title: Intestinal mucosal lipid peroxidation and absorptive function in Salmonella typhimurium mediated intestinal infection.
abstract: S. typhimurium infection is associated with neutrophil infiltration within the intestinal mucosa. Neutrophil activation provides a major source of reactive oxygen species (ROS). The mucosal pathology of S. typhimurium infection may be in part due to the excessive production of these reactive species. This study was carried out to investigate if ROS play a role in mediating the changes in the structural components and functional properties of brush border membrane (BBM) in rats during S. typhimurium infection. This was done by determining the changes in the BBM extent of lipid peroxidation and absorptive function. A significant increase in the extent of lipid peroxidation of BBM during S. typhimurium infection was observed as judged by malondialdehyde (MDA) and conjugated diene formation and depletion of alpha-tocopherol and protein associated thiol groups. A significant decrease in the BBMV (brush border membrane vesicle) transport of amino acids was also observed. However there was no change in the transport of D-glucose. The decrease in amino acid transport further led to a significant decrease in the enterocyte level of protein synthesis. Exposure of BBMV to a free radical donor, cumene hydroperoxide, also led to an increase in the extent of lipid peroxidation and a decrease in the amino acid transport. Possibly ROS might play a significant role in mediating the mucosal damage during S. typhimurium infection.
authors.affiliation: Department of Pediatrics, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
authors.forename: A
authors.initials: A
authors.lastname: Mehta
authors.forename: S
authors.initials: S
authors.lastname: Singh
authors.forename: V
authors.initials: V
authors.lastname: Dhawan
authors.forename: N K
authors.initials: NK
authors.lastname: Ganguly
mesh_terms: D000409:Alanine / Q000493:pharmacokinetics; D000818:Animals; D001224:Aspartic Acid / Q000493:pharmacokinetics; D005759:Gastroenteritis / Q000378:metabolism* / Q000382:microbiology; D005947:Glucose / Q000493:pharmacokinetics; D007408:Intestinal Absorption; D007413:Intestinal Mucosa / Q000378:metabolism* / Q000382:microbiology; D008054:Lipid Peroxides / Q000378:metabolism*; D008239:Lysine / Q000493:pharmacokinetics; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008871:Microvilli / Q000378:metabolism / Q000382:microbiology; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D012481:Salmonella Infections, Animal / Q000378:metabolism* / Q000382:microbiology; D012486:Salmonella typhimurium; D014810:Vitamin E / Q000378:metabolism
chemical_list: D008054:Lipid Peroxides; D017382:Reactive Oxygen Species; D014810:Vitamin E; D001224:Aspartic Acid; D008315:Malondialdehyde; D005947:Glucose; D008239:Lysine; D000409:Alanine