Intestinal mucosal oxidative damage and bacterial translocation in cirrhotic rats.
BACKGROUND
Bacterial translocation plays an important role in the pathogenesis of spontaneous bacterial peritonitis mainly due to intestinal bacterial overgrowth. Alterations in the functional integrity of the intestinal barrier caused by an increased production of free radical metabolites as a consequence of portal hypertension could also facilitate bacterial translocation in cirrhotic rats.


OBJECTIVE
The aim of the study was to determine intestinal mucosal lipid peroxidation and neutrophil infiltration and their relationship with portal hypertension and bacterial translocation in cirrhotic rats.


METHODS
Eighteen male Sprague-Dawley rats with cirrhosis induced by carbon tetrachloride, administered by gavage, and eight control rats were included in the study.


METHODS
Samples of jejunum, ileum and caecum were obtained by laparotomy for the determination of malondialdehyde and myeloperoxidase as indexes of lipid peroxidation and neutrophil infiltration, respectively. Samples of ascitic and pleural fluids, mesenteric lymph nodes and ileal stools were obtained for the culture of microoganisms.


RESULTS
The concentration of malondialdehyde was significantly higher in ileal and caecal, but not in jejunal mucosa, in cirrhotic rats, mainly in those with ascites (P< 0.01), as compared to control rats (P< 0.01), and in cirrhotic rats with bacterial translocation compared to those without bacterial translocation (P< 0.01). No differences between groups were observed in the concentrations of myeloperoxidase in jejunum, ileum or caecum. A direct correlation between ileal malondialdehyde and portal pressure was observed (P< 0.01).


CONCLUSIONS
Cirrhotic rats, particularly those with ascites and bacterial translocation, show increased malondialdehyde levels in ileal and caecal mucosa. These results suggest that mucosal oxidative damage in ileum and caecum could favour bacterial translocation in cirrhotic rats.
Chiva
Maite
M
Liver Section, Department of Gastroenterology, Hospital de la Santa Creu i Sant Pau, Sant Antoni M Claret 167, 08025 Barcelona, Spain.
Guarner
Carlos
C
Peralta
Carmen
C
Llovet
Teresa
T
Gómez
Gloria
G
Soriano
Germán
G
Balanzó
Joaquín
J
D000818:Animals; D018988:Bacterial Translocation / Q000502:physiology*; D015415:Biomarkers / Q000032:analysis; D002251:Carbon Tetrachloride; D002432:Cecum / Q000378:metabolism / Q000382:microbiology; D013293:Enterococcus faecalis / Q000502:physiology; D016984:Enterococcus faecium / Q000502:physiology; D004926:Escherichia coli / Q000502:physiology; D006975:Hypertension, Portal / Q000209:etiology / Q000378:metabolism; D007082:Ileum / Q000378:metabolism / Q000382:microbiology; D007413:Intestinal Mucosa / Q000378:metabolism* / Q000382:microbiology; D007583:Jejunum / Q000378:metabolism / Q000382:microbiology; D015227:Lipid Peroxidation / Q000502:physiology*; D008106:Liver Cirrhosis, Experimental / Q000150:complications / Q000378:metabolism* / Q000382:microbiology; D008297:Male; D008315:Malondialdehyde / Q000032:analysis; D020556:Neutrophil Infiltration / Q000502:physiology; D009195:Peroxidase / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley
D015415:Biomarkers; D008315:Malondialdehyde; D002251:Carbon Tetrachloride; D009195:Peroxidase