Exploring the Use of Inducible Nitric Oxide Synthase to Enhance Compost Nitrogen Content

The goal of our research is to find and present new ways to introduce an inducible nitric oxide synthase to plants to better control nitrogen levels. We also looked at ways to introduce the synthase through compost. We are trying to answer the question of: Will the introduction of inducible nitric oxide synthase in the compost mixture increase the nutrient richness? Our results will indicate whether there are adequate mechanisms to introduce inducible nitric oxide synthase in compost mixtures. A literature review was conducted to look at previous methods used to introduce the inducible nitric oxide synthase (iNOS). We also looked at methods that are being used to accelerate the composting process. Lastly, we looked at any overlap between the synthase introduction methods and composting acceleration methods. The results indicated that compost acceleration can be accomplished by adding organic materials that are high in nitrogen, maintaining a stable and warmer temperature, and maintaining an aerobic process. When introducing the inducible nitric oxide synthase into the compost there is no prior knowledge that says the compost can process the synthase. The synthase will go to benefit the plants when it comes to their growth and resisting pathogens. If this application is successful, the composting industry will be able to market a more nitrogen heavy product to consumers, specifically farms

In vitro and in vivo TNFa synthesis modulation by methylguanidine, an uremic catabolyte

Original article can be found at: http://www.sciencedirect.com/science/journal/00243205 Copyright Elsevier Inc.We have investigated whether methylguanidine (MG), an uremic toxin, modulates the expression of the inducible nitric oxide synthase (iNOS) and nitric oxide (NO) release in vitro in LPS-induced J774 macrophages.Peer reviewe

Okanin, a chalcone found in the genus Bidens, and 3-penten-2-one inhibit inducible nitric oxide synthase expression via heme oxygenase-1 induction in RAW264.7 macrophages activated with lipopolysaccharide

Excess production of nitric oxide by activated macrophages via inducible nitric oxide synthase leads to the development of various inflammatory diseases. Heme oxygenase-1 expression via activation of nuclear factor-erythroid 2-related factor 2 inhibits nitric oxide production and inducible nitric oxide synthase expression in activated macrophages. Okanin is one of the most abundant chalcones found in the genus Bidens (Asteraceae) that is used as various folk medications in Korea and China for treating inflammation. Here, we found that okanin (possessing the α-β unsaturated carbonyl group) induced heme oxygenase-1 expression via nuclear factor-erythroid 2-related factor 2 activation in RAW264.7 macrophages. 3-Penten-2-one, of which structure, as in okanin, possesses the α-β unsaturated carbonyl group, also induced nuclear factor-erythroid 2-related factor 2-dependent heme oxygenase-1 expression, while both 2-pentanone (lacking a double bond) and 2-pentene (lacking a carbonyl group) were virtually inactive. In lipopolysaccharide-activated RAW264.7 macrophages, both okanin and 3-penten-2-one inhibited nitric oxide production and inducible nitric oxide synthase expression via heme oxygenase-1 expression. Collectively, our findings suggest that by virtue of its α-β unsaturated carbonyl functional group, okanin can inhibit nitric oxide production and inducible nitric oxide synthase expression via nuclear factor-erythroid 2-related factor 2-dependent heme oxygenase-1 expression in lipopolysaccharide-activated macrophages

Leishmania guyanensis suppressed inducible nitric oxide synthase provoked by its viral endosymbiont

Inducible nitric oxide synthase (iNOS) is essential to the production of nitric oxide (NO), an efficient effector molecule against intracellular human pathogens such a

Inducible nitric oxide synthase links NF-κB to PGE(2 )in polyunsaturated fatty acid altered fibroblast in-vitro wound healing

BACKGROUND: This study investigated mechanisms of altered fibroblast collagen production induced by polyunsaturated fatty acids. 3T3-Swiss fibroblasts were grown in medium containing either eicosapentaenoic or arachidonic acid. The effects of nuclear factor-kappaB activation by lipopolysaccharide on inducible nitric oxide synthase, nitric oxide, prostaglandin E(2), collagen production, and in-vitro wound healing were studied. RESULTS: Eicosapentaenoic acid treated cells produced less prostaglandin E(2 )but had increased inducible nitric oxide synthase expression, nitric oxide production, collagen formation, and recoverage area during in-vitro wound healing than cells treated with arachidonic acid. Activation of nuclear factor-kappaB with lipopolysaccharide increased inducible nitric oxide synthase expression, the production of nitric oxide, prostaglandin E(2), collagen, and the in-vitro wound recoverage area. The nitric oxide synthase inhibitor, N(G)-nitro-L-arginine methyl ester, decreased lipopolysaccharide-induced nitric oxide, but the amount of nitric oxide was greater in eicosapentaenoic acid treated cells. N(G)-nitro-L-arginine methyl ester plus lipopolysaccharide treatment increased collagen production and cellular recoverage area while treatment with N(G)-nitro-L-arginine methyl ester alone decreased it in wounded fibroblasts. CONCLUSION: The activation of the NF-κB pathway and PGE(2 )can be linked by the cross-talk of iNOS and NO in the PUFA altered fibroblast collagen production and wound healing. Additional studies are needed to determine how polyunsaturated fatty acids can be used as adjuvants in combination with other treatments (i.e, drugs) to design therapies to either enhance healthy collagen production or inhibit production and reduce fibrosis

Inhibition of inducible nitric oxide synthase ameliorates rat lung allograft rejection

AbstractRecently, the inducible isoform of nitric oxide synthase has been shown to be an important immunomodulation molecule in allograft rejection. We have observed the production of nitric oxide during rejection and the effect of nitric oxide synthase inhibition on allograft rejection in a rat lung transplant model. Rat left lung allotransplants were performed in two strain combinations: brown Norway–to–F344 (major histocompatibility complex incompatible); and Lewis-to-F344 (minor loci incompatible) as severe and mild rejection models respectively. Syngeneic F344-to-F344 transplants were performed as a negative control. Nitric oxide production during rejection was determined by measuring the recipient's serum nitrite/nitrate levels as a stable end product of nitric oxide. The progression of rejection was evaluated radiographically and the grade of rejection was determined histologically. After operation, recipients of allotransplantation were randomly divided into two groups and received either aminoguanidine (200 mg/kg, intraperitoneal every 6 hours), a potent inducible nitric oxide synthase inhibitor, or normal saline treatment. The levels of serum nitrite and nitrate in recipients increased in the early phase of rejection in both allotransplant combinations. However, in the terminal phase of rejection, the serum nitrite/nitrate level decreased significantly compared with the peak level in the brown Norway–to–F344 recipients. The serum nitrite/nitrate levels in the syngeneic transplant recipients were normal during the entire observation period. In aminoguanidine-treated animals, serum nitrite/nitrate levels remained normal in both allograft combinations. Significant suppression of rejection in aminoguanidine-treated recipients was observed histologically and radiographically in comparison with untreated recipients in the brown Norway–to–F344 combination. In the Lewis-to-F344 combination, aminoguanidine treatment significantly ameliorated histologic rejection but did not affect radiologic appearance. We therefore conclude nitric oxide is produced during early allograft rejection and may prove to be a marker and mediator of early rejection. The inhibition of inducible nitric oxide synthase results in significant reduction in rat lung allograft rejection. (J THORAC CARDIOVASC SURG 1995;110:1449-60

Neuroprotective roles of asiaticoside on hydrogen peroxide-induced toxicity in SH-SY5Y cells

This study aims to determine whether the neuroprotective role of asiaticoside at maximum non-toxic dose (MNTD) or half MNTD (½MNTD) on H2O2-induced neurotoxicity in SH-SY5Y cells was mediated by regulation of reactive oxygen species (ROS) and nitric oxide (NO) through inducible nitric oxide synthase (iNOS) and heme-oxygenase 1 (HO-1). The levels of ROS, NO, iNOS and HO-1 in SH-SY5Y cells pre-treated with asiaticoside ½MNTD were significantly reduced by 15.3, 55.6, 24.8 and 6.7 %, respectively as compared to the H2O2 treatment group. Cells pre-treated MNTD only reduced the iNOS level significantly. Asiaticoside, particularly at ½MNTD reduced the ROS, NO and iNOS levels. Contrarily, the HO-1 expression was down-regulated when treated with asiaticoside, which further suggest that asiaticoisde exerted its neuroprotective effects via HO-1 regulation.Keywords: Asiaticoside; Heme-oxygenase 1; Inducible nitric oxide synthase; Nitric oxide; Reactive oxygen species

Delay of phagosome maturation by a mycobacterial lipid is reversed by nitric oxide.

Mycobacterium tuberculosis is a facultative intracellular pathogen that inhibits phagosome maturation in macrophages thereby securing survival and growth. Mycobacteria reside in an early endocytic compartment of near-neutral pH where they upregulate production of complex glycolipids such as trehalose dimycolate. Here, we report that trehalose dimycolate coated onto beads increased the bead retention in early phagosomes, i.e. at a similar stage as viable mycobacteria. Thus, a single mycobacterial lipid sufficed to divert phagosome maturation and likely contributes to mycobacterial survival in macrophages. Previous studies showed that activated macrophages promote maturation of mycobacterial phagosomes and eliminate mycobacteria through bactericidal effectors including nitric oxide generated by inducible nitric-oxide synthase. We show that deceleration of bead phagosome maturation by trehalose dimycolate was abolished in immune-activated wild type, but not in activated nitric-oxide synthase-deficient macrophages, nor when hydroxyl groups of trehalose dimycolate were chemically modified by reactive nitrogen intermediates. Thus, specific host defence effectors of activated macrophages directly target a specific virulence function of mycobacteria