Does N-acetylcysteine have an effect on acetylcholine-induced contractions and histopathological changes on isolated rat ileum?

OBJECTIVE: To investigate the action of N-acetylcysteine (NAC) on rat isolated ileal contractility, and to determine the effects of NAC on histopathological changes on ileal tissue. METHODS: The study took place at the Faculty of Medicine, Ankara University, Ankara, Turkey, in January 2003. Adult Wistar rats were used in all experiments. Two groups were designed. The experimental group, to which NAC 0.5 g/Kg/day was administered orally by adding to their water for 7 days, and the control group to which only saline was administered. At the end of the experimental periods, one cm pieces of terminal ileum segments were removed for testing ileal contractility, and one cm pieces of ileum segments were removed for histopathological experiments. The acetylcholine (ACh)-induced contraction was recorded, and the ileal tissue examined using light and electron microscopic technics for histopathological changes. RESULTS: The average peak amplitude of ACh-induced contraction recorded in standard tyrode solution of the experimental group was decreased significantly when compared to the control group in standard and calcium-Free tyrode solution. On histopathological findings, there were swollen mitochondria with disturbed cristae in the ileal muscle. CONCLUSION: Our data suggest that the NAC in the present experiment decreased the ACh-induced contractility on rat-isolated ileum.

Selenium treatment protects diabetes-induced biochemical and ultrastructural alterations in liver tissue.

We have shown that a single dose of streptozotocin (STZ) (50 mg/kg body weight) injected into rats caused significant changes in some antioxidant enzyme activities, such as glutathione peroxidase, glutathione reductase, glutathione-S-transferase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase activities, and acid-soluble sulfhydryl levels of the liver tissue with respect to the control rats. Furthermore, these alterations in the activities of the antioxidant enzymes were accompanied by significant changes in the ultrastructure of the liver tissue; mainly intercellular biliary canaliculi were distended and contained stagnant bile, swollen mitochondria in hepatocytes and disoriented and disintegrating cristae, dilatation of the rough endoplasmic reticulum (rER) with detachment of ribosomes, and dissociation of polysomes. Both diabetic and normal rats were treated with sodium selenite (5 micromol/kg/d, intra peritoneally) for 4 wk following 1 wk of diabetes induction. This treatment of diabetic rats improved significantly diabetes-induced alterations in liver antioxidant enzymes. Moreover, treating of diabetic rats with sodium selenite prevented primarily the variation in staining quality of hepatocytes nuclei, increased density and eosinophilia of the cytoplasm, focal sinusoidal dilatation and congestion, and increased numbers of mitochondria with different size and shape. In summary, treatment of diabetic rats with sodium selenite has beneficial effects on both antioxidant system and the ultrastructure of the liver tissue. These findings suggest that diabetes-induced oxidative stress can be responsible for the development of diabetic complications and antioxidant treatment can protect the target organs against diabetes.

Effects of intracameral lidocaine on ocular tissues.

PURPOSE: To investigate the ultrastructural changes in iris and corneal tissue induced by intracameral 1% lidocaine infusion applied during lens extraction in a rabbit model. METHODS: The study was conducted using New Zealand rabbits. Eight rabbits received 0.2 mL 1% lidocaine hydrochloride intracamerally and lens extraction was performed, keeping the posterior capsule intact. After lens extraction, cornea and iris tissue samples were obtained for electron microscopy. Eight eyes were included as a control group. RESULTS: Electron microscopy revealed morphological abnor-malities in both cornea and iris of the lidocaine injected eyes, different from the control group. Cytoplasmic vacuolization, phagosomes and residual bodies were observed in epithelial cells. Corneal fibroblasts contained fluid-filled vacuoles, which could be due to the influx of water into the cells as a result of corneal endothelial damage. Mitochondrial swelling and residual bodies were also seen in the cytoplasm of fibroblasts. Blood vessels in the iris contained fluid material composed of fibrin and proteinaceous material and many vacuoles showed vascular endothelial injury. CONCLUSION: Even a short period of exposure of intra-cameral lidocaine to the ocular tissues can induce histo-logical changes that may result in functional defects.