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Gopabandhu Jena - One of the best experts on this subject based on the ideXlab platform.
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Role of α-lipoic acid in dextran sulfate sodium-induced ulcerative colitis in mice: studies on inflammation, oxidative stress, DNA damage and fibrosis.
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2013Co-Authors: Priyanka Trivedi, Gopabandhu JenaAbstract:Ulcerative colitis affects many people worldwide. Inflammation and oxidative stress play a vital role in its pathogenesis. Previously, we reported that ulcerative colitis leads to systemic genotoxicity in mice. The present study was aimed at elucidating the role of α-lipoic acid in ulcerative colitis-associated local and systemic damage in mice. Experimental colitis was induced using 3%w/v dextran sulfate sodium in drinking water for 2 cycles. α-Lipoic acid was administered in a co-treatment (20, 40, 80 mg/kg bw) and post-treatment (80 mg/kg bw) schedule. Various biochemical parameters, histological evaluation, comet and micronucleus assays, immunohistochemistry and western blot analysis were employed to evaluate the effect of α-lipoic acid in mice with ulcerative colitis. The protective effect of α-lipoic acid was mediated through the modulation of nuclear factor kappa B, cyclooxygenase-2, interleukin 17, signal transducer and activator of transcription 3, nuclear erythroid 2-related factor 2, NADPH: quinone Oxidoreductase-1, matrix metalloproteinase-9 and connective tissue growth factor. Further, ulcerative colitis led to an increased gut permeability, plasma lipopolysaccharide level, systemic inflammation and genotoxicity in mice, which was reduced with α-lipoic acid treatment. The present study identifies the underlying mechanisms involved in α-lipoic acid-mediated protection against ulcerative colitis and the associated systemic damage in mice.
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Effect of melatonin on the expression of Nrf2 and NF-κB during cyclophosphamide-induced urinary bladder injury in rat
Journal of pineal research, 2010Co-Authors: Durga Nand Tripathi, Gopabandhu JenaAbstract:Urotoxicity is one of the major problems associated with cyclophosphamide (CP) chemotherapy in cancer patients. Melatonin is a potent antioxidant and reduces CP-induced urotoxicity. However, the molecular mechanisms of protection offered by melatonin are not yet clear. The present study investigated the role of nuclear erythroid 2-related factor 2 (Nrf2) and nuclear factor-kappa B (NF-kappaB) on melatonin-mediated protection against CP-induced urotoxicity. CP was administered intraperitoneally at the dose of 150 mg/kg to induce urotoxicity in male Sprague-Dawley rats. Melatonin treatment (10 mg/kg) was initiated 3 days before and continued for 1 day after the CP administration. Melatonin treatment reduced the CP-induced oxidative stress and DNA damage in the urinary bladder as observed by abrogation in thiobarbituric acid-reactive substances and glutathione levels as well as comet and modified comet assay parameters. Melatonin treatment reduced the bladder damage and apoptosis as observed by histological analysis and TUNEL assay. Melatonin increased the expression of transcription factor Nrf2 as well as associated phase-II enzymes NADPH: quinone Oxidoreductase-1 and heme oxygenase-1. Further melatonin treatment reduced the expression of transcription factor NF-kappaB. The results of the present study provide evidence that melatonin treatment favorably alters Nrf2 and NF-kappaB expression and, this appears to be at least in part responsible for observed protection against CP-induced urotoxicity.
G B Jena - One of the best experts on this subject based on the ideXlab platform.
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Ulcerative colitis-induced hepatic damage in mice: studies on inflammation, fibrosis, oxidative DNA damage and GST-P expression.
Chemico-biological interactions, 2012Co-Authors: P P Trivedi, G B JenaAbstract:There exists a close relationship between ulcerative colitis and various hepatic disorders. The present study was aimed to evaluate the hepatocellular damage in experimental colitis model. Ulcerative colitis was induced in Swiss mice by cyclic treatment with 3% w/v dextran sulfate sodium in drinking water. The severity of colitis was assessed on the basis of disease activity index and colon histology. The effect of ulcerative colitis on the liver was assessed using various biochemical parameters, histological evaluation, sirius red staining, immunohistochemical staining with peroxisome proliferator-activated receptor γ, 8-oxo-7,8-dihydro-2'-deoxyguanosine and placental glutathione S-transferase, comet assay (alkaline and modified), Terminal Deoxynucleotidyl Transferase-mediated dUTP Nick End Labeling assay and western blot analysis to detect the protein expression of nuclear factor kappa B, cyclooxygenase-2, nuclear erythroid 2-related factor 2 and NADPH: quinone Oxidoreductase-1. Dextran sulfate sodium induced severe colitis in mice as evident from an elevated disease activity index and histological abnormalities. Ulcerative colitis increased the permeability of colon as apparent from a significant reduction in the expression of tight junction protein, occludin. Further, the bacterial translocation assay as well as the analysis of lipopolysaccharide level revealed the existence of various bacterial species in the liver of ulcerative colitis-induced mice. There was a significant increase in the plasma alanine and aspartate transaminases and liver triglyceride levels, expression of peroxisome proliferator-activated receptor γ, inflammatory markers, oxidative stress, fibrosis, oxidative DNA damage and apoptosis in the liver of mice. Moreover, there was an increase in the expression of nuclear factor kappa B and cyclooxygenase-2 and a reduction in the expression of nuclear erythroid 2-related factor 2 and NADPH: quinone Oxidoreductase-1 in the liver of severe ulcerative colitis-induced mice. The results of the present study provide evidence that ulcerative colitis is accompanied with hepatic damage in mice.
Shuzhe Ding - One of the best experts on this subject based on the ideXlab platform.
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Endurance exercise causes mitochondrial and oxidative stress in rat liver: effects of a combination of mitochondrial targeting nutrients.
Life sciences, 2009Co-Authors: Lijuan Sun, Weili Shen, Zhongbo Liu, Shangyi Guan, Jiankang Liu, Shuzhe DingAbstract:Endurance exercise causes fatigue due to mitochondrial dysfunction and oxidative stress. In order to find an effective strategy to prevent fatigue or enhance recovery, the effects of a combination of mitochondrial targeting nutrients on physical activity, mitochondrial function and oxidative stress in exercised rats were studied. Rats were subjected to a four-week endurance exercise regimen following four weeks of training. The effects of exercise and nutrient treatment in rat liver were investigated by assaying oxidative stress biomarkers and activities of mitochondrial complexes. Endurance exercise induced an increase in activities of complexes I, IV, and V and an increase in glutathione (GSH) levels in liver mitochondria; however, levels of ROS and malondialdehyde (MDA) and activities of complexes II and III remained unchanged. Exercise also induced a significant increase in MDA and activities of glutathione S-transferase and NADPH-Quinone-Oxidoreductase 1 (NQO-1) in the liver homogenate. Nutrient treatment caused amelioration of complex V and NQO-1 activities and enhancement of activities of complex I and IV, but had no effect on other parameters. These results show that endurance exercise can cause oxidative and mitochondrial stress in liver and that nutrient treatment can either ameliorate or enhance this effect, suggesting that endurance exercise-induced oxidative and mitochondrial stress may be either damaging by causing injury or beneficial by activating defense systems.
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Endurance exercise causes mitochondrial and oxidative stress in rat liver: effects of a combination of mitochondrial targeting nutrients.
Life Sciences, 2009Co-Authors: Lijuan Sun, Weili Shen, Zhongbo Liu, Shangyi Guan, Jiankang Liu, Shuzhe DingAbstract:Abstract Aims Endurance exercise causes fatigue due to mitochondrial dysfunction and oxidative stress. In order to find an effective strategy to prevent fatigue or enhance recovery, the effects of a combination of mitochondrial targeting nutrients on physical activity, mitochondrial function and oxidative stress in exercised rats were studied. Main methods Rats were subjected to a four-week endurance exercise regimen following four weeks of training. The effects of exercise and nutrient treatment in rat liver were investigated by assaying oxidative stress biomarkers and activities of mitochondrial complexes. Key findings Endurance exercise induced an increase in activities of complexes I, IV, and V and an increase in glutathione (GSH) levels in liver mitochondria; however, levels of ROS and malondialdehyde (MDA) and activities of complexes II and III remained unchanged. Exercise also induced a significant increase in MDA and activities of glutathione S-transferase and NADPH-Quinone-Oxidoreductase 1 (NQO-1) in the liver homogenate. Nutrient treatment caused amelioration of complex V and NQO-1 activities and enhancement of activities of complex I and IV, but had no effect on other parameters. Significance These results show that endurance exercise can cause oxidative and mitochondrial stress in liver and that nutrient treatment can either ameliorate or enhance this effect, suggesting that endurance exercise-induced oxidative and mitochondrial stress may be either damaging by causing injury or beneficial by activating defense systems.
J S Zigler - One of the best experts on this subject based on the ideXlab platform.
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identification and characterization of the enzymatic activity of zeta crystallin from guinea pig lens a novel nadph quinone Oxidoreductase
Journal of Biological Chemistry, 1992Co-Authors: C M Krishna, J S ZiglerAbstract:Abstract zeta-Crystallin is a major protein in the lens of certain mammals. In guinea pigs it comprises 10% of the total lens protein, and it has been shown that a mutation in the zeta-crystallin gene is associated with autosomal dominant congenital cataract. As with several other lens crystallins of limited phylogenetic distribution, zeta-crystallin has been characterized as an "enzyme/crystallin" based on its ability to reduce catalytically the electron acceptor 2,6-dichlorophenolindophenol. We report here that certain naturally occurring quinones are good substrates for the enzymatic activity of zeta-crystallin. Among the various quinones tested, the orthoquinones 1,2-naphthoquinone and 9,10-phenanthrenequinone were the best substrates whereas menadione, ubiquinone, 9,10-anthraquinone, vitamins K1 and K2 were inactive as substrates. This quinone reductase activity was NADPH specific and exhibited typical Michaelis-Menten kinetics. Activity was sensitive to heat and sulfhydryl reagents but was very stable on freezing. Dicumarol (Ki = 1.3 x 10(-5) M) and nitrofurantoin (Ki = 1.4 x 10(-5) M) inhibited the activity competitively with respect to the electron acceptor, quinone. NADPH protected the enzyme against inactivation caused by heat, N-ethylmaleimide, or H2O2. Electron paramagnetic resonance spectroscopy of the reaction products showed formation of a semiquinone radical. The enzyme activity was associated with O2 consumption, generation of O2- and H2O2, and reduction of ferricytochrome c. These properties indicate that the enzyme acts through a one-electron transfer process. The substrate specificity, reaction characteristics, and physicochemical properties of zeta-crystallin demonstrate that it is an active NADPH:quinone Oxidoreductase distinct from quinone reductases described previously.
Makoto Fujii - One of the best experts on this subject based on the ideXlab platform.
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fisetin induces transcription of nadph quinone Oxidoreductase gene through an antioxidant responsive element involved activation
International Journal of Oncology, 2001Co-Authors: Masahiro Fukuda, Koji Miyamori, Miharu Ushikai, Jeffrey A Johnson, Makoto FujiiAbstract:Induction of phase II enzymes such as NADPH: quinone Oxidoreductase (QR) can reduce carcinogen-induced mutagenesis and tumor formation. In our search for novel dietary anticarcinogens, fisetin, a flavonol widely distributed in fruits and vegetables was found to induce QR activity in murine hepatoma 1c1c7 cells. The cells were treated with various concentrations of fisetin, and then were assessed for cell growth, QR activity, QR mRNA expression and transcription activation of the QR gene. The results showed that fisetin induced QR activity in time- and dose-dependent manner in the concentration range of 0.1 to 10 μM, and the activity induction was associated with QR mRNA expression as detected by reverse transcription-PCR. Furthermore, transfection studies using a human QR antioxidant/ electrophile-response element (ARE/EpRE) reporter construct demonstrated that fisetin activated the ARE/EpRE. These results show that fisetin increases QR activity by transcriptional activation of the ARE/EpRE, suggesting a novel mechanism by which dietary fisetin may be implicated in cancer chemoprevention.
