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Mucosal barrier

Although iron deficiency is a common problem, about 10% of the population are genetically at risk of iron overload (hemochromatosis), and elemental iron can lead to nonen2ymic generation of free radicals. Absorption of iron is stricdy regulated. Inorganic iron is accumulated in intestinal mucosal cells bound to an intracellular protein, ferritin. Once the ferritin in the cell is saturated with iron, no more can enter. Iron can only leave the mucosal cell if there is transferrin in plasma to bind to. Once transferrin is saturated with iron, any that has accumulated in the mucosal cells will be lost when the cells are shed. As a result of this mucosal barrier, only about 10% of dietary iron is normally absorbed and only 1-5% from many plant foods. [Pg.478]

V represents the volume of the mucosal compartment and A the surface area of the mucosal barrier. Passive paracellular solute flux is also proportional to mucosal solute concentration, where the proportionality constant is the ratio of the... [Pg.184]

Mucus is produced by the mucus neck cells and by the surface epithelial cells of the stomach wall. A thick layer of mucus adheres to the wall of the stomach, forming the gastric mucosal barrier. The function of this barrier is to protect the gastric mucosa from injury — specifically, from the corrosive actions of HCl and pepsin. Together with bicarbonate ion released into the lumen of the stomach, mucus neutralizes the acid and maintains the mucosal surface at a nearly neutral pH. [Pg.292]

Bacterial translocation is defined as the passage of viable indigenous bacteria from the GI tract to extraintesti-nal sites, such as the mesenteric lymph node complex, liver, spleen and bloodstream [183], Three major mechanisms promote bacterial translocation intestinal bacterial overgrowth, deficiencies in host immune defenses and increased permeability or damage to the intestinal mucosal barrier [184], These mechanisms can act in concert to promote synergistically the systemic spread of indigenous translocating bacteria to cause lethal sepsis. [Pg.53]

There was an increased incidence of a mycoplasma respiratory tract infection in rats exposed to 260 ppm hexachloroethane for 6 weeks but not in rats exposed to lower doses or in other species. This could indicate compromised immune function or a weakened mucosal barrier along the respiratory epithelium. There were no studies identified that evaluated a wide range of immunological parameters. Therefore, there are no reliable LOAELs or NOAELs for this end point. Increases in spleen weights are not classified as LOAELs since they were not accompanied by histopathological changes. [Pg.42]

It is apparent that patients with gluten-induced enteropathy respond to the administration of gluten differently from other people. It is obvious from consideration of the evidence already presented that the reason for this may lie in inadequacy of the small intestinal mucosal barrier. It is clear that the intestinal mucosa or extracts of it will inactivate the deleterious agent(s) in gluten this is a thermolabile reaction, presumably enzymatic in nature. Patients with gluten-induced... [Pg.108]

When bacteria overcome the cutaneous or mucosal barriers and penetrate body tissues, a bacterial infection is present Frequently the body succeeds in removing the invaders, without outward signs of disease, by mounting an immune response. If bacteria multiply faster than the body s defenses can destroy them, infectious disease develops with inflammatory signs, e.g., purulent wound infection or urinary tract infectioa Appropriate treatment employs substances that injure bacteria and thereby prevent their further multiplication, without harming cells of the host organism (1). [Pg.266]

Gastrointestinal Erosive gastritis, peptic ulceration PGE2-mediated suppression of gastric acid secretion, which helps maintain mucosal barrier and regulate microcirculation COX-1... [Pg.427]

Degradative enzymes Resistance of mucosal barrier Membrane transporters Metabolism at mucosa pH changes Disease conditions... [Pg.341]

The ideal permeation enhancer is safe, effective, pharmacologically inactive, chemically inert, and has a reversible effect (does not compromise the mucosal barrier function for extended periods) [10]. It is noticeable that the majority of the most widely investigated permeation enhancers have surfactant-like properties, and those that are water soluble seem to be most active at concentrations above the critical micelle concentration. The following have been investigated as a means of enhancing buccal permeability. [Pg.205]

Peng X, Yan H, You Z, et al. Effects of enteral supplementation with glutamine granules on intestinal mucosal barrier function in severe burned patients. Bums. 2004 30 135-139. [Pg.38]

Spiekermann GM, Finn PW, Ward ES, et al. Receptor-mediated immunoglobulin G transport across mucosal barriers in adult life functional expression of FcRn in the mammalian lung. J Exp Med 2002 196(3) 303-10. [Pg.274]

In order to obtain a clinical effect by an orally administered drug, it is, for example, required that the drug is (i) dissolved and released from its formulation, (ii) transported over the mucosal barrier, and (iii) has passed from the lumen to the systemic blood circulation without being metabolized by, for example, the lumen or the liver. The drug dissolution rate and the rate of absorption of the dissolved active substance as well as the relation between these processes are important, in particular the dissolution process since the absorption of undissolved drug particles can be disregarded. [Pg.1194]

Desai, H.G., Venugopalan, K., Philipose, M. (1977). Effect of red chili powder on gastric mucosal barrier and acid secretion. Indian J. Med. Res. 66 440-8. [Pg.171]


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Bioavailability mucosal barrier

Gastric mucosal barrier

Gastric mucosal barrier damage

Mucosal

Mucosal barrier agents

Mucosal barrier presence

Mucosal epithelial barrier

Mucositis

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