Reductive stress, characterised by an increased NADH:NAD+ ratio, may be as common and as important a consequence of redox imbalance as oxidative stress. It may also be an important predisposing cause of the generation of reactive oxygen species. Considerable experimental and indirect clinical evidence suggests that protection against reductive stress depends on biomolecules with electrophilic methyl groups (EMG) such as S-adenosylmethionine, betaine, carnitine and phosphatidylcholine. Pathological processes leading to reductive stress and their relief by such protective agents is reviewed and the proposed molecular mechanism is outlined. These and other EMG-containing biomolecules are part of the daily diet and may represent an important control system for redox balance.

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Electrophilic methyl groups present in the diet ameliorate pathological states induced by reductive and oxidative stress: a hypothesis.

Composition of phospholipid classes and phosphatidylcholine molecular species of gastric mucosa and mucus.

The old wives tale of an 'inside lining' protecting the stomach wall against acid retains a certain intuitive appeal, which has found refuge in the concept of a gastric mucosal barrier to the back-diffusion of hydrogen ions. Preference for a physical barrier arose from the many fundamental physiological studies of Horace Davenport and coworkers in the 1950s-1970s,' 2 and offered many theoretical advantages over alternative mechanisms proposed for mucosal protection.3 Davenport envisaged the gastric mucosal barrier as distinct from the mucus layer or mucus/bicarbonate blanket4 which, arguably, offers inadequate protection because refined mucus is too permeable to hydrogen ions while mucus is absent from the extremely corrosive environment of the oxyntic duct and sparse, if not absent,5 from considerable areas of the lumen of the stomach, especially in certain monogastric mammals such as the dog.

https://gut.bmj.com/content/gutjnl/39/5/621.full.pdf

Gastric surfactant and the hydrophobic mucosal barrier.

Surfactant approach to the gastric mucosal barrier: Protection of rats by banana even when acidified

The protective capacities of fresh green (unripe) sweet bananas and of phosphatidylcholine and pectin (banana ingredients) against acute (ethanol- or indomethacin-induced) and chronic (indomethacin-induced) gastric mucosal lesions were evaluated in rats. Banana pulp was mixed with saline and given by gavage, as a pretreatment in a single dose. The identical protocol was used for pectin and phosphatidylcholine solution, and the dosages were adjusted to equal the amount of ingredients in the banana mixture, but higher concentrations were also given. The banana suspension reduced acute lesions, as did pectin and phosphatidylcholine in higher concentrations, but in concentrations as in fresh fruit no protective effects were observed except by pectin against indomethacin injury. In the model of chronic ulcers the banana suspension provided an incomplete and temporary protective effect. We conclude that the protective capacity of fresh green sweet bananas cannot be confined to only one active component. Pectin and phosphatidylcholine may protect gastric mucosa by strengthening the mucous-phospholipid layer, but the mechanism of protection afforded by bananas has to be further elucidated.

Green banana protection of gastric-mucosa against experimentally-induced injuries in rats - a multicomponent mechanism

The role of the gastric nonwettable hydrophobic layer (surfactant) was investigated in the mucosal protection against the damage induced by ethanol in the rat. Although aluminium hydroxide inhibited t

H. Engler

Papers

Cytoprotective Role of Gastric Surfactant in the Ethanol-Produced Gastric Mucosal Injury of the Rat