Comparative studies of xanthine oxidase inhibitors viz. allopurinol and febuxostat against induced hyperuricaemia in a poultry model.

In this study, an attempt was made to evaluate the relative efficacy of two important anti-gout agents, viz. allopurinol and febuxostat, in the control of hyperuricaemia/gout using a poultry model. A 21-day study was conducted on 48 Vencobb-400 broiler chicks randomly divided into four groups. In one group hyperuricaemia/gout was induced by the oral administration of diclofenac (group D); in two other groups the ameliorative effect of the two drugs under study was investigated by providing both simultaneously, i.e. diclofenac and allopurinol (group DA), diclofenac and febuxostat (group DF); and the fourth group was kept un-induced and untreated as a control (group C). Both allopurinol and febuxostat inhibit xanthine oxidase enzymes, thereby reducing the production of uric acid. The birds kept on diclofenac alone exhibited the highest level of hyperuricaemia, clinical signs of gout, and overt adverse changes in the visceral organs, whereas these changes were lesser in allopurinol- and febuxostat-treated groups. Furthermore, haematological, biochemical, patho-morphological, and ultra-structural studies using transmission electron microscopy were carried out to evaluate the pathology and, thus, the ameliorative effect of allopurinol and febuxostat. The findings proved that allopurinol and febuxostat carry definite ameliorative potential as anti-hyperuricemic and anti-gout agents in poultry, which was better expressed by febuxostat compared to allopurinol.

Influence and Implications of the Molecular Paradigm of Nitric Oxide Underlying Inflammatory Reactions of the Gastrointestinal Tract of Dog: A Major Hallmark of Inflammatory Bowel Disease.

Nitric oxide (NO), a pleiotropic free radical messenger molecule, is responsible for the various cellular function of the gastrointestinal mucosa. It plays a major role in the maintenance of perfusion, regulation of microvascular, epithelial permeability, and immune functions. Nitric oxide exerts its beneficial effect on the initiation and maintenance of inflammation in human inflammatory bowel disease (IBD). But the accelerated production of NO triggers activation of the inducible form of the NO synthase enzyme (iNOS) that leads to damages of the intestinal membrane. Nitric oxide synthase enzyme is responsible for the higher production of NO from l-arginine and causes an inflammatory condition in the intestinal epithelium. Nitric oxide induces nitrative DNA damage and oxidative DNA damage in the cellular system. Accelerated production of NO enhances iNOS activity that is associated with cytotoxicity and apoptosis of gastrointestinal epithelial cells in the dog. Chronic inflammation leads to angiogenesis that is modulated by the immune system in IBD. Chronic inflammation is a major risk factor for the development of gastrointestinal malignancies. Nitric oxide participates in mucosal inflammation in the intestine through invigoration of NO synthase enzyme. The intrinsic complex mechanism is correlated with the inflammation in the gastrointestinal tract and is also correlated with the expression of iNOS, enzymatic activity and NO production. Nitric oxide employs a significant role in modulating epithelial permeability with accelerated immune response in acute colitis. But the enormous generation of NO causes adverse effects on the mucosal cell during the inflammatory process in IBD. In this review, a complex episode of NO generation with altered biochemical pathways was assessed for the regulation of mucosal inflammation in inflammatory bowel disease of dogs. This review is a unique compilation of the role of NO in the pathogenesis of inflammatory bowel disease of dogs. Nitric oxide plays a key role in modulating cancer in the gastrointestinal tract. This review seeks to explore the characteristics of NO as a major hallmark of canine inflammatory bowel diseases.

Inflammatory bowel disease (IBD), the most significant chronic inflammatory condition, is characterized by the painful infection in the gastrointestinal tract among dogs. Nitric oxide (NO) plays a significant role in counteracting the inflammation in the mucosa of the intestine. But prolonged chronic inflammation in the submucosal layers leads to accelerated production of NO that causes harmful effects on the cellular system of the intestine of IBD cases. In IBD, a complex mechanism has occurred in the intestine of dogs.

Prospects and future perspectives of selenium nanoparticles: An insight of growth promoter, antioxidant and anti-bacterial potentials in productivity of poultry.

Nanoparticles have been attracted attention in poultry research due to their low toxicity, higher bio-availability, high surface area with sustained drug release. Dietary supplementation with selenium nanoparticles (Se-NPs) plays a regulatory role in maintaining growth performance, feed conversion ratio (FCR), antioxidant defense as well as microbial control. Se-NPs have emerging importance in modulating intestinal health through the maintenance of beneficial microbes (microflora) as well as the production of short-chain fatty acids (SCFA). Se-NPs regulate intrinsic redox status by scavenging free radicals. The antioxidant potentiality of Se-NPs is influenced by the activation of the seleno-enzymes such as thioredoxin reductase and glutathione peroxidase family (GPx) involved in scavenging of Reactive Oxygen Species (ROS). The emerging significance of Se-NPs on antimicrobial activity has been exploited due to their bio-accumulative effects and biocompatibility potentiality in the cellular systems against poultry pathogens. The present review highlights on growth performance, antioxidant defense, and anti-bacterial potentiality of Se-NPs in poultry and also provide insight into its significance in the poultry industry.

Inhibition of Oxidative Stress and Enhancement of Cellular Activity by Mushroom Lectins in Arsenic Induced Carcinogenesis.

Chronic arsenicosis is a major environmental health hazard throughout the world, including India. Animals and human beings are affected due to drinking of arsenic contaminated ground water, due to natural mineral deposits, arsenical pesticides or improperly disposed arsenical chemicals. Arsenic causes cancer with production of free radicals and reactive oxygen species (ROS) that are neutralized by an elaborate antioxidant defense system consisting of enzymes and numerous non-enzymatic antioxidants. Dietary antioxidant supplements are useful to counteract the carcinogenesis effects of arsenic. Oyster mushroom lectins can be regarded as ingredients of popular foods with biopharmaceutical properties. A variety of compounds have been isolated from mushrooms, which include polysaccharides and polysaccharopeptides with immune-enhancing effects. Lectins are beneficial in reducing arsenic toxicity due to anticarcinogenetic roles and may have therapeutic application in people suffering from chronic exposure to arsenic from natural sources, a global problem that is especially relevant to millions of people on the Indian subcontinent.

Evidence of antiapoptotic properties of Pleurotus florida lectin against chronic arsenic toxicity in renal cells of rats.

Chronic arsenic exposure results in toxicity in humans and causes many toxicologic manifestations. Apoptosis was measured by cell adhesion, morphologic alterations, cell proliferation, terminal deoxyuridine triphosphate nick-end labeling (TUNEL), and caspase-3/CPP32 fluorometric protease assay. Results of the present study suggested that arsenic administration in rats caused apoptosis by elevating morphologic alterations, TUNEL-positive nuclei, caspase-3 activity, and DNA damage and by reducing cell adhesion and cell proliferation in a time-dependent manner. The apoptosis in renal cells of arsenic-exposed rats reverted to normal values after coadministration of mushroom lectin. This study provided significant evidence that Pleurotus florida lectin has an antiapoptotic property by protecting from arsenic-induced toxicity. The beneficial effect of Pleurotus florida lectin was proportional to its duration of exposure. This finding might be of therapeutic benefit in people suffering from chronic exposure to arsenic from natural sources, a global problem that is especially relevant to millions of people on the Indian subcontinent.

Mushroom lectin protects arsenic induced apoptosis in hepatocytes of rodents.

Acute and chronic arsenic exposure result in toxicity both in human and animal beings and cause many hepatic and renal manifestations. The present study stated that mushroom lectin prevents arsenic-induced apoptosis. Apoptosis was measured by morphological alterations, cell proliferation index (CPI), phagocytic activity (nitro blue tetrazolium index; NBT), nitric oxide (NO) production, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, DNA fragmentation and caspase-3 activity. Arsenic exposure at 5 µM in the form of sodium arsenite resulted in significant elevation of deformed cells, NO production, TUNEL stained nuclei of hepatocytes, DNA fragmentation and caspase-3 activity. But the CPI and NBT index were significantly declined in arsenic-treated hepatocytes. The beneficial effect of mushroom lectin at 10 µg/mL, 20 µg/mL and 50 µg/mL) showed increased CPI and phagocytic activity. Mushroom lectin at those concentrations reduced deformed cells, NO production, DNA fragmentation and caspase-3 activity of hepatocytes. But significant better protection was observed in 50 µg/mL mushroom lectin-treated hepatocytes. This finding may be of therapeutic benefit in people suffering from chronic arsenic exposure.