Intestinal prostaglandin E2 expression in rats with obstructive jaundice.

AIM: How obstructive jaundice causes the intestinal barrier to be injured is still controversially discussed. In this study, we hypothesize that intestinal prostaglandin E (2), a cytoprotective factor, may be affected by the bile duct obstruction. MATERIALS AND METHODS: Four groups of Wistar-Albino rats were used: in Groups 1 and 3, the rats underwent a sham operation. In Groups 2 and 4, the common bile duct was doubly ligated. Relaparotomy was performed after one week in Groups 1 and 2, and after two weeks in Groups 3 and 4, and specimens of the jejunum, ileum and liver were obtained for intestinal PGE (2) analysis and histopathological evaluation. RESULTS: Jejunal and ileal PGE (2) levels had significantly decreased in two-week bile duct-ligated rats compared to one-week ligated rats and the sham group (p < 0.01). Tissue injury scores (Chiu score) of the ileum were significantly higher in the two-week and one-week ligated rats than in the controls (p < 0.01 and p < 0.05, respectively). The jejunal injury score was significantly higher in the two-week ligated rats compared to controls (p < 0.05). The ileal and jejunal injury scores were higher in the two-week ligated rats than in the one-week ligated rats (p < 0.01 and p < 0.05, respectively). Precirrhotic fibrosis was detected in all two-week ligated rats, but in only 7 of 10 one-week ligated rats. CONCLUSIONS: Obstructive jaundice associated with intestinal tissue injury and precirrhotic changes leads to reduced intestinal PGE (2)-levels, suggesting an adverse effect on the intestinal cytoprotective process.

The role of cadmium in the peroxidative response of kidney to stress.

Since the kidney is a main target for cadmium, its accumulation in the kidney tissue by increasing peroxidative damage make the kidney functions vulnerable to stress. For this reason, the effect of cadmium-induced peroxidative damage to kidney responses to stress was investigated in this study. Two-month-old albino rats receiving 15 micrograms/mL containing Cd drinking water for 30 d were exposed to restraint and cold stress for 6 h, and their responses were compared with those of unstressed counterparts. Lipid peroxidation was found to be significantly higher in the cortical portion of kidney in cadmium-exposed rats than that of unexposed animals. The mean thiobarbutyric acid reactive substance (TBARS) level rose from 211.6 +/- 64.2 to 303.4 +/- 46.4 nmol/g protein (p < 0.01). Six hours of cold and restraint stress caused an elevation in the cortical TBARS level in control animals without affecting its level in cadmium-exposed rats. Despite unaltered cortical TBARS, its medullar levels increased significantly in cadmium-exposed rats because of stress. These results suggested that cadmium accumulation in the kidney increases the susceptibility of medulla against peroxidative damage. However, further functional studies are necessary to explain the role of cadmium in the stress-induced deterioration of medullar functions.