Liver lipid peroxidation in experimental Escherichia coli peritonitis: the role of myeloperoxidase and nitric oxide inhibition.

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(5) (low E. coli) or 2 x 10(8) CFU/ml (high E. coli) E. coli isolated from a bacteriemic patient. A nonspecific nitric oxide synthase inhibitor, L-N(G)-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 (p0.001) 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 (p0.01). Liver myeloperoxidase (MPO) activities were increased in the high E. coli group (p0.01), 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.

Does two episodes of acute urinary retention lead to additional ischemia-reperfusion injury in rat bladder?

AIM: To determine whether two episodes of acute urinary retention lead to additional ischemia-reperfusion injury due to decompression of the bladder, or not. MATERIALS AND METHODS: Sham, retention and recurrent retention groups consisting of 5, 8 and 8 Wistar Albino male rats were randomized, respectively. After the bladders of rats were emptied with 3F catheter, penile urethras were clamped with aneurism clamp and waited for 30 min after diuresis was forced. At the end of this period, penile clamps were removed and the bladder was again decompressed with 3F catheter and after 30 min removed for examination. In the recurrent retention group, the same process was repeated after an interval of one week. Malonedialdehyde (MDA) levels, indicator of lipid peroxidation and myeloperoxidase (MPO) levels, indicator of leukocyte activation, were examined biochemically in the tissues of the removed bladders. RESULTS: In the retention and recurrent retention groups, the average increase in bladder MDA and MPO values was higher than the values of sham group (P < 0.05), however, no significant difference was determined between retention and recurrent retention groups (P > 0.05). CONCLUSION: In the bladder tissue, due to acute urinary retention and following decompression process, ischemia-reperfusion injury occurs. Two episodes of acute urinary retention do not lead to additional the ischemia-reperfusion injury that develops in the bladder.

The effect of partial unilateral ureteral obstruction release and allopurinol on the renal malondialdehyde and glutathione levels.

PURPOSE: The aim of the present study was to evaluate whether relief of partial unilateral ureteral obstruction (PUUO) with or without antioxidant drug affect renal tissue malonedialdehyde (MDA) and glutathion (GSH) levels. MATERIALS AND METHODS: A total of 25 rats were used in this PUUO study. Partial unilateral ureteral obstruction was created by the burial of the upper one-third of the left ureter in the psoas muscle. The rats were sacrificed on 28th day following PUUO. Relief of the obstruction was performed twenty minutes before sacrifice by cutting the proximal ureter in reperfusion group. 50 mg/kg intraperitoneal allopurinol was administered 20 minutes before relief of obstruction in the antioxidant group. Renal tissue MDA and GSH levels were measured in both kidneys. RESULTS: At the end of the study 5, 7 and 7 rats could only be interpreted in sham, reperfusion and antioxidant groups, respectively. While the mean left and right renal MDA and GSH levels were statistically different from each other in reperfusion group (P < 0.001), there were no significant differences in the sham (P > 0.05) and antioxidant (P > 0.05) group. Both the mean sham group left and right renal tissue MDA or GSH levels were significantly different from reperfusion group, but only the mean sham group left renal tissue MDA and right renal tissue GSH levels were not statistically different from antioxidant group (P < 0.05). The mean left or right renal MDA and GSH tissue levels of the antioxidant group were statistically different from reperfusion group (P < 0.05) except for the right renal tissue GSH level (P > 0.05). CONCLUSION: Partial unilateral ureteral obstruction leads to oxidative injury by relief of obstruction in both kidneys. The antioxidant allopurinol has a beneficial effect on renal MDA and GSH levels in both kidneys.

Mycotoxin-forming ability of two Penicillium roqueforti strains in blue moldy tulum cheese ripened at various temperatures.

Isolated and identified toxigenic and nontoxigenic Penicillium roqueforti (PR) strains from moldy tulum cheeses were inoculated into tulum cheeses made in the laboratory and ripened at 5 and 12 degrees C. Mycotoxin (patulin, penicillic acid, PR toxin, and roquefortine) formation in the control and mold-inoculated cheeses were detected by thin-layer chromatography on the first through fourth months of ripening. Patulin, penicillic acid, and PR toxin were not detected in the experimental cheeses. Only roquefortine was detected in cheese inoculated with the toxigenic strain of the mold and ripened at 5 and 12 degrees C on the third and first months of ripening, respectively. Toxin in cheeses ripened at 5 and 12 degrees C was 2.1 to 2.4 and 2.1 to 3.8 mg/kg cheese, respectively.