title: Acute and chronic acidosis influence on antioxidant equipment and transport proteins of rat jejunal enterocyte.
abstract: Acidosis elicits the formation of oxidants and, in turn, ROS (reactive oxygen species)-induced intestinal diseases cause acidosis. This research investigated whether both acute and chronic acidosis influence the antioxidant enzymatic equipment of rat jejunocyte, including γ-GT activity, involved in GSH (glutathione) homoeostasis. Lipid peroxidation level and the expressions of (Na+, K+)-ATPase and GLUT2 were also investigated. The possible influence of acidosis on ROS action was tested. Isolated apical membranes, everted sac preparations and homogenates from acidotic rats were used. γ-GT activity is inhibited after incubation of isolated membranes at acidic pH, but using the whole intestinal tract this inhibition disappears, while SOD (superoxide dismutase) and GR (glutathione reductase) activities are enhanced. Also, in conditions of chronic acidosis, γ-GT activity is unaffected, but no variations of antioxidant activities are apparent. (Na+, K+)-ATPase expression increases, while GLUT2 decreases in acidotic animals. Lipid peroxidation level is unaffected by acidosis. H2O2 inhibits γ-GT activity only in isolated membranes; in the whole tissue, it enhances CAT (catalase) and SOD activities and reduces GLUT2 expression. The pattern of responses to oxidant agents is unaffected by acidosis. Although jejunum seems quite resistant to acidosis, results, suggesting specific responses to this condition, may direct further research on antioxidant supplementation.
authors.affiliation: Dipartimento di Scienze Biomolecolari e Biotecnologie, Università di Milano, I20133 Milano, Italy. marisa.tosco@unimi.it
authors.forename: Marisa
authors.initials: M
authors.lastname: Tosco
authors.forename: Cristina
authors.initials: C
authors.lastname: Porta
authors.forename: Chiara
authors.initials: C
authors.lastname: Sironi
authors.forename: Umberto
authors.initials: U
authors.lastname: Laforenza
authors.forename: Maria Novella
authors.initials: MN
authors.lastname: Orsenigo
mesh_terms: D000138:Acidosis / Q000201:enzymology* / Q000378:metabolism; D000208:Acute Disease; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002352:Carrier Proteins / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D002908:Chronic Disease; D020895:Enterocytes / Q000201:enzymology* / Q000378:metabolism; D051273:Glucose Transporter Type 2 / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D007583:Jejunum / Q000166:cytology*; D015227:Lipid Peroxidation; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D005723:gamma-Glutamyltransferase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D002352:Carrier Proteins; D051273:Glucose Transporter Type 2; C495683:Slc2a2 protein, rat; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005723:gamma-Glutamyltransferase; D000254:Sodium-Potassium-Exchanging ATPase