title: Are the increases in local tumour necrosis factor and lipid peroxidation observed in pre-starved mice infected with Salmonella typhimurium markers of increased liver damage?
abstract: Pathogenic microorganisms are known to sense and process signals within their hosts, including those resulting from starvation. Therefore, an attempt was made to evaluate the extent and the possible underlying mechanism of Salmonella typhimurium-induced hepatic damage using pre-starved laboratory mice. The following parameters were analysed, comparing control, fed infected, starved, and starved infected mice: the bacterial load in the liver, fluctuations in liver-derived enzymes alanine-aminotransferase and aspartate-aminotransferase, histopathological changes, lipid peroxidation as well as estimation of reduced glutathione, superoxide dismutase and catalase, along with the TNF content in livers. The number of bacterial cells recovered from starved infected livers at 3 days post-S. typhimurium inoculation was comparable to the number recovered from fed infected livers at 5 days post-Salmonella inoculation, indicating an early increase in the development of the bacteria in starved mice. A marked elevation in liver-derived enzymes in mouse serum and significant histopathological changes are markers of liver damage of higher amplitude in starved infected mice. Analysis of the liver indicated a significant increase in lipid peroxidation in starved infected mice compared to their control counterparts, a process coupled with increased TNF level. Although the reduced glutathione levels showed a marked increase in the starved infected mice, there was a significant decrease in superoxide dismutase and catalase activities in this group.
authors.affiliation: Department of Microbiology, Basic Medical Sciences Block, Panjab University, Chandigarh, India. rishipraveen@yahoo.com
authors.forename: Praveen
authors.initials: P
authors.lastname: Rishi
authors.forename: Harsimran
authors.initials: H
authors.lastname: Kaur
authors.forename: Naveen
authors.initials: N
authors.lastname: Tirkey
authors.forename: Kanwaljit
authors.initials: K
authors.lastname: Chopra
authors.forename: Sushma
authors.initials: S
authors.lastname: Bharrhan
authors.forename: Vishal
authors.initials: V
authors.lastname: Chanana
authors.forename: Ashwani
authors.initials: A
authors.lastname: Koul
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D015415:Biomarkers; D002374:Catalase / Q000032:analysis; D015169:Colony Count, Microbial; D005978:Glutathione / Q000032:analysis; D006651:Histocytochemistry; D015227:Lipid Peroxidation; D008099:Liver / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D012481:Salmonella Infections, Animal / Q000378:metabolism / Q000382:microbiology / Q000473:pathology*; D012486:Salmonella typhimurium / Q000302:isolation & purification*; D013217:Starvation / Q000150:complications*; D013482:Superoxide Dismutase / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D014409:Tumor Necrosis Factor-alpha; D002374:Catalase; D013482:Superoxide Dismutase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D005978:Glutathione