Studies on Toxicity,Anti—stress and Hepato—Protective properties of Kombucha Tea

Objective :The objective of the study was to evaluate toxicity,anti-stress activity and hepatoprotective properties of Kombucha tea.Method :Kombucha tea was fed orally for 15 days using three different doses i.e.normal dose,five and ten times the dose,Rats were then sacrficed and various biochemical,and histological parameters were estimated.Anti-stress activity was evaluated either by 1)by exposing animals to cold and hypoxia and estimating the levels of malondialdehyde and reduced glutathione in plasma/blood or 2) by subjecting the animals to restraint stress and recording faecal output.Hepato-toxicity was induced by challenging the animals to an acute dose of paracetamol(1gm/kg)orally and determining the plasma levels of SGPT,SGOT and MDA.REsults:The effect of oral administration of different doses of K-tea to albion rats was examined and the results indicate that K-tea has no significant toxicity as revealed by various biochemical and histopathological parameters.K-tea has been found to prevent lipid peroxidation and fall in reduced glutathione level when rats were exposed to cold and hypoxia in simulated chamber.Further,K-tea has also been found to decrease the Wrap-restraint faecal pellet output in rats.K-tea has also been found to decrease paracetamol induced hepatotoxicity significantly.Conclusion:The study shows that K-tea has anti-stress and hepato-protective activities.     

Hypoglycemic and antioxidant activities of Caesalpinia ferrea Martius leaf extract in streptozotocininduced diabetic rats

Objective: To evaluate the antidiabetic and antioxidant ef ects of aqueous ethanolic extract of Caesalpinia ferrea(C. ferrea) leaf in normal and streptozotocin(STZ) induced diabetic rats.Methods: Male Sprague-Dawley rats divided into 6 groups of 6 rats each were assigned into diabetic and non-diabetic groups. Diabetes was induced in rats by single intraperitoneal administration of STZ(65 mg/kg body weight). C. ferrea extract at the doses of 250 and 500 mg/kg body weight was orally administered to both diabetic and non-diabetic animals for a period of 30 days. After completion of experimental duration serum, liver and pancreas were used for evaluating biochemical and histopathological changes.Results: Oral administration of C. ferrea leaf extract significantly reduced elevated serum glucose, α-amylase, liver function levels and signii cantly increased serum insulin, total protein and body weight as well as improved lipid proi le due to diabetes. Furthermore, the treatment resulted in a marked increase in glutathione peroxidase, superoxide dismutase, catalase and reduced glutathione, and diminished levels of lipid peroxidation in liver and pancreas of diabetic rats. Histopathological studies demonstrated the reduction in the pancreas and liver damage and coni rmed the biochemical i ndings.Conclusions: From the present study, it can be concluded that the C. ferrea leaf extract ef ectively improved hyperglycaemia while inhibiting the progression of oxidative stress in STZ-induced diabetic rats. Hence, it can be used in the management of diabetes mellitus.     

Protective role of Triphala,an Indian traditional herbal formulation,against the nephrotoxic effects of bromobenzene in Wistar albino rats

OBJECTIVE: The purpose of the present study was to evaluate the nephroprotective and antioxidant properties of Triphala against bromobenzene-induced nephrotoxicity in female Wistar albino rats. METHODS: Animals were divided into five groups of six rats and treated as follows: Group I was a normal control and received no treatment, Group II received only bromobenzene(10 mmol/kg), Groups III and IV received bromobenzene and Triphala(250 and 500 mg/kg, respectively), Group V received Triphala alone(500 mg/kg), and Group VI received bromobenzene and silymarin(100 mg/kg). Antioxidant status and serum kidney functional markers were analyzed.RESULTS: Bromobenzene treatment resulted in significant(P < 0.05) decreases in the activities of antioxidant enzymes such as catalase, superoxide dismutase, glutathione-S-transferase and glutathione peroxidase as well as total reduced glutathione. There was a significant(P < 0.05) increase in lipid peroxidation in kidney tissue homogenates. There were significant(P < 0.05) reductions in the levels of serum total protein and albumin as well as significant(P < 0.05) increases in serum creatinine, urea and uric acid. The oral administration of two different doses(250 and 500 mg/kg) of Triphala in bromobenzene-treated rats normalized the tested parameters. The histopathological examinations of kidney sections of the experimental rats support the biochemical observations. CONCLUSION: Triphala treatment alleviated the nephrotoxic effects of bromobenzene by increasing the activities of antioxidant enzymes and reducing the levels of lipid peroxidation and kidney functional markers.     

Inhibitory Effect of Estrogens,Phytoestrogens,and Caloric Restriction on Oxidative Stress and Hepato-toxicity in Aged Rats

Objective To investigate the protective effect of 17β-estradiol （E2）, peganum harmala extract （PHE） administration and calorie restriction （CR） treatment （60%） on oxidative stress and hepato-toxicity in aged rats. Methods Eighteen months old animals that were treated at the age of 12 months were divided into 4 groups： normal control group with free access to food, E2 treatment group, PHE treatment group and CR treatment group of the food given to control group. Six male rats at the age of 4 months were used as a reference group. Results Aging significantly decreased superoxide dismutase （SOD）, catalase （CAT） and glutathione peroxidase （GPX）, and increased lactate deshydrogenase （LDH）, gamma-glyiamyl transferase （GGT）, pbosphatase alkalines （PAL）, aspartate and lactate transaminase （AST and ALT） activities in the liver. Aging also induced an increased lipid peroxidation level, histological changes and a decreased E2 level. However, treatment with E2, PHE, and CR increased 17β-estradiol, and decreased hepatic dysfunction parameters and lipid peroxidation as well as histological changes in the liver of aged rats. Conclusion The antioxidant and hepatoprotective activity of PHE and CR is possibly attributed to its ability to increase E2 level, which as an antioxidant, acts as a scavenger of ROS. Further studies on the pharmaceutical functions of E2 in males may contribute to its clinical application.     

Antioxidant properties of magnesium lithospermate B contribute to the cardioprotection against myocardial ischemia/reperfusion injury invivo and invitro

OBJECTIVE: To determine the cardioprotective effect of magnesium lithospermate B (MLB) on myocardial ischemia/reperfusion (MI/R) injury and to investigate the antioxidant potential in vivo and in vitro. METHODS: MI/R injury was induced by the occlusion of left anterior descending coronary artery for 30 min followed by reperfusion for 3 h in rats. After reperfusion, hearts were harvested to assess infarct size, histopathological damages, the levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH) and malondialdehyde (MDA). Blood samples were col- lected to determine serum levels of creatine kinase-MB (CK-MB), cardiac troponin (cTnI) and lactate dehydrogenase (LDH). Furthermore, simulatedischemia/reperfusion (SI/R) injury in vitro was established by oxygen and glucose deprivation (OGD) for 2 h followed by 24-hour recovery period in cardiomyocytes. The activity of LDH in the cultured supernatant and the levels of intracellular reactive oxygen species (ROS), SOD and MDA in cardiomyocytes were also measured. Finally, cardiomyocytes apoptosis was determined with flow cytometry. RESULTS: MLB significantly limited infarct size, ameliorated histopathological damages and prevented leakage of CK-MB, cTnI and LDH. Additionally, SOD, CAT, GPx and GSH activities were notably increased by MLB, along with the MDA content decreased as compared with the model group in rats. In vitro study, MLB also decreased LDH activity in the cultured supernatant, increased SOD activity in cardiomyocytes, reduced intracellular ROS and MDA levels, and significantly suppressed cardiomyocytes apoptosis. CONCLUSION: MLB possessed remarkably cardioprotective effects on MI/R injury in vivo and in vitro. The protection of MLB may contribute to its antioxidant properties.     

Effects of Carpobrotus edulis Extract on Oxidative Stress and 158N Oligodendrocyte Death

Objective Age-related diseases, including neurodegenerative diseases, are associated with oxidative stress and lipid peroxidation, and increase the levels of cholesterol auto-oxidation products such as 7β-hydroxycholesterol(7β-OHC). Thus, it is imperative to identify agents that can prevent 7β-OHC-induced side-effects. Methods We evaluated the potential protective effects of Carpobrotus edulis ethanol-water extract(EWe) on murine oligodendrocytes(158 N) cultured in the absence or presence of 7β-OHC(20 μg/mL, 24 h). The cells were incubated with EWe(20-200 μg/mL) 2 h before 7β-OHC treatment. Mitochondrial activity and cell growth were evaluated with the MTT assay. Photometric methods were used to analyze antioxidant enzyme [catalase(CAT) and glutathione peroxidase(GPx)] activities and the generation of lipid and protein oxidation products [malondialdehyde(MDA), conjugated diene(CD), and carbonylated proteins(CPs)]. Results Treatment with 7β-OHC induced cell death and oxidative stress(reflected by alteration in CAT and SOD activities). Overproduction of lipid peroxidation products(MDA and CDs) and CPs was also reported. The cytotoxic effects associated with 7β-OHC were attenuated by 160 μg/mL of EWe of C. edulis. Cell death induced by 7β-OHC treatment was ameliorated, GPx and CAT activities were restored to normal, and MDA, CD, and CP levels were reduced following C. edulis extract treatment. Conclusion These data demonstrate the protective activities of C. edulis EWe against 7β-OHC-induced disequilibrium in the redox status of 158 N cells, indicative of the potential role of this plant extract in the prevention of neurodegenerative diseases.     

Protective effect of diosmin against diabetic neuropathy in experimental rats

OBJECTIVE： The present study was undertaken to evaluate the effect of diosmin in diabetic neuropathy in type 2 diabetic rats. METHODS： Type 2 diabetes was induced in male Sprague-Dawley rats by single intraperitoneal injection of streptozotocin （35 mg/kg） and high-fat diet. Four weeks after the confirmation of diabetes, diabetic rats were treated with diosmin （50 and 100 mg/kg, p.o.） for next 4 weeks. Rats were evaluated for biochemical, behavioral and oxidative stress parameters. Eddy＇s hot plate and tail immersion test were performed on 6th, 7th, 8th, 9th and 10th weeks of experiment to assess thermal hyperalgesia and cold allodynia respectively. Further, the walking function test was performed for assessing the motor responses at the end of the treatment schedule. RESULTS： Rats were fed with high-fat diet throughout the experiment schedule and administration of low-dose streptozotocin induced significant elevation in blood glucose level and insulin resistance which was confirmed by oral glucose tolerance test. Treatment with diosmin at doses of 50 and 100 mg/kg significantly restored the reduced body weight, elevated blood sugar and lipid profiles. Further the dose-dependent improvement was observed in thermal hyperalgesia, cold allodynia and walking function in diabetic rats treated with diosmin. Elevated levels of malondialdehyde, and nitric oxide and decreased glutathione levels and superoxide dismutase activity in diabetic rats were restored significantly after the 4 weeks of diosmin treatment. CONCLUSION： Diosmin has shown beneficial effect in preventing the progression of early diabetic neuropathy in rats.     

Changes of Selenium Metabolism Glutathione Peroxidase Activity and Lipid Peroxides Content in Severely Scalding-injured Rats

The changes of sclenium metabolism, glutathione peroxidase activity and lipid peroxidescontent in the tissues of rats suffering from 30% TBSA full thickness scalding were observed in thefirst 7 days after injury. It was found that selenium content in the rat tissues decreased remarkably af-ter injury, which in turn resulted in serious reduction of glutathione peroxidasc activity and significantincrease of lipid peroxides in the scrum, crythrocytcs and liver. However the muscular tissue showedno significant changes. These facts imply that after burn injury, the body is in a state of selenium deficiency, the lossof selenium might be responsible for the reduction of anti - peroxidation ability of glutathioneperoxidase, and conscqucntly there is an increase of lipid peroxides in the tissues. Only the musculartissue is insensitive to lipid peroxidation. It is believed that the reduction of anti-peroxidation abilityof glutathione peroxidasc after bum injury might be one of the main causes to intensify, the injury re-suiting from free radicals.     

Preventive and Therapeutic Role of Vitamin E in Chronic Plumbism

The ability of vitamin E to prevent or treat experimental lead intoxication was investigatedin rats.Lead ingestion(10 mg/kg,lead as lead acetate,orally fbr 6 weeks)significantly inhibitedthe activity of blood δ-aminolevulinic acid dehydratase(ALAD),reduced the brain dopamine(DA)contents,enhanced the blood zinc protoporphyrin,and enhanced the urinary excretion ofδ-aminolevulinic acid(ALA).Lead exposure also elevated brain norepinephrine,homovanillicacid,and 5-hydroxyindole acetic acid(5-HIAA)levels and concentration of lead in blood andtissue.Simultaneous supplementation of vitamin E along with lead significantly reduced theinhibition of blood ALAD activity,brain DA and 5-HIAA levels,and elevation of urinary ALAexcretion.Blood and liver lead concentrations were also significantly reduced by simultaneoussupplementation with vitamin E.Postlead exposure treatment with vitamin E was ineffective inreducing the lead-induced effects,except that the inhibition of blood ALAD activity was slightlyreduced.The present results suggest that vitamin E given simultaneously with lead is effectivein reducing the severity of lead intoxication.1989 Academic Press.Inc.     

Protective Efficacy of Calcium Channel Blockers in Sulphur Mustard Poisoning

The present study was designed to ascertain the in vivo protective efficacy of Ca^2 -channel blockers against dermally applied sulphur mustard(SM).Male albino mice were exposed to 1.5LD50 of SM(232mg/kg0percutaneously and the control group received an equal volume of vehicle(polyethylene glycol 300),Prior to SM application,the animals were administered nifedipine and dextrose saline containing antibiotic by intraperitoneal route,The protection assessed by the mean survival time(MST)was detrermined by Dunnett‘s method.The MST was significantly increased in nifedipine treated group.Te characteristic biochemical indices of SM intoxication.i.e.lipid peroxidation and reduced glutathione(GSH)were determined in liver from animals sacrificed at 24,48 and 72 after exposure.Sm application(1 LD50)caused a reduction in GSH level which was restored in nifedipine treated grop.Sm-induced lipid peroxidation was also prevented by nifedipine administration.The protective effect of nifedipine may be related to its capacity of attenuating SM-induced lipid peroxidation and glutathione depletion.     

铅致幼鼠脑脂质过氧化的实验研究

目的 :探讨铅致发育期中枢神经系统脂质过氧化作用。方法 :通过大鼠孕期及哺乳期不同剂量染铅及用维生素E(VitaminE ,VE)干预所致幼鼠模型 ,测定出生后第 7,2 1d幼鼠脑的脂质过氧化产物 (lipidperoxidativeproduct ,LPO)水平 ,谷胱甘肽 (glutathione ,GSH)含量及超氧化物歧化酶 (superoxidedismutase ,SOD)、谷胱甘肽过氧化物酶 (glutathioneperoxidase ,GSH PX)、过氧化氢酶 (catalase ,CAT)活力。 结果 :无论出生后 7d还是 2 1d ,中、高剂量染铅组幼鼠脑组织LPO水平升高、SOD活力下降 (P <0 .0 5 ,P <0 .0 1) ;出生后 7d幼鼠高剂量染铅组GSH含量下降 (P <0 .0 5 ) ;出生后 2 1d中剂量染铅组CAT活力下降 (P <0 .0 5 ) ;且VE拮抗了这种脂质过氧化作用 (P <0 .0 5 )。结论 :铅可能通过增强脑组织脂质过氧化过程而致发育期神经系统的损伤。     

Effect of morin on the levels of circulatory liver markers and redox status in experimental chronic hyperammonaemic rats

INTRODUCTION: Hyperammonaemia is a major contributing factor to neurological abnormalities observed in hepatic encephalopathy and in congenital defects of ammonia detoxication. Ammonia toxicity results in free radical generation that leads to oxidative stress and tissue damage. Morin is a bioflavonoid, a constituent of many herbs and fruits that are used as herbal medicines and also several biological activities. Our aim was to investigate the effect of morin on circulatory liver markers, lipid peroxidation and antioxidant status in ammonium chloride (AC)-induced hyperammonaemic rats. METHODS: Male albino Wistar rats weighing 180-200 g were used for the study. The hyperammonaemia was induced by interaperitonial injection of AC (100 mg/kg body weight). Rats were treated with morin (30 mg/kg body weight) via oral administration. Administration of morin in hyperammonaemic rats reduced the levels of ammonia and urea. The antioxidant property of morin was studied by assessing the activities of thiobarbituric acid reactive substances (TBARS), hydroperoxides (HP) and liver markers (alanine transaminase, aspartate transaminase and alkaline phosphatase) and the levels of glutathione peroxidase, superoxide dismutase, catalase, reduced glutathione, vitamins A, C and E in AC-treated rats. RESULTS: Oxidative stress was effectively modulated by morin administration. Morin significantly improved the status of antioxidants and decreased the levels of ammonia, urea, TBARS, HP and liver markers enzymes, as compared to the AC-treated group. CONCLUSION: The study offers evidence for the antihyperammonaemic, hepatoprotective and antioxidant effects of morin against oxidative stress induced by AC.     

Lipid peroxidation and antioxidant status in patients with breast cancer

INTRODUCTION: The present study was undertaken to evaluate the status of lipid peroxidation and antioxidants as biomarkers in human plasma. METHODS: The extent of lipid peroxidation as evidenced by the formation of thiobarbituric acid reactive substances (TBARS) and conjugated dienes (CD) as well as the status of the antioxidants superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), glutathione peroxidase (GPx) and glutathione S-transferase (GST) in serum samples of 40 breast cancer patients in and around Coimbatore, India, were studied. Controls consisted of members of the public with no previous history of breast cancer or other cancer-related diseases. RESULTS: The plasma samples of the breast cancer patients showed enhanced level of lipid peroxidation when compared to the corresponding controls. This was accompanied by a significant elevation in both enzymic and non-enzymic antioxidants. CONCLUSION: These findings indicate the significant increase in lipid peroxidation as evidenced by the level of TBARS and antioxidant status such as elevated SOD, CAT, GPx, GSH and GST in samples from breast cancer patients compared to controls.     

Alteration of lipid peroxidation and antioxidant enzymes in young Malaysian IDDM patients

The present study was designed to explore the relationship between lipid peroxidation and antioxidant enzymes in young Malaysian insulin dependant diabetes mellitus (IDDM) patients. Indicative parameters of lipid peroxidation, activities of antioxidant enzymes and diabetes parameters were evaluated in single blood samples from 30 young type 1 diabetic patients and 30 healthy control subjects. Antioxidant enzymes namely superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were significantly decreased while plasma malondialdehyde (MDA), an indicator for lipid peroxidation was significantly increased in IDDM patients compared to control subjects. Positive correlations between HbA1c and MDA; fasting blood glucose (FBG) and MDA and negative correlations between HbA1c and SOD; MDA and SOD were observed in these patients. No significant correlation existed between HbA1c and fasting blood glucose, GPx or CAT in the diabetic patients. The strong correlations found between lipid peroxidation, antioxidant enzymes and diabetes parameters confirms the existence of oxidative stress in our IDDM patients.     

Changes in antioxidant enzyme activities and lipid peroxidation related to bromoethylamine-induced renal cytotoxicity

BACKGROUND: The effect of bromoethylamine (BEA) administration on lipid peroxidation and on the activities of antioxidant enzymes was studied. METHODS: Adult rats received BEA at 1.2 mmol/kg, a dose that produces renal papillary necrosis. Lipid peroxidation assessed by maximal rate in MDA formation, the activities of catalase, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and the levels of non-protein sulfhydryls (NPSH) were measured in renal cortex and papilla of control and BEA-treated animals. RESULTS: After BEA treatment, an increment in lipid peroxidation in papilla and cortex was found after 1.5 and 24 hours of treatment. Catalase activity decreased in both regions, but earlier in cortex. CONCLUSION: These data suggest some role of oxidative stress in the mechanism of BEA-induced papillary necrosis.     

铅与脂多糖协同对大鼠肝细胞TNF-α的影响

目的:铅增强脂多糖所诱发的肿瘤坏死因子-ɑ的表达及肝脏伤害的机制。方法:以尾静脉注射方式,单独给予大鼠不同剂量的醋酸铅(0,5,10,15mg/kg)或合并给予脂多糖(100μg/kg),测量其血液中肿瘤坏死因子-ɑ的浓度、一氧化氮产量、脂质过氧化程度和肝功能受损指标天门冬酸转胺酶以及氨基丙酸转胺酶,建立铅增强脂多糖肿瘤坏死因子的活性及肝脏伤害的机制,并以抑制剂阻断的方式,来探讨醋酸铅合并脂多糖所诱导的信号传递路径。结果:单独给予不同剂量的铅,对各项测量指标并无显著的影响;在合并脂多糖后,大鼠血中肿瘤坏死因子-ɑ活性、一氧化氮产量、脂质过氧化程度及肝脏伤害明显增加。结论:大鼠实验的结果显示,高铅暴露具有加成性地增强脂多糖所诱导的肝脏伤害,可能是经由剌激巨噬细胞的作用,循着蛋白激酶C(PKC)和细胞外信号调节激酶(ERK)的信号途径,来促进肿瘤坏死因子的过度表达和一氧化氮的增加所致,其中一氧化氮的增加会造成脂质过氧化作用。     

Antioxidative effect of folate–modified chitosan nanoparticles

ObjectiveTo evaluate the potency of carboxymethyl chitosan-2, 2′ ethylenedioxy bis-ethylamine-folate (CMC-EDBE-FA) on tissue injury, antioxidant status and glutathione system in tissue mitochondria and serum against nicotine–induced oxidative stress in mice.MethodsCMC-EDBE-FA was prepared on basis of carboxymethyl chitosan tagged with folic acid by covalently linkage through 2, 2′ ethylenedioxy bis-ethylamine. Animals were divided into four groups, i.e., control, nicotine (1 mg/kg bw/day), CMC-EDBE-FA (1 mg/kg bw/day) and nicotine (1 mg/kg bw/day) and CMC-EDBE-FA (1 mg/kg bw/day) for 7 days. Levels of lipid peroxidation, oxidized glutathione level, antioxidant enzyme status and DNA damage were observed and compared.ResultsThe significantly increase of lipid peroxidation, oxidized glutathione levels and DNA damage was observed in nicotine treated group as compared with control group; those were significantly reduced in CMC-EDBE-FA supplemented group. Moreover, significantly reduced antioxidant status in nicotine treated group was effectively ameliorated by the supplementation of CMC-EDBE-FA. Only CMC-EDBE-FA treated groups showed no significant change as compared with control group; rather than it repairs the tissue damage of nicotine treated group.ConclusionsThese findings suggest that CMC-EDBE-FA is non–toxic and ameliorates nicotine–induced toxicity.     

Impact of dietary oils and fats on lipid peroxidation in liver and blood of albino rats

Objective

To investigate the effects of different dietary fat and oils (differing in their degree of saturation and unsaturation) on lipid peroxidation in liver and blood of rats.

Methods

The study was conducted on 50 albino rats that were randomly divided into 5 groups of 10 animals. The groups were fed on dietary butter (Group I), margarine (Group II), olive oil (Group III), sunflower oil (Group IV) and corn oil (Group V) for 7 weeks. After 12 h of diet removal, livers were excised and blood was collected to measure malondialdehyde (MDA) levels in the supernatant of liver homogenate and in blood. Blood superoxide dismutase activity (SOD), glutathione peroxidase activity (GPx), serum vitamin E and total antioxidant capacity (TAC) levels were also measured to determine the effects of fats and oils on lipid peroxidation.

Results

The results indicated that no significant differences were observed in SOD activity, vitamin E and TAC levels between the five groups. However, there was significant decrease of GPx activity in groups IV and V when compared with other groups. The results indicated that feeding corn oil caused significant increases in liver and blood MDA levels as compared with other oils and fats. There were positive correlations between SOD and GPx, vitamin E and TAC as well as between GPx and TAC (r: 0.743; P<0.001) and between blood MDA and liver MDA (r: 0.897; P<0.001). The results showed also negative correlations between blood MDA on one hand and SOD, GPx, vitamin E and TAC on the other hand.

Conclusions

The results demonstrated that feeding oils rich in polyunsaturated fatty acids (PUFA) increases lipid peroxidation significantly and may raise the susceptibility of tissues to free radical oxidative damage.