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Melatonin, a pineal secretory product, is a potent scavenger of a variety of free radicals. We investigated the role of melatonin on water avoidance stress (WAS)-induced degenerations of the liver parenchyme. Wistar albino rats were exposed to acute WAS (aWAS group) or chronic WAS (cWAS group). Before exposing animals to acute (aWAS + mel group) or chronic WAS (cWAS + mel group), 10 mg/kg melatonin was injected i.p. The liver samples were investigated under light and transmission electron microscope. Malondialdehyde (MDA) and glutathione (GSH) levels were also determined. Prominent vascular congestion and dilated sinusoids, activated Kupffer cells with prominent morphology, dilated granular endoplasmic reticulum membranes, and focal picnotic nuclei were observed in the aWAS group; these morphological changes were severe in the cWAS group. MDA level was increased and GSH level was decreased significantly in the cWAS group. The morphology of liver parenchme in both the aWAS + mel and the cWAS + mel group showed that melatonin significantly reduced the degeneration in liver; besides, a significant decrease in MDA and an increase in GSH levels were observed in the cWAS + mel group. Based on the results, melatonin treatment significantly prevented WAS-induced morphological and biochemical changes in liver parenchyma. [ABSTRACT FROM AUTHOR]

Experiments have shown that chronic nicotine administration caused oxidative damage in various organs by increasing lipid peroxidation products and decreasing the activity of endogenous antioxidants. The aim of this study was to investigate the effects of taurine treatment on nicotine-induced oxidative changes in rat thoracic aorta and heart and to explore the possible mechanisms of action. Male Wistar albino rats (200–250 g) were injected with nicotine hydrogen bitartrate (0.6 mg/kg; i.p.) or saline for 21 days. Taurine was administered (50 mg/kg; i.p.) alone or along with nicotine injections. After decapitation, the thoracic aorta and heart tissues were excised. The aorta was used for in vitro contractility studies or stored along with the heart samples for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content. Tissue samples were also examined histologically. Serum samples were stored for the measurement of MDA, GSH and lactate dehydrogenase (LDH) activity. Chronic nicotine treatment impaired both the contraction and relaxation responses of the aortic rings to phenylephrine and acetylcholine, respectively. It increased lipid peroxidation, MPO levels and tissue collagen content of both aorta and heart samples. Taurine supplementation to nicotine-treated animals reversed the contractile dysfunction and restored the endogenous GSH levels and decreased high lipid peroxidation and MPO activities in both tissues. These data suggest that taurine supplementation effectively attenuates the oxidative damage because of chronic nicotine administration possibly by its antioxidant effects. [ABSTRACT FROM AUTHOR]

We investigated the effect of aqueous garlic extract (AGE) on water avoidance stress (WAS)-induced degeneration of the gastric and ileal mucosa and liver parenchyma. Wistar albino rats were exposed to WAS (WAS group) for 5 days. After exposure of the animals to WAS, a 1 ml/kg aqueous garlic extract (AGE) was injected i.p. (WAS+AGE group). The stomach, ileum, and liver samples were investigated under light microscope for general morphology. Topography of gastric and ileal mucosa was investigated by scanning electron microscopy, and hepatocyte ultastructure by transmission electron micsroscopy. Malondialdehyde (MDA) and glutathione (GSH) levels of all tissues were also determined. In the WAS group, the epithelium of the stomach showed ulceration in some areas, dilatations of the gastric glands, and degeneration of gastric glandular cells. Severe vascular congestion and degeneration of ileal epithelium were observed. Prominent vascular congestion and dilated sinusoids, activated Kupffer cells with prominent morphology, dilated granular endoplasmic reticulum membranes, and focal picnotic nuclei were observed in liver parenchyma. AGE treatment reduced the degeneration of the gastric and ileal mucosa and liver parenchyma. Increased MDA levels and decreased GSH levels in the WAS group were reversed to control values after AGE treatment. Based on these results, AGE treatment significantly prevented WAS-induced degeneration in both morphology and biochemistry of gastrointestinal mucosa and liver parenchyma due to its potent free radical scavenging and antioxidant properties.

Objective: To investigate the role of aqueous garlic extract (AGE) on the water-avoidance stress (WAS)-induced degeneration of the urinary bladder in a rat model., Materials and Methods: Wistar albino rats were exposed to WAS for 2 h/day for 5 days (WAS group), after which, AGE (1 mL/kg) was injected intraperitoneally into the rats (WAS + AGE group). Urinary bladder samples were investigated with both light and scanning electron microscopy, and lipid peroxidation and glutathione levels were also measured in the samples., Results: In the WAS group there was inflammatory cell infiltration, more mast cells and ulcerated areas in the mucosa. In the WAS + AGE group there was relatively normal urothelial alignment, moderate inflammatory cell infiltration and fewer mast cells in the mucosa. The increased lipid peroxidation and decreased glutathione levels in WAS rats were reversed by AGE treatment., Conclusions: These results show that AGE has a protective effect on WAS-induced degenerative changes in the urinary bladder.

We investigated the role of taurine, is a potent free radical scavenger, on water avoidance stress (WAS)-induced degeneration of the gastric, ileal, and colonic mucosa and liver parenchyma. Wistar albino rats were exposed to chronic WAS (WAS group) 2 hr daily for 5 days. After exposing animals to chronic WAS (WAS + taurine group), 50 mg/kg taurine was injected IP for 3 days. Control animals received vehicle solution only. The stomach, ileum, colon, and liver samples were investigated under light microscope for histopathologic changes. To demonstrate the topography of the luminal mucosa of the stomach, ileum, and colon, scanning electron microscope was used and for hepatocyte ultastructure transmission electron microscope was used. Malondialdehyde (MDA, a biomarker of oxidative damage) and glutathione (GSH, a biomarker of protective oxidative injury) levels were also determined in all tissues. In the WAS group, the stomach epithelium showed ulceration in some areas, dilatations of the gastric glands, and degeneration of gastric glandular cells; prominent congestion of the capillaries was apparent. In the WAS group, severe vascular congestion was observed along with degeneration of ileal and colonic epithelium. Prominent vascular congestion and dilated sinusoids, activated Kupffer cells, dilated granular endoplasmic reticulum membranes, and focal pyknotic nuclei were observed in liver parenchyma. MDA levels (stomach, P < 0.01; ileum, colon, and liver P < 0.05) were increased and GSH levels (P < 0.01) were decreased in all tissues in the WAS group compared with the control group. The morphology of gastric, ileal, and colonic mucosa and liver parenchyma in the WAS + taurine group (stomach and ileum, P < 0.05; colon and liver, P < 0.01) showed a significant amelioration when compared to the WAS group. Increased MDA and decreased GSH levels in the WAS group were ameliorated with taurine treatment. Based on the results, taurine supplementation effectively attenuates the oxidative damage of gastrointestinal mucosa and liver because of WAS induction possibly by its antioxidant effects.

The present study was designed to investigate the putative protective effects of taurine on protamine sulfate (PS) induced bladder injury. Wistar albino female rats were catheterized and intravesically infused with phosphate buffered solution (control group) or PS (PS group) dissolved in phosphate buffered solution. In the PS + taurine (PS+Tau) group, after the PS instillation, taurine (50 mg/kg) was injected intraperitoneally for 3 days. Histopathological changes were investigated by light and scanning electron microscopy. Tissue samples were also obtained to determine bladder malondialdehyde (MDA) (a biomarker of oxidative damage) and glutathione (GSH) (a biomarker of protective oxidative injury) levels. In the PS group ulcerated areas, an irregular mucus layer, inflammatory cell infiltration, and increased number of mast cells were observed. In the PS+Tau group, a relatively normal urothelial topography, glycosaminoglycan layer, and decreased number of mucosal mast cells and inflammatory cells were observed. Increased MDA levels as a result of PS induction lead us to propose that free radicals may have a critical role in this injury. The significant decrease in MDA and increase in GSH levels in the PS+Tau group compared to PS group was in accordance with morphological findings. Based on the results, taurine treatment significantly prevented PS induced degenerative morphological and biochemical changes of urinary bladder mucosa.

This morphological and biochemical study aims to investigate the antioxidant effects of chronic administration of aqueous garlic extract (AGE) on protamine sulfate (PS)-induced bladder injury. Wistar albino female rats were catheterized and intravesically infused with phosphate-buffered solution (control group) or PS (PS group) dissolved in phosphate-buffered solution. In the PS + AGE group after the PS instillation, AGE (1 ml/kg, i.p., corresponding to 250 mg/kg) was injected intraperitoneally for 3 days. Bladder morphology was investigated by light and scanning electron microscopy. Tissue samples were also obtained to determine bladder malondialdehyde (MDA) and glutathione levels. In the PS group, ulcerated areas, an irregular mucus layer, inflammatory cell infiltration and an increased number of mast cells were observed. In the PS + AGE group a relatively normal urothelial topography, glycosaminoglycan layer and a decreased number of mucosal mast cells and inflammatory cells were observed. Increased MDA levels as a result of PS induction led us to propose that free radicals may have a critical role in this injury. The significant decrease in MDA and increase in glutathione levels in the PS + AGE group was in accordance with morphological findings. Based on the results, AGE treatment significantly prevented PS-induced degenerative morphological and biochemical changes of urinary bladder mucosa.

Several studies demonstrate that taurine treatment prevents tissue damage in various models of inflammation. Experiments have shown that chronic nicotine administration caused oxidant damage in various organs by increasing lipid peroxidation products and decreasing the activity of endogenous antioxidants. The aim of this study was to investigate the effects of taurine treatment on nicotine-induced oxidative changes in rat urinary bladder and kidney and to explore the possible mechanisms of action. Male Wistar albino rats were injected with nicotine hydrogen bitartrate (0.6 mg/kg i.p.) or saline for 21 days. Taurine was administered (50 mg/kg i.p.) alone or along with nicotine injections. At the end of the treatment period bladder tissue was used for in vitro contractility studies, or stored along with kidney tissue for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content. Tissue samples were also examined histologically. Serum samples were stored for the measurement of MDA, GSH, blood urea nitrogen, creatinine and lactate dehydrogenase activity. Chronic nicotine treatment decreased the contractile activity of the bladder strips to carbachol and increased lipid peroxidation, MPO levels and tissue collagen content of the bladder and kidney samples. Taurine supplementation to nicotine-treated animals reversed the contractile dysfunction of the bladder strips. It also preserved the renal functions, restored the endogenous GSH levels and decreased high lipid peroxidation and MPO activities in both urinary bladder and kidney tissues. These data suggest that taurine supplementation effectively counteracts the deleterious effect of chronic nicotine administration on bladder and kidney functions and attenuates oxidative damage possibly by its antioxidant effects., (Copyright (c) 2005 S. Karger AG, Basel)

We investigated the role of melatonin on water avoidance stress (WAS)-induced degeneration of the gastric, ileal and colonic mucosa. Wistar albino rats were exposed to acute WAS (aWAS group) or chronic WAS (cWAS group). Before exposing animals to acute (aWAS + mel group) or chronic WAS (cWAS + mel group), 10 mg/kg melatonin was injected i.p. The stomach, ileum and colon samples were investigated under light and scanning electron microscope. Malondialdehyde (MDA) and glutathione (GSH) levels were also determined. In both aWAS and cWAS groups, the epithelium of stomach showed ulceration in some areas, dilatations of the gastric glands and degeneration of gastric glandular cells; prominent congestion of the capillaries after WAS was apparent. In the cWAS group, severe vascular congestion was observed along with degeneration of ileal and colonic epithelium. MDA levels were increased and GSH levels were decreased in all tissues in both the aWAS and cWAS groups. The morphology of gastric, ileal and colonic mucosa in both aWAS + mel and cWAS + mel groups showed that the indole significantly reduced degeneration of the gastrointestinal mucosa. Decreased MDA and increased GSH levels were observed in the WAS + mel groups. Based on the results, melatonin treatment significantly prevented WAS induced degenerative morphological and biochemical changes of gastrointestinal mucosa.