Anti oxidant enzymes

Gastrointestinal stromal tumours (GIST) are rare mesenchymal neoplasms in the gastrointestinal tract. The metachronous existence of GIST and gastric adenocarcinoma, though are tumours of distinct histotype, and very rare, have been reported in medical case reports in recent years. We report a case of a 74 year old man who initially presented with moderately differentiated adenocarcinoma of the stomach, underwent Billroth 2 gastrectomy followed by chemotherapy. Subsequently, after 15 months he developed a GIST of small bowel with metastasis from adenocarcinoma of stomach. Taking into consideration the fact that metachronous occurrence of GIST of the gastrointestinal tract and adenocarcinoma of stomach is rare and further metastasis of one tumour into the other makes this case a rare one as per available literature.

Growth hormone (GH) excess causes an increment in the metabolic rate and in reactive oxygen species generation, which accelerate the ageing process in mammals. Considering that there is no information on this subject in fish, the aim of the present study was to evaluate the excess GH effect on senescence in a zebrafish (Danio rerio) transgenic model. In order to reach this objective, we analyzed the phenotype of spinal curvature and expression of genes related to the anti-oxidant defense system and myogenesis in muscle of 8 and 30 months old GH-transgenic males. Gene expression analyses revealed that both superoxide dismutase isoforms were down-regulated only in 30 months old animals, while glutamate cysteine ligase was down-regulated in GH-transgenic zebrafish. Acceleration of the spinal curvature and a reduction in the expression of miogenin at both ages and MyoD in the old fish were also observed. Although neurolipofuscin accumulation was not significant in GH-transgenic zebrafish, the estimation of maximum longevity based on the von Bertalanffy growth function was significantly lower in this group. The results obtained here indicate that GH overexpression reduces the transcription of anti-oxidant defense system and myogenesis-related genes, which probably accelerates senescence in the zebrafish transgenic model used.

Mechanisms of interleukin-18 (IL-18) and interleukin-10 (IL-10) in lipopolysaccharide (LPS) induced endotoxemia are not clear; their protective role is being investigated so that they may effectively modulate the host cytokine levels during endotoxemia. The aim of the study was to evaluate protective effects of IL-18 and IL-10 in experimentally induced endotoxemia in mice correlating the changes in tissue anti-oxidant enzymes and circulating cytokines. Liver injury was determined by estimation of serum glutamate oxalate transaminase (SGOT) and serum glutamate pyruvate transaminase (SGPT), serum nitric oxide (NOx), hepatic anti-oxidant enzyme and cytokine content in LPS (250 microg/kg) induced endotoxemic mice receiving either IL-18 (500 ng/mouse) or IL-10 (600 ng/mouse) treatment. Mice (87% of IL-10 treated and 74% of IL-18 treated) survived when administered prior to LPS challenge. Pre-treatment of mice with either IL-10 or IL-18 followed by LPS, lead to reduction in SGPT and SGOT ...

Ethanol and ionizing radiation exposure are independently known to cause tissue damage through various mechanisms. The non-enzymatic and enzymatic metabolism of ethanol, the latter via the cytochrome P 450 2E1dependent pathway produces free radicals, which deplete cellular glutathione (GSH). Ionizing radiation exposure has been shown to induce lipid peroxidation, DNA damage, protein oxidation and GSH depletion. It was postulated that cells sensitized by ethanol will be susceptible to additional insult, such as by radiation through increased oxidative stress. In this investigation, cultured liver cells (HepG2, human hepatocellular liver carcinoma) were exposed to ethanol, followed by ionizing radiation. The antioxidant status of the cells was evaluated by an array of techniques. Levels of glutathione, cysteine (CYS), and malondialdehyde (MDA) were measured by HPLC. Activities of antioxidant enzymes, catalase and glutathione reductase (GR) were determined enzymatically. Apoptosis was evaluated by the caspases-3 assay and fluorescence microscopy. The data showed that combined treatment with ethanol and radiation resulted in the lowest levels of GSH, and highest MDA level compared with the control. The catalase activity was lower in the combined exposure groups, when compared with the single agent exposure groups, and the glutathione reductase activity was the highest in the combined exposure groups and lowest in the control. These findings suggest that a combination of ethanol and ionizing radiation results in greater toxicity in vitro through elevated oxidative stress.

Ethanol and ionizing radiation exposure are independently known to cause tissue damage through various mechanisms. The non-enzymatic and enzymatic metabolism of ethanol, the latter via the cytochrome P 450 2E1dependent pathway produces free radicals, which deplete cellular glutathione (GSH). Ionizing radiation exposure has been shown to induce lipid peroxidation, DNA damage, protein oxidation and GSH depletion. It was postulated that cells sensitized by ethanol will be susceptible to additional insult, such as by radiation through increased oxidative stress. In this investigation, cultured liver cells (HepG2, human hepatocellular liver carcinoma) were exposed to ethanol, followed by ionizing radiation. The antioxidant status of the cells was evaluated by an array of techniques. Levels of glutathione, cysteine (CYS), and malondialdehyde (MDA) were measured by HPLC. Activities of antioxidant enzymes, catalase and glutathione reductase (GR) were determined enzymatically. Apoptosis was evaluated by the caspases-3 assay and fluorescence microscopy. The data showed that combined treatment with ethanol and radiation resulted in the lowest levels of GSH, and highest MDA level compared with the control. The catalase activity was lower in the combined exposure groups, when compared with the single agent exposure groups, and the glutathione reductase activity was the highest in the combined exposure groups and lowest in the control. These findings suggest that a combination of ethanol and ionizing radiation results in greater toxicity in vitro through elevated oxidative stress.

This study was carried out to assess the anti-hyperglycaemic effects if any of novel synthetic binary chromium (III)-amino acid complexes in a high sucrose (HS) induced insulin resistance (IR) and or impaired glucose tolerant male Sprague Dawley (SD) rat model. Aqueous solutions of chromium chloride hexahydrate (CrCl3.6H2O) and D/L amino acids were mixed in 1:3 molar ratios, refluxed at 80°C for 4 hours and the resultant crude greenish-violet solid was extracted with acetone, dried in a hot air oven and their elemental composition and structure were determined. The chromium- amino acid [Cr-(AA)3] complexes were administered orally (~45 μg/kg body weight/day up to 12 weeks) to adult male SD rats in which IR and or impaired glucose tolerance were induced by feeding a HS diet. In line with literature reports, Cr-D-(Phe)3 complex improved insulin sensitivity and oral glucose tolerance in the HS fed rats. Interestingly, Cr-L-(Phe)3 complex also improved these parameters. Increased phosphorylation of insulin receptor substrate- 1 and Akt and increased glucose transporter-4 expression in skeletal muscle were associated with these changes suggesting modulation of insulin sensitivity by Cr-L/D-(Phe)3 complexes. Further, sub chronic administration of Cr-(AA)3 complexes significantly improved lipid metabolism. Modulation of oxidative stress and/ or antioxidant status of the animals seem to be associated with/underlie these beneficial effects in HS induced insulin resistant SD rats.