Abstract

Background: The pathogenic mechanism of peritonitis is complex. The role of nitric oxide (NO) and myeloperoxidase (MPO) in liver lipid peroxidation accompanying bacterial peritonitis was evaluated.
Material/Methods: Peritonitis was induced by 0.2-ml intraperitoneal application of 10[sup]5[/sup] (low E. coli) or 2×10[sup]8[/sup] CFU/ml (high E. coli) E. coli isolated from a bacteriemic patient. A nonspecific nitric oxide synthase inhibitor, L-N[sup]G[/sup]-nitroarginine methyl ester (L-NAME, 8 mg/kg i.p.) was given to determine the potential involvement of nitric oxide. Female mice were divided into five groups: controls, low E. coli, low E. coli + L-NAME, high E. coli, and high E. coli + L-NAME. After 24 hours, peritoneal lavage fluids and hepatic tissue samples were obtained for microbiological and biochemical evaluation. Hepatic tissue malondialdehyde (MDA) levels were measured to determine the free radical-induced lipid peroxidation in peritonitis.
Results: MDA levels were increased in the high, but not in the low, E. coli group (p<0.001) compared with the controls. MDA levels were lower in the high E. coli + L-NAME group than in the high E. coli group, but still higher than in the control group (p<0.01). Liver myeloperoxidase (MPO) activities were increased in the high E. coli group (p<0.01), but not in the low E. coli group. L-NAME increased myeloperoxidase activities in both groups.
Conclusions: These results are consistent with the notion that NO and MPO contribute in liver tissue lipid peroxidation in peritonitis. NO may have different effects in hepatic damage depending on the severity of infection.

Keywords: Escherichia coli - physiology, Ascitic Fluid - microbiology, Lipid Peroxidation, Liver - microbiology, Malondialdehyde - metabolism, Mice, Inbred BALB C, Nitric Oxide - metabolism, Peritonitis - microbiology, Peroxidase - metabolism