Mucin degradation in the intestine

Rat intestinal mucin was labelled biologically by intraperitoneal injection of radioactive amino acids and monosaccharides 3–6 h prior to killing, followed by isolation and purification of the mucin from mucosal scrapings. The labelled product was then introduced into intestinal segments of rats under ether anesthesia for periods up to 3 h, removed by washing and assessed for evidence of degradation. In segments containing the pancreatic ducts the total mucin precipitable by cetyltrimethylammonium bromide fell from 80% to 5% in 3 h. At 3 h, chromotography on Sephadex G-100 and Sepharose 4B revealed multiple products, including very small molecular weight fragments deficient in carbohydrate label. With the introduction of neomycin sulfate into the segments to reduce bacterial growth, only two products were found, one corresponding in size to the original mucin and one somewhat smaller, although still in excess of 200 000 daltons. These products occurred independently of the presence of the pancreatic ducts in the segments, and in chronically pancreatectomized rats. The smaller product could not be produced by incubation with trypsin or elastase. Both products were altered antigenically as compared with the original mucin. Both products also retained the same ratio of carbohydrate and protein label as the original. It is concluded that mucins undergo early degradative changes in the intestine which do not involve deglycosylation but which involve partial loss of antigenicity and a fall in molecular weight. The pancreas is not responsible for these changes.     

Luminal alkalinization in the intestine of the goby

Summary The rate of luminal alkalinization in vitro byGillichthys mirabilis posterior intestine as measured by a manual pH stat technique was 0.70±0.05 Equiv/cm² h; acidification of the mucosal medium was never observed. The rate of HCO ₃ ^– secretion (J ^HCO ₃) was reduced by ouabain, serosally-applied DIDS, removal of serosal HCO ₃ ^– and replacement of media Cl^– with gluconate. HCO ₃ ^– secretion was enhanced replacement of Cl^– with isethionate and unaffected by mucosal DIDS, furosemide or acetazolamide.J ^HCO ₃ was reduced at mucosal pH above or below 7.5. These results support active HCO ₃ ^– secretion via a Cl^–/HCO ₃ ^– exchange mechanism on the basolateral membrane and a conductive exit pathway for HCO ₃ ^– , H⁺ or OH^– on the apical membrane.Abbreviations DIDS diisothiocyanostilbene-2,2-disulfonic acid - TEP transepithelial potential - GBR Gillichthyts bicarbonate Ringer - GUR Gillichthys unbuffered, bicarbonate-free Ringer - GER Gillichthys EPPS-buffered, bicarbonate-free Ringer - EPPS N-(2-hydroxyethyl)piperazine-N-3-propanesulfonic acid     

Redox biology of the intestine

Abstract

The intestinal tract, known for its capability for self-renew, represents the first barrier of defence between the organism and its luminal environment. The thiol/disulfide redox systems comprising the glutathione/glutathione disulfide (GSH/GSSG), cysteine/cystine (Cys/CySS) and reduced and oxidized thioredoxin (Trx/TrxSS) redox couples play important roles in preserving tissue redox homeostasis, metabolic functions, and cellular integrity. Control of the thiol-disulfide status at the luminal surface is essential for maintaining mucus fluidity and absorption of nutrients, and protection against chemical-induced oxidant injury. Within intestinal cells, these redox couples preserve an environment that supports physiological processes and orchestrates networks of enzymatic reactions against oxidative stress. In this review, we focus on the intestinal redox and antioxidant systems, their subcellular compartmentation, redox signalling and epithelial turnover, and contribution of luminal microbiota, key aspects that are relevant to understanding redox-dependent processes in gut biology with implications for degenerative digestive disorders, such as inflammation and cancer.