Urtica dioica L (UD) on lipid peroxidation, antioxidant enzyme systems and liver enzymes in CCl4-treated rats. METHODS: Fifty-six healthy male Wistar albino rats were used in this study. The rats were randomly allotted into one of the four experimental groups: A (CCU-only treated), B (CCU+UD treated), C (CCU+NS treated) and D (CCl4+UD+NS treated), each containing 14 animals. All groups received CCU (0.8 mL/kg of body weight, sc, twice a week for 60 d). In addition, B, C and D groups also received daily i.p. injections of 0.2 mL/kg NS or/and 2 mL/kg UD oils for 60 d. Group A, on the other hand, received only 2 mL/kg normal saline solution for 60 d. Blood samples for the biochemical analysis were taken by cardiac puncture from randomly chosen-seven rats in each treatment group at beginning and on the 60th d of the experiment. RESULTS: The CCl4 treatment for 60 d increased the lipid peroxidation and liver enzymes, and also decreased the antioxidant enzyme levels. NS or UD treatment (alone or combination) for 60 d decreased the elevated lipid peroxidation and liver enzyme levels and also increased the reduced antioxidant enzyme levels. The weight of rats decreased in group A, and increased in groups B, C and D. CONCLUSION: NS and UD decrease the lipid peroxidation and liver enzymes, and increase the antioxidant defense system activity in the CCl4-treated rats.     

Red cell lipid peroxidation and antioxidant enzymes in iron deficiency

Whether iron deficient RBC in humans have a reduced, or an increased, susceptibility to lipid peroxidation was studied in the iron deficiency states of primary proliferative polycythaemia and iron deficiency anaemia and related to changes in the activities of iron-dependent and non-iron dependent antioxidant enzymes. Susceptibility of RBCs to lipid peroxidation was increased when expressed per g Hb. However, this was a result of the low RBC Hb giving an increased membrane lipid: Hb ratio in the incubations. Results were normal when expressed either per cell, or per ml, RBC. Glutathione reductase was normal. Increased RBC superoxide dismutase activity in iron deficiency may be explained by the younger RBC population and reductions in glutathione peroxidase and catalase activities by the microcytic hypochromic changes and the lack of availability of iron, respectively. There is no evidence of an increased susceptibility of RBC to lipid peroxidation in iron deficiency.     

Met-enkephalin modulates lipid peroxidation and total sialic acid level in CBA mice in age- and sex-dependent manners

Age- and sex-associated differences in lipid peroxidation (LPO), and total sialic acid content (TSA) in response to abuse of drugs have been reported both in humans and experimental animals. However, no data on the influence of gender and age on these parameters have been reported for methionine-enkephalin (MENK). In this study we examined the influence of age and gender on MENK-induced LPO levels in the liver and TSA content in splenocytes of CBA mice. LPO production, which was age- and gender-associated was differentially regulated by MENK at a dose of 10 mg or 2.5 mg/kg body weight. At the higher dose, MENK stimulated LPO production in younger males and females but suppressed only in older male mice. At the lower dose, MENK induced strong suppression in males while being without any effect in females. In TSA levels, the age-associated increase was greater in males and much lower in females, with higher TSA levels in younger (2.5, 4.5 months) and decreased levels in older female mice (9 months) being observed. Contrary to the effect on LPO level, TSA level in MENK-treated mice was suppressed in both sexes but only in young 2.5-month-old mice. These data provide evidence that some immunomodulatory properties of MENK are age- and gender-associated which may be relevant to the potential use of MENK as adjuvant therapy in patients with immunocompromised status.     

Melatonin and tryptophan counteract lipid peroxidation and modulate superoxide dismutase activity in ringdove heterophils in vivo. Effect of antigen-induced activation and age

Aging is associated with an increased production of free radicals and alterations in the mechanisms of adaptation to stress. A number of studies have shown a causal connection between age-related oxidant/antioxidant imbalance and the diminution of an organism’s melatonin levels in old age. Restoration of this rhythm may contribute to the re-stabilization of cellular homeostasis. The present work was aimed at examining the effect of the administration of melatonin or its precursor, the amino acid tryptophan, on heterophil lipid peroxidation (LPO) levels and superoxide dismutase (SOD) activity in heterophils from young (4–5 year) and old (12–14 year) ringdoves (Streptopelia risoria) under both basal and antigen-induced (stressful) conditions. Young animals were treated for 3 consecutive days with a single daily oral dose (0.25 mg) of melatonin at 1900 hours while old animals were treated for 3 consecutive days with either an oral dose (2.5 mg) of melatonin at 1900 hours or an oral capsule of 300 mg/kg body weight of l-tryptophan at 0900 hours. Non-treated old animals presented lower circulating levels of melatonin at night and higher levels of malonaldehyde (MDA) both day and night when compared to young birds. In both age groups, LPO levels were lower at night than during the day. Melatonin or tryptophan treatments significantly increased serum melatonin levels, reinforced SOD activity, and reduced MDA levels induced by the antigen. Melatonin and tryptophan may be useful agents for the treatment of disease states and processes in which an excessive production of oxidative damage occurs.     

Effect of chronic smoking on lipid peroxidation and antioxidant status in gastric carcinoma patients

Oxidative stress plays an important role in malignant transformation and is postulated to be associated with increased lipid peroxidation. We determined the effects of chronic cigarette smoking on lipid peroxidation and antioxidant status in 100 male patients with gastric cancer and an equal number of age-matched healthy control subjects. The mean (SD) level of thiobarbituric acid reactive substances (TBARS) was higher in plasma (healthy non-smokers 3.1 [0.2]; healthy smokers 4.6 [0.2]; gastric cancer non-smokers 6.5 [1.0]; gastric cancer smokers 8.9 [3.1]) and erythrocytes (3.3 [0.6]; 4.6 [0.1]; 8.3 [0.9]; 13.2 [5.1]) from gastric cancer patients when compared with control subjects. TBARS level was higher in smokers than non-smoking gastric cancer patients. The activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-treansferase, reduced glutathione, and vitamins A, E and C were decreased in gastric cancer patients who were smokers as compared to other groups (p<0.001). Thus, there occurs lipid peroxidation and possible breakdown of antioxidant status in cigarette smoking, which may increase the risk of gastric cancer.     

蛇床子素对四氯化碳诱导小鼠脂质过氧化反应的影响

目的:研究蛇床子素(Ost)对四氯化碳(CCl_4)诱导小鼠脂质过氧反应的影响.方法:40只昆明种小鼠随机平均分为4组:正常对照组、模型组、Ost治疗1组(50 g/kg)、Ost治疗2组(100 g/kg).除对照组外,其余各组腹腔注射1 g/L CCl_4花生油溶液.16 h后分别测定血清SOD和T-AOC及肝组织MDA,NO和T-AOC.结果:与模型组相比,50 g/kg Ost显著升高肝组织NO含量(F=6.171,P=0.01);100 g/kg Ost显著降低CCl_4中毒小鼠肝组织中MDA含量(F=3.547,P=0.04),升高NO(F=3.698,P =0.009)和T-AOC(P=0.000)以及血清中提高SOD活性(F=4.797,P=0.04)和T-AOC(F= 3.103,P=0.02).结论:蛇床子素有抗脂质过氧化作用.     

高砷水对机体氧化与抗氧化能力的影响

目的研究高砷水区人群血中氧化与抗氧化能力的影响,探讨高砷水对机体的危害及机理。方法对不同人群血中超氧化物歧化酶(SOD)总量、谷胱甘肽过氧化物酶(GSH鄄Px)、谷胱甘肽(GSH)和脂质过氧化物(LPO)进行测定和分析。结果SOD随饮水砷浓度增高而代偿性增高,在36～55岁年龄段最明显,该年龄段对照组LPO明显低于高水砷组(P<0.05);GSH对照组高于高水砷组(P<0.05);GSH鄄Px变化不大,只有55岁以上年龄段对照组高于高水砷组。结论饮用高砷水可影响机体氧化与抗氧化系统,在轻中度砷中毒时,可引起抗氧化物代偿性增加和脂质过氧化的发生,并对机体造成损伤。     

Effect of age on lipid peroxidation in a short-lived species of reptile, Calotes versicolor

The lipid peroxidation potential, measured as a thiobarbituric acid-reactive substance (TBA-RS) increased with advancing age in liver, brain and kidney of a short-lived species of reptile, Calotes versicolor. The same parameter did not show a significant change in an ageing heart. The pattern of age changes in lipid peroxidation potential in this species shows similarity with the findings in a majority of mammalian species. While suggesting a commonality in a basic mechanism of ageing between reptiles and mammals, the results also partially support the free radical theory of ageing.     

Effect of age on lipid peroxidation in a short-lived species of reptile, Calotes versicolor

The lipid peroxidation potential, measured as a thiobarbituric acid-reactive substance (TBA-RS) increased with advancing age in liver, brain and kidney of a short-lived species of reptile, Calotes versicolor. The same parameter did not show a significant change in an ageing heart. The pattern of age changes in lipid peroxidation potential in this species shows similarity with the findings in a majority of mammalian species. While suggesting a commonality in a basic mechanism of ageing between reptiles and mammals, the results also partially support the free radical theory of ageing.     

Studies on cumene hydroperoxide-induced lipid peroxidation in the isolated perfused rat heart

In the isolated, perfused rat heart, lipid peroxidation, induced by cumene hydroperoxide (Cum OOH), is accompanied by the release of malondialdehyde (MDA). Using a modified perfusion technique resulting in the separate collection of coronary and interstitial effluent, it can be shown that upon Cum OOH (0.5 mM) perfusion there is an immediate release of MDA in the coronary effluent and a delayed release in the interstitial fluid, indicating the susceptibility and coronary vascular tissue towards free radical-induced lipid peroxidation. Perfusion with Cum OOH leads to an initial increase of the coronary flow and a depressed contractility followed by a cardiac arrest concomitantly with the onset of MDA release in the interstitial fluid. Finally, during prolonged perfusion the coronary flow diminishes and contracture of the heart muscle ('stone heart') develops. These phenomena resemble those occurring during the 'calcium paradox'. Although the contractility diminishes immediately after the perfusion with Cum OOH the tissue ATP level and energy charge (formula; see text) remain constant. From the moment of cardiac arrest the ATP and creatine phosphate levels gradually decrease and the energy charge drops simultaneously with the appearance of MDA in the interstitial fluid. In contrast to the calcium paradox there is no simultaneous increase in the myocardial AMP level. Various mitochondrial enzymes (cytochrome c oxidase, monoamine oxidase, carnitinepalmitoyltransferase I and palmitoyl CoA synthetase) were tested and not affected by Cum OOH perfusion. During the development of contracture after 20 min of Cum OOH perfusion massive contraction band necrosis of cardiac tissue occurs. However, overall protein release is lower when compared with the protein release during the calcium paradox.(ABSTRACT TRUNCATED AT 250 WORDS)     

Antioxidant,lipid peroxidation inhibition and free radical scavenging efficacy of a diterpenoid compound sugiol isolated from Metasequoia glyptostroboides

Objective:To investigate the antioxidant enicacy of a biologically active dilerpenoid compound sugiol isolated from Metasequoia glyptostroboides(M.glyptostroboides)in various antioxidant models.Methods:An abietane type diterpenoid sugiol,isolated from ethyl acetate extract of M.glyptostroboides cones,was analyzed for its antioxidant efficacy as reducing power ability and lipid peroxidation inhibition as well as its ability to scavenge free radicals such as 1,1-diphenyl-2-picryl hydrazyl,nitric oxide,superoxide and hydroxyl radicals.Results:The sugiol showed significant and concentration-dependent antioxidant and free radical scavenging activities.Consequently,the sugiol exerted lipid peroxidation inhibitory effect by 76.3%as compared to a-tocopherol(80.13%)and butylaled hydroxyanisole(76.59%).In addition,the sugiol had significant scavenging activities of l,l-diphenyl-2-picryl hydrazyl,nitric oxide,superoxide and hydroxyl free radicals in a concentration-dependent manner by 78.83%,72.42%,72.99%and 85.04%,when compared to the standard compound ascorbic acid(81.69%,74.62%,73.00%and 73.79%)and a-tocopherol/butylated hydroxyanisole(84.09%,78.61%,74.45%and 70.02%),respectively.Conclusions:These findings justify the biological and traditional uses of M.glyptostroboides or its secondary metabolites as confirmed by its promising antioxidant efficacy.     

高血压患者过氧化损伤及血清一氧化氮水平分析

目的 :探讨脂质过氧化损伤水平和血清一氧化氮 (NO)浓度及其与血压的关系。方法 :随机选取一个社区 2 3～ 5 9岁人群 2 0 0例 ,按年龄分为 2 3～、30～、4 0～和 5 0～ 5 9岁 4组 ,分别进行常规体检和测定NO、超氧化物歧化酶 (SOD)和丙二醛 (MDA)活性 ,探讨上述 3个指标与高血压 (≥ 14 0 / 90mmHg ,1mmHg =0 .133kPa)之间的关系。结果 :①随年龄的增加 ,心电图和肝胆B超检查异常率均逐渐上升 ,血清总胆固醇水平随年龄增长也呈现增加趋势 ,而三酰甘油水平在 4组之间未发现明显差异 ;②随年龄的增加 ,原发性高血压 (EH)发病率上升 ,血浆NO水平逐渐下降 ,而MDA含量则呈上升趋势 ,其中血浆NO水平与EH的关系非常密切 (r =- 0 .986 ,P <0 .0 5 )。结论 :脂质过氧化损伤和血浆NO水平下降可能共同促进了EH的发生和发展     

砷中毒对小鼠脏器脂质过氧化的影响及VE干预作用的研究

目的研究不同水平的砷对小鼠脏器组织脂质过氧化的影响,并观察维生素E(VE)对砷毒作用的干预作用。方法昆明种小鼠按2因素3水平析因实验设计分为9组,不同实验组的动物通过喂饲法给三氧化二砷和VE复制亚慢性砷中毒动物模型。三氧化二砷的分组剂量按照其对小鼠经口半数致死量LD50进行分组,VE按照我国青少年每日推荐量进行分组。2个月后,采用试剂盒,研究砷对小鼠脏器组织中超氧化物歧化酶(SOD)活力、谷胱甘肽过氧化物酶(GSH-Px)活力及丙二醛(MDA)含量的影响以及给于VE处理后的干预作用。结果染毒组动物脏器组织中SOD、GSH-Px活力低于正常对照组动物(P<0.05),MDA含量高于正常对照组(P<0.05);VE处理后动物脏器组织中SOD、GSH-Px活力增强,MDA含量降低(P<0.05)。结论砷能引起小鼠脏器组织中氧化与抗氧化系统失衡,VE可拮抗砷对小鼠脏器氧化水平与抗氧化能力的影响。     

Clinicopathological significance of lipid peroxidation in carotid plaques

Several reports have suggested an association between lipid peroxidation and human carotid atherosclerosis, but few reports have demonstrated a link between lipid peroxidation and carotid plaques in humans. In this study, we investigated the relationship between clinical features, histopathological characteristics and lipid peroxidation in patients undergoing carotid endarterectomy (CEA). Forty-one carotid plaques were obtained. A portion of the most severe lesions was subjected to histopathologic examination, and the remainder of the plaques examined for lipid peroxidation. Thiobarbituric acid-reactive substances (TBARS) values were determined as a marker for lipid peroxidation. The lipid-rich core (LC) and macrophage infiltration (Mφ) component as a percentage of total plaque area were measured morphometrically. Based on the results, all plaques were classified into four groups. Group I (GI): LC <10%; Group IIa (GIIa): LC 10–30%, Mφ <5%; Group IIb (GIIb): LC 10–30%, Mφ ≥5%, and Group III (GIII): LC ≥30%. The plaque TBARS values of GIII were significantly higher than those of GI, GIIa, and GIIb. The TBARS values of GIIb were one-and-a-half times higher than those of GIIa. Our results show that lipid peroxidation in carotid plaques is significantly associated with carotid atherosclerosis, especially plaque instability. These findings provide direct evidence of an association between lipid peroxidation and human atherosclerosis.     

慢性愤怒应激对衰老大鼠学习记忆能力的影响及其脂质过氧化机制

目的 观察慢性愤怒应激对D-半乳糖(D-gal)引起的衰老大鼠空间学习记忆能力的影响,并从脂质过氧化与抗氧化角度解释其作用机制.方法 采用夹尾间接激怒法诱导被攻击大鼠产生愤怒应激,观察慢性愤怒应激对衰老大鼠空间学习记忆能力和血清SOD活性及心、肝组织MDA、LPF含量的影响,分析心、肝MDA、LPF含量与血清SOD活性的相关性.结果 愤怒D-gal组大鼠较D-gal组寻台时间显著延长(P＜0.05),血清SOD活性显著降低(P＜0.05),心、肝组织MDA、LPF含量显著提高(P＜0.05,P＜0.01),心、肝MDA、LPF含量与血清SOD活性呈负相关.结论 慢性愤怒应激可降低衰老大鼠的学习记忆能力,加速衰老进程.抑制机体抗氧化能力,加重心、肝等重要脏器组织脂质过氧化可能是其机制之一.     

Relationship between oxidative and occupational stress and aging in nurses of an intensive care unit

Stressful conditions lead to formation of excessive reactive oxygen species (ROS) and cause oxidative stress and aging. The aim of this study was to determine superoxide dismutase (SOD) and catalase (CAT) activity, and malondialdehyde (MDA) levels in nurses of a hospital intensive care unit according to demographic and occupational parameters, and to analyse the relationship with aging. Thirty-two nurses working in an intensive care unit and 35 aged-matched healthy individuals of both sexes as a control group were surveyed. No significant variations with respect to sex were detected in SOD, CAT, MDA and burnout levels. MDA levels increased with age in both the control group and the nurses, and we observed significant differences in MDA levels between the control group and nurses for all age groups. Significant variations in MDA levels were detected between single (286.12 ± 8.41) and married (318.82 ± 6.02), people, between those who frequently practice some kind of sport (281.41 ± 7.32) and those who never participate in sport (298.24 ± 8.11) ,and between those who frequently eat fruit and greens (289.75 ± 8.41) and those who never eat them (315.12 ± 7.21). Significant differences were detected between smokers and nonsmokers in SOD, CAT and MDA, but not for alcohol, coffee, tea or cola consumption. Higher SOD activity and MDA levels were detected in nurses on evening and night shifts (P < 0.01); these nurses also scored significantly higher on burnout subscales. These results suggest that: (1) occupational stress increases oxidative stress levels as a response to elevated ROS generation; (2) occupational stress increases MDA levels as a response to an elevation in free radical generation and can lead to aging; (3) working evening and night shifts increases oxidative and burnout levels. It is evident that preventive changes in job conditions and lifestyle are necessary to improve the quality of life of nurses who work in intensive care units.     

Lactoferrin inhibits lipid peroxidation in patients with chronic hepatitis C.

Lactoferrin is a milk protein with inhibitory effect on lipid peroxidation induced by oxidative stress. Oxidative stress plays an important role in the pathogenesis of chronic hepatitis C (CHC). The aim of this study was to evaluate the effect of bovine lactoferrin (bLF) monotherapy on lipid peroxidation, hepatic inflammation and iron metabolism in patients with CHC. Ninety Japanese patients with CHC were randomly assigned to two groups: bLF group (n=47) treated with bLF at a dose of 3.6g/day and a control group (n=43) that remained untreated. Plasma 8-isoprostane levels and clinical laboratory data including iron metabolism parameters were measured. Plasma 8-isoprostatne level was significantly decreased from 8.6+/-3.7 to 6.9+/-2.1pg/ml in the bLF group (P<0.05). Plasma levels of 8-isoprostane did not significantly change in the control group. The decline in plasma 8-isoprostane levels was positively correlated with improvement in the level of ALT in the bLF group. No significant change in serum HCV RNA levels or iron metabolism markers was found after bLF treatment. Therapy with bLF was associated with improvement in lipid peroxidation and ALT levels in CHC. Administration of bLF is a promising therapeutic approach for suppressing oxidative stress in non-responders to antiviral therapy.     

硒与GSH联合对氟致大鼠脂质过氧化作用的影响

目的　研究抗氧化剂硒及与不同剂量 GSH联合对氟所致脂质过氧化作用的影响。方法　采用动物实验。结果　饮含氟化钠 (15 0 mg/ L)水可使大鼠肝、肾及血清中 L PO含量显著增加 ;SOD活性、GSH- Px活性、GSH含量均显著下降 ;饮含氟水同时给亚硒酸钠 ,可使血清中 L PO含量显著下降 ;SOD活性、GSH- Px活性、GSH含量显著升高。说明硒对氟引起的脂质过氧化有拮抗作用。饮含氟水同时给 Se与不同剂量 GSH后 ,结果显示 :Se与低、中、高 3个剂量 GSH均可使血清中 L PO含量显著下降 ,全血中 SOD活性显著增强 ,呈剂量—效应关系 ,使肝、肾及全血中 GSH- Px活性不同程度增强 ,表明 Se与 GSH联合可有效拮抗氟所致的脂质过氧化作用 ,恢复机体抗氧化能力。结论　 1氟可引起大鼠肝、肾及全血中脂质过氧化物含量升高 ,抗氧化能力下降 ;2硒及与不同剂量 GSH联合具有不同程度拮抗氟诱导的脂质过氧化作用 ,恢复机体的抗氧化能力     

依达拉奉对实验性肝纤维化大鼠脂质过氧化的影响

目的探讨依达拉奉（EDA）对实验性肝纤维化大鼠脂质过氧化的影响。方法以四氯化碳诱导大鼠肝纤维化模型。30只Sprague—Dawley大鼠随机分为对照组（10只）、肝纤维化模型组（10只）和EDA防治组（10只）。检测各组大鼠血清谷丙转氨酶、谷草转氨酶水平及肝组织羟脯氨酸、丙二醛含量和超氧化物歧化酶活性。结果EDA防治大鼠血清谷丙转氨酶和谷草转氨酶水平分别为714．2±28．2U／L和766．0±11．0U／L,较模型组（1110．3±45．9U／L和1640．3±26．7U／L,P〈0．05和P〈0．01）明显降低;EDA组大鼠肝组织羟脯氨酸和丙二醛含量分别为0．4±0．1μg／mg和5．5±2．3nmol／gl,较模型组（0．8±0．1μg／mg和7．5±2．1nmol／gl,P均〈0．01）显著下降;EDA组大鼠超氧化物歧化酶活性为129．7±2．3u／g,较模型组（933±3．9u／g,P〈0．01）明显升高;EDA组和模型组大鼠肝组织纤维化评分分别为2．7±1．0和3．5±0．7,差异显著（P〈0．01）。结论EDA对大鼠肝纤维化有一定的防治作用,其机制很可能与抗脂质过氧化损伤有关。     

Effects of ethanol on antioxidant capacity in isolated rat hepatocytes

AIM: To investigate dose-response and time-course of the effects of ethanol on the cell viability and antioxidant capacity in isolated rat hepatocytes. METHODS: Hepatocytes were isolated from male adult Wistar rats and seeded into 100-mm dishes. Hepatocytes were treated with ethanol at concentrations between 0 (C), 10 (E10), 50 (E50), and 100 (E100) mmol/L (dose response) for 12, 24, and 36 h (time course). Then, lactate dehydrogenase (LDH) leakage, malondialdehyde (MDA) concentration, glutathione (GSH) level, and activities of glutathione peroxidase (GPX), glutathione reductase (GRD), superoxide dismutase (SOD), and catalase (CAT) were measured. RESULTS: Our data revealed that LDH leakage was significantly increased by about 30% in group E100 over those in groups C and E10 at 24 and 36 h, The MDA concentration in groups C, E10 and E50 were significantly lower than that in group E100 at 36 h. Furthermore, the concentration of MDA in group E100 at 36 h was significantly higher by 4.5- and 1.7-fold, respectively, than that at 12 and 24 h. On the other hand, the GSH level in group E100 at 24 and 36 h was significantly decreased, by 32% and 28%, respectively, compared to that at 12 h. The activities of GRD and CAT in group E100 at 36 h were significantly less than those in groups C and E10. However, The GPX and SOD activities showed no significant change in each group. CONCLUSION: These results suggest that longtime incubation with higher concentration of ethanol (100 mmol/L) decreased the cell viability by means of reducing GRD and CAT activities and increasing lipid peroxidation.