The association between colonization of the stomach by Helicobacter pylori and peptic ulcer disease has stimulated a renewal of interest in the factors that render the gastric mucosa resistant to injury induced by endogenous secretions and ingested toxins. Mucosal defense consists of a complex network of components that function in concert with one another. This network includes: 1) the extramucosal components such as acid, mucus, surface-active phospholipids, and bicarbonate; 2) the epithelium itself; 3) the microcirculation and sensory afferent neurons beneath the epithelium; 4) the mucosal immune system; and 5) the ability of the mucosa to undergo repair. In the past two decades, an enormous amount has been learned about the cellular and molecular basis of the various components of mucosal defense, including a better understanding of the chemical substances that coordinate mucosal responses to injury. In this paper, we review the factors that contribute to mucosal defense, the cellular and molecular mechanisms through which mucosal defense is modulated, and the chemical mediators that play key roles in this process.

The cellular and molecular basis of gastric mucosal defense.

Respiratory tract lining fluids (RTLFs) are a heterogeneous group of substances covering the respiratory tract epithelial cells (RTECs) from nasal mucosa to alveoli. Antioxidant contained in the RTLFs can be expected to provide an initial defense against inhaled environmental toxins. The major antioxidants in RTLF include mucin, uric acid, protein (largely albumin), ascorbic acid, and reduced glutathione (GSH). RTLF antioxidants can be augmented by such processes as transudation/exudation of plasma constituents; RTEC secretory processes, including glandular mucus secretion; and cellular antioxidants derived from lysis of RTECs and of inflammatory cells. The antioxidant composition of RTLFs and their role in modulating normal and pathophysiologic RTEC functions under conditions of oxidative stress are yet to be fully characterized.

https://escholarship.org/content/qt2j0943mc/qt2j0943mc.pdf?t=qajobr

Oxidants, Antioxidants, and Respiratory Tract Lining Fluids

Alginate, an algal polysaccharide, is widely used in the food industry as a stabilizer, or as a thickening or emulsifying agent. As an indigestible polysaccharide, alginate may also be viewed as a source of dietary fiber. Previous work has suggested that dietary fibres may protect against the onset and continuation of a number of cardiovascular and gastrointestinal diseases. This article aims to examine what is currently understood about the fiber-like activities of alginate, particularly its effects on intestinal absorption and the colon, and therefore aims to gauge the potential use of alginate as a dietary supplement for the maintenance of normal health, or the alleviation of certain cardiovascular or gastrointestinal diseases.

Alginate as a source of dietary fiber

https://docs.lib.purdue.edu/cgi/viewcontent.cgi?article=1082&context=bmepubs

Oxygen radicals in ulcerative colitis.

Free radicals and other reactive oxygen metabolites in inflammatory bowel disease: cause, consequence or epiphenomenon?

The gastrointestinal epithelium is continuously exposed to reactive oxygen metabolites that are generated within the lumen. In spite of this exposure, the healthy epithelium appears unaffected, suggesting efficient mechanisms for protection against these potentially cytotoxic oxidants. The objective of this study is to characterize the interaction between purified gastric mucin and hydroxyl radicals generated from the interaction between ferric iron and ascorbic acid. We found that both native and pronase-treated mucin effectively scavenged hydroxyl radical and that the scavenging properties were not significantly different. The effective concentration of mucin required for a 50% reduction in malondialdehyde production was approximately 10 mg/ml for both native and pronase-treated mucin. In addition, the iron-ascorbic system produced a dramatic decrease (greater than 50%) in the specific viscosity of mucin that was inhibited by catalase, deferoxamine, and mannitol. Superoxide dismutase had no effect. These data suggest that hydroxyl radicals derived from the iron-catalyzed decomposition of hydrogen peroxide are responsible for the depolymerization of native mucin. We propose that mucin may provide protection to the surface epithelium of the gastrointestinal tract by scavenging oxidants produced within the lumen; however, it does so at the expense of its viscoelastic properties.

B. F. Smith

Papers

Interaction between oxygen radicals and gastric mucin.