OBJECTIVE: To evaluate the effect of melatonin on the intestinal apoptosis along with oxidative damage in endotoxemic infant rats. DESIGN AND SETTING: Prospective animal study in a university-based experimental research laboratory. SUBJECTS AND INTERVENTIONS: Wistar albino 7-day-old rat pups (n=21). The animals were randomized into three experimental groups: (1) controls; (2) endotoxemia; (3) endotoxemia treated with melatonin (10mg/kg). Endotoxemia was induced in rats by intraperitoneal injection of lipopolysaccharide (Escherichia coli serotype 0111:B4; 3 mg/kg). MEASUREMENTS AND RESULTS: Four hours after LPS injection, the antioxidant enzyme activities, including superoxide dismutase (SOD), glutathione peroxidase (GPx), and thiobarbituric acid reactive substance (TBARS) levels as an indicator of lipid peroxidation, were determined. Intestinal apoptosis was assessed by hematoxylin-eosin staining and terminal deoxynucleotide transferase-mediated fluorescein-dUTP nick end labeling. The administration of melatonin into endotoxemic rats prevented the increase in the TBARS levels, and increased the activities of antioxidant enzymes and attenuated apoptotic cell death in both intestinal epithelium and lamina propria. CONCLUSIONS: Melatonin diminished the intestinal oxidative stress and apoptotic damage induced by endotoxemia in infant rats.
OBJECTIVE: To evaluate the effect of melatonin on the intestinal apoptosis along with oxidative damage in endotoxemic infantrats. DESIGN AND SETTING: Prospective animal study in a university-based experimental research laboratory. SUBJECTS AND INTERVENTIONS: Wistar albino 7-day-old rat pups (n=21). The animals were randomized into three experimental groups: (1) controls; (2) endotoxemia; (3) endotoxemia treated with melatonin (10mg/kg). Endotoxemia was induced in rats by intraperitoneal injection of lipopolysaccharide (Escherichia coli serotype 0111:B4; 3 mg/kg). MEASUREMENTS AND RESULTS: Four hours after LPS injection, the antioxidant enzyme activities, including superoxide dismutase (SOD), glutathione peroxidase (GPx), and thiobarbituric acid reactive substance (TBARS) levels as an indicator of lipid peroxidation, were determined. Intestinal apoptosis was assessed by hematoxylin-eosin staining and terminal deoxynucleotide transferase-mediated fluorescein-dUTP nick end labeling. The administration of melatonin into endotoxemic rats prevented the increase in the TBARS levels, and increased the activities of antioxidant enzymes and attenuated apoptotic cell death in both intestinal epithelium and lamina propria. CONCLUSIONS:Melatonin diminished the intestinal oxidative stress and apoptotic damage induced by endotoxemia in infantrats.
Authors: D Ozdemir; N Uysal; S Gonenc; O Acikgoz; A Sonmez; A Topcu; N Ozdemir; M Duman; I Semin; H Ozkan Journal: Physiol Res Date: 2005 Impact factor: 1.881
Authors: Juan C Mayo; Rosa M Sainz; Dun-Xian Tan; Rüdiger Hardeland; Josefa Leon; Carmen Rodriguez; Russel J Reiter Journal: J Neuroimmunol Date: 2005-08 Impact factor: 3.478
Authors: Massimo Antonelli; Elie Azoulay; Marc Bonten; Jean Chastre; Giuseppe Citerio; Giorgio Conti; Daniel De Backer; François Lemaire; Herwig Gerlach; Johan Groeneveld; Goran Hedenstierna; Duncan Macrae; Jordi Mancebo; Salvatore M Maggiore; Alexandre Mebazaa; Philipp Metnitz; Jerôme Pugin; Jan Wernerman; Haibo Zhang Journal: Intensive Care Med Date: 2008-01-04 Impact factor: 17.440