[13] Catalase in vitro

Aebi, H.

doi:10.1016/s0076-6879(84)05016-3

Cited by 21,314 publications

(9,888 citation statements)

References 9 publications

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“…Catalase-Catalase was estimated at 240 nm by monitoring the disappearance of H 2 O 2 as described by Aebi [1]. The reaction mixture (1 ml, vol) contained 0.02 ml of suitably diluted cytosol in phosphate buffer (50 mM, pH 7.0) and 0.1ml of 30 mM H 2 O 2 in phosphate buffer.…”

Section: Assay Methodsmentioning

confidence: 99%

Protective effect of arginine on oxidative stress in transgenic sickle mouse models

Dasgupta

Hebbel

Kaul

2006

Free Radical Biology and Medicine

129

101

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Sickle cell disease (SCD) is characterized by reperfusion injury and chronic oxidative stress. Oxidative stress and hemolysis in SCD result in inactivation of nitric oxide (NO) and depleted arginine levels. We hypothesized that augmenting NO production by arginine supplementation will reduce oxidative stress in SCD. To this end, we measured the effect of arginine (5% in mouse chow) on NO metabolites (NOx), lipid peroxidation (LPO) and selected antioxidants in transgenic sickle mouse models. Untreated transgenic sickle (NY1DD) mice (expressing ~75% β S -globin of all β-globins; mild pathology) and knockout sickle (BERK) mice (expressing exclusively hemoglobin S; severe pathology) showed reduced NOx levels and significant increases in the liver LPO compared with C57BL mice, with BERK mice showing maximal LPO increase in accordance with the disease severity. This was accompanied by reduced activity of antioxidants (glutathione [GSH], total superoxide dismutase [SOD], catalase and glutathione peroxidase [GPx]). However, GSH levels in BERK were higher than in NY1DD mice indicating a protective response to greater oxidative stress. Importantly, dietary arginine significantly increased NOx levels, reduced LPO and increased antioxidants in both sickle mouse models. In contrast, L-NAME, a potent non-selective NOS inhibitor, worsened the oxidative stress in NY1DD mice. Thus, attenuating effect of arginine on oxidative stress in SCD mice suggests its potential application in the management of this disease.

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Section: Assay Methodsmentioning

confidence: 99%

Protective effect of arginine on oxidative stress in transgenic sickle mouse models

Dasgupta

Hebbel

Kaul

2006

Free Radical Biology and Medicine

129

101

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“…26 The assay is based on the determination of the rate constant (s 71 , k) of hydrogen peroxide decomposition. The rate constant was calculated using the formula k=(2.3/Dt)(a/ b)log(A 1 /A 2 ), where A 1 and A 2 are the absorbance values of hydrogen peroxide at times t 1 (0th second) and t 2 (15th second), (`a' is a dilution factor, and`b' is the protein content of the supernatant).…”

Section: Antioxidant Enzyme Assaysmentioning

confidence: 99%

Pentoxifylline reduces biochemical markers of ischemia-reperfusion induced spinal cord injury in rabbits

et al. 2002

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Study design: Occlusion of the infrarenal abdominal aorta with administration of pentoxifylline was applied to adult rabbits, followed by removal of aortic clamp and reperfusion. Tissue levels of cytokines, lipid peroxides, and antioxidant enzymes were assayed and compared within groups. Objectives: To examine the e ect of pentoxifylline (PTX) on cytokine levels, lipid peroxidation, and antioxidant enzymes in a rabbit model of spinal cord ischemia-reperfusion injury induced by aortic occlusion. Setting: Isparta, Turkey. Methods: Rabbits were randomly allocated into four groups of sham laparotomy (SHAM), sham laparotomy with PTX administration (SHAM+PTX), aortic occlusion and reperfusion (AOR), aortic occlusion and reperfusion with PTX administration (AOR+PTX). An intravenous bolus of 50 mg/kg PTX was given just before aortic cross clamping. An atraumatic microvascular clamp was then placed on the abdominal aorta immediately distal to the left renal artery for 30 min. PTX was infused at a rate of 0.5 mg/kg/min during the aortic occlusion. Animals were subjected to 120 min of reperfusion after removal of the aortic clamp. All animals were sacri®ced at the end of reperfusion. The lumbosacral segments of spinal cords were quickly harvested and stored at 7788C for biochemical assays of IL-6, TNF-a, MDA, SOD, and CAT levels. Di erences among groups were analyzed by one-way analysis of variance followed by a post hoc Tukey's honestly signi®cant di erence test. Results: No di erences in mean levels of IL-6, TNF-a, MDA, SOD, and CAT were noted between SHAM and SHAM+PTX groups (P40.05). There was a signi®cant increase in all biochemical parameters in the AOR group (P50.05). Administration of PTX signi®cantly attenuated the levels of all biochemical parameters in the AOR+PTX group (P50.05). Conclusion: PTX pretreatment attenuated ischemia-reperfusion induced spinal cord injury in a rabbit model, in terms of biochemical parameters of ischemia and reperfusion.

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“…Catalase activity was determined by a slightly modified version of Aebi (1984). Ten ml of absolute ethanol was added per 100 ml of tissue extract and then placed in an ice bath for 30 min.…”

Section: Methodsmentioning

confidence: 99%

Dose Response of Carboplatin‐Induced Nephrotoxicity in Rats

Husain¹,

Jagannathan²,

Hasan³

et al. 2002

Pharmacology & Toxicology

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Carboplatin, a second-generation platinum-containing anticancer drug, is currently being used against a variety of cancers. High-dose carboplatin chemotherapy can cause renal tubular injury in cancer patients. However, the biochemical mechanism of carboplatin-induced renal injury has not been well studied. This study investigated the dose response of carboplatin-induced changes in endogenous antioxidants, lipid peroxidation and platinum content in rat kidney. Male Wistar rats (250-300 g) were divided into five groups and treated as follows: (1) control (saline, intraperitoneally); (2) carboplatin (64 mg/kg, intraperitoneally); (3) carboplatin (128 mg/kg, intraperitoneally); (4) carboplatin (192 mg/kg, intraperitoneally); and (5) carboplatin (256 mg/kg, intraperitoneally). The animals were sacrificed four days after treatment. The blood and kidneys were isolated and analyzed. Plasma creatinine and blood urea nitrogen levels were increased significantly in response to carboplatin in a dose-dependent manner. Renal superoxide dismutase and catalase activities were decreased significantly due to carboplatin at dosages of 128 mg/kg and above. The protein expressions of renal copper/zinc-superoxide dismutase and manganese-superoxide dismutase significantly depleted after carboplatin. Carboplatin (192 and 256 mg/kg) significantly increased lipid peroxidation (malondialdehyde concentration) in rat kidneys. Carboplatin dose-dependently increased the renal platinum concentration, with significance at dosages of 128 mg/kg and above. Carboplatin (256 mg/kg) significantly increased renal xanthine oxidase activity, while ratio of reduced to oxidized glutathione depleted significantly. The data suggested that carboplatin caused dose-dependent oxidative renal injury, as evidenced by renal antioxidant depletion, enhanced lipid peroxidation, platinum content, plasma creatinine and blood urea nitrogen levels in rats.

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[13] Catalase in vitro

Cited by 21,314 publications

References 9 publications

Protective effect of arginine on oxidative stress in transgenic sickle mouse models

Protective effect of arginine on oxidative stress in transgenic sickle mouse models

Pentoxifylline reduces biochemical markers of ischemia-reperfusion induced spinal cord injury in rabbits

Dose Response of Carboplatin‐Induced Nephrotoxicity in Rats

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