MICRODETERMINATION OF CYTOCHROME OXIDASE IN RAT TISSUES BY THE OXIDATION OF N-PHENYL-<i>p</i>-PHENYLENEDIAMINE OR ASCORBIC ACID

Pearl, William; Cascarano, Joseph; Zweifach, Benjamin W.

doi:10.1177/11.1.102

Cited by 95 publications

(43 citation statements)

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“…ATPase [28] were assayed. The Activities of mitochondrial enzymes such as isocitrate dehydrogenase [29], a-ketoglutarate dehydrogenase [30], succinate dehydrogenase [31], malate dehydrogenase [32], NADH-dehydrogenase [33] and cytochrome C-oxidase [34] were assessed according to the published papers. …”

Section: Evaluation Of Biochemical Estimationsmentioning

confidence: 99%

Exploring the Potential Role of Chemopreventive Agent, Hesperetin Conjugated Pegylated Gold Nanoparticles in Diethylnitrosamine-Induced Hepatocellular Carcinoma in Male Wistar Albino Rats

et al. 2015

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Liver cancer is the fifth most common cancer and is still one of the leading causes of death world wide, due to food additives, alcohol, fungal toxins, air, toxic industrial chemicals, and water pollutants. Chemopreventive drugs play a potential role in liver cancer treatment. Obviously in the production of anticancer drugs, the factors like poor solubility, bioavailability, biocompatibility, limited chemical stability, large amount of dose etc., plays a major role. Against this backdrop, the idea of designing the chemopreventive nature of bio flavanoid hesperetin (HP) drug conjugated with pegylated gold nanoparticles to increasing the solubility, improve bioavailability and enhance the targeting capabilities of the drug during diethylnitrosamine (DEN) induced liver cancer in male wistar albino rats. The dose fixation studies and the toxicity of pure HP and HP conjugated gold nanoparticles (AumPEG (5000) -S-HP) were analysed. After concluded the dose fixation and toxicity studies the experimental design were segregated in six groups for the anticancer analysis of DEN induced HCC for 16 weeks. After the experimental period the body weight, relative liver weight, number of nodules and size of nodules, the levels of tumor markers like CEA, AFP and the level of lipid peroxidation, lipid hydroperoxides and the activities of antioxidant enzymes were assessed. The administration of DEN to rats resulted in increased relative liver weight and serum marker enzymes aspartate transaminase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase, and gamma glutamyl transpeptidase. The levels of lipid peroxides elevated (in both serum and tissue) with subsequent decrease in the final body weight and tissue antioxidants like superoxide dismutase, catalase, reduced glutathione, glutathione peroxidise, and glutathione reductase. HP supplementation (20 mg/kg b.wt) significantly attenuated these alterations, thereby showing potent anticancer effect in liver cancer and the HP loaded gold nanoparticels (AumPEG (5000) -S-HP) treated animals shows the better treatment than the pure HP due to the solubility of drug, bioavailability and the target drug delivery of the biodegradable polymer. Histological observations were also carried out, which added supports to the chemopreventive action of the pure HP and HP loaded gold nanoparticles (Au-mPEG (5000) -S-HP) against DEN induction during liver cancer progression. These findings suggest that HP loaded gold nanoparticels (Au-mPEG (5000) -S-HP) shows better efficacy than the pure HP against lipid peroxidation, hepatic cell damage and protects the antioxidant system in DEN induced hepatocellular carcinogenesis.

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Section: Evaluation Of Biochemical Estimationsmentioning

confidence: 99%

Exploring the Potential Role of Chemopreventive Agent, Hesperetin Conjugated Pegylated Gold Nanoparticles in Diethylnitrosamine-Induced Hepatocellular Carcinoma in Male Wistar Albino Rats

et al. 2015

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“…The activity of cytochrome-C-oxidase in the heart mitochondrial fraction was assayed by the method of Pearl et al (1963). The reaction mixture contained 1.0 ml of phosphate buffer, 0.2 ml of 0.2% N-phenyl-p-phenylene diamine, 0.1 ml of 0.01% cytochrome-C, and 0.5 ml of distilled water.…”

Section: Assay Of Cytochrome-c-oxidasementioning

confidence: 99%

Caffeic acid protects rat heart mitochondria against isoproterenol-induced oxidative damage

Kumaran

Prince

2010

Cell Stress and Chaperones

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Cardiac mitochondrial dysfunction plays an important role in the pathology of myocardial infarction. The protective effects of caffeic acid on mitochondrial dysfunction in isoproterenol-induced myocardial infarction were studied in Wistar rats. Rats were pretreated with caffeic acid (15 mg/kg) for 10 days. After the pretreatment period, isoproterenol (100 mg/kg) was subcutaneously injected to rats at an interval of 24 h for 2 days to induce myocardial infarction. Isoproterenol-induced rats showed considerable increased levels of serum troponins and heart mitochondrial lipid peroxidation products and considerable decreased glutathione peroxidase and reduced glutathione. Also, considerably decreased activities of isocitrate, succinate, malate, α-ketoglutarate, and NADH dehydrogenases and cytochrome-C-oxidase were observed in the mitochondria of myocardial-infarcted rats. The mitochondrial calcium, cholesterol, free fatty acids, and triglycerides were considerably increased and adenosine triphosphate and phospholipids were considerably decreased in isoproterenol-induced rats. Caffeic acid pretreatment showed considerable protective effects on all the biochemical parameters studied. Myocardial infarct size was much reduced in caffeic acid pretreated isoproterenol-induced rats. Transmission electron microscopic findings also confirmed the protective effects of caffeic acid. The possible mechanisms of caffeic acid on cardiac mitochondria protection might be due to decreasing free radicals, increasing multienzyme activities, reduced glutathione, and adenosine triphosphate levels and maintaining lipids and calcium. In vitro studies also confirmed the free-radicalscavenging activity of caffeic acid. Thus, caffeic acid protected rat's heart mitochondria against isoproterenolinduced damage. This study may have a significant impact on myocardial-infarcted patients.

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“…The activity of cytochrome c oxidase was assayed according to the method of Pearl et al 34 One milliliter of phosphate buffer, 0.2 mL of 0.2% N-phenyl-p phenylene diamine, 0.1 mL of 0.01% cytochrome c, 0.5 mL of distilled water were mixed and incubated at 25 C for 5 min. Mitochondrial suspension of 0.2 mL was added and the change in absorbance was recorded at 550 nm for 5 min at intervals of 15 sec.…”

Section: Cytochrome C Oxidase Activitymentioning

confidence: 99%

Protective effect of administration ofWithania somiferaagainst bromobenzene induced nephrotoxicity and mitochondrial oxidative stress in rats

2014

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Background: The present study was conducted to elucidate the protective role of Withania somnifera against bromobenzene induced nephrotoxicity and mitochondrial dysfunction in rats. Methods: In this study, Wistar albino rats of either sex were divided into six groups consisting of six animals each. The first one was control, those in group II received bromobenzene (10 mmol/kg, intragastric intubation) once, but group III and IV animals received W. somnifera (250 and 500 mg/kg, orally), respectively for 8 days followed by bromobenzene once on the 8th day and silymarin (100 mg/kg, orally) was given for 8 days to group V animals and then bromobenzene on the last day. Group VI animals received only W. somnifera (500 mg/kg) for 8 days. Results: The levels of renal lipid peroxidation, lysosomal enzymes and glycoprotein were increased significantly (p50.05) in the bromobenzene alone treated rats and antioxidant status and mitochondrial enzymes were found to be decreased, when compared to the control group. The levels of kidney functional markers (urea, uric acid and creatinine) were also found to be abnormal in serum of bromobenzene alone treated rats. On the other hand, administration of W. somnifera (250 and 500 mg/kg) along with bromobenzene offered a significant dose-dependent protection to the biochemical alterations as observed in the bromobenzene alone treated rats, which was also evidenced by histopathology. Conclusion: Thus, the oral administration of W. somnifera significantly protected against the bromobenzene induced nephrotoxicity and renal mitochondrial dysfunction in rats.

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MICRODETERMINATION OF CYTOCHROME OXIDASE IN RAT TISSUES BY THE OXIDATION OF N-PHENYL-p-PHENYLENEDIAMINE OR ASCORBIC ACID

Cited by 95 publications

References 0 publications

Exploring the Potential Role of Chemopreventive Agent, Hesperetin Conjugated Pegylated Gold Nanoparticles in Diethylnitrosamine-Induced Hepatocellular Carcinoma in Male Wistar Albino Rats

Exploring the Potential Role of Chemopreventive Agent, Hesperetin Conjugated Pegylated Gold Nanoparticles in Diethylnitrosamine-Induced Hepatocellular Carcinoma in Male Wistar Albino Rats

Caffeic acid protects rat heart mitochondria against isoproterenol-induced oxidative damage

Protective effect of administration ofWithania somiferaagainst bromobenzene induced nephrotoxicity and mitochondrial oxidative stress in rats

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