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AIM Oxidative stress participates in the cell carcinogenesisby inducing DNA mutations.Our aim was to assess whetherascorbic acid,an antioxidant,could have a role in preventingROS(Reactive Oxygen Species)generation in experimentalgastric carcinoma in a rat model.METHODS:Experimental gastric cancer was induced intwelve Wistar male rats(weighting 250-350 g)by profoundduodeno-gastric reflux throught split gastrojenunostomy.Therats were allocated to the following groups:Group Ⅰ(n=6)was the control;Group Ⅱ(n=6)which was mantained withdaily intake of tape water with Vitamin C(30 mg/Kg).After6 or 12 months,samples of gastric tumor or non tumormucosa were taken from the anastomosis of both groups.Oxidative stress was measured by superoxide quantificationthrough lucigenin-amplified chemiluminescence base andby staining with Nitrobluetetrazolium.The histopathologicconfirmation of adenocarcinoma was made by eosin-hemathoxilin method.RESULTS:The intestinal type of gastric adenocarcinomawas microscopically identified in all animals of group Ⅰwhereas only 3 rats of group Ⅱ showed an adenocarcinomawithout macroscopic evidence of them.The cancers werelocated in the anastomosis in all cases.Basal luminescencefrom tumor gastric tissue generated 38.4±6.8 count perminute/mg/×10~6(mean±SD)and 14.9±4.0 count perminute/mg/×10~6,respectively,in group Ⅰ and Ⅱ animals(P<0.05).The Nitrobluetetrazolium method showed intensestaining in tumor tissues but not in non neoplasic mucosa.CONCLUSION:Experimental gastric tumors seem toproduce more reactive oxygen species than non neoplasicgastric tissue.The reduction of oxidative stress and gastrictumor incidence in rats were induced by the intake of ascorbicacid.Therefore,it may have a role in the prevention ofgastric carcinoma
AIM Oxidative stress participates in the cell carcinogenesis by inducing DNA mutations. Our aim was to assess whetherascorbic acid, an antioxidant, could have a role in preventing ROS (Reactive Oxygen Species) generation in experimental gastric carcinoma in a rat model. METHODS: Experimental gastric cancer was induced Group 2 (n = 6) was the control; Group Ⅱ (n = 6) which was mantained with daily intake of tape water with Vitamin C (30 mg / Kg) .After 6 or 12 months, samples of gastric tumor or non tumormucosa were taken from the anastomosis of both groups. Oxidative stress was measured by superoxide quantificationthrough lucigenin-amplified chemiluminescence base andbystan staining Nitrobluetetrazolium. The histopathologicconfirmation of adenocarcinoma was made by eosin-hemathoxilin method .RESULTS: The intestinal type of gastric adenocarcinomawas micr oscopically identified in all animals of group Iwhereas only 3 rats of group II showed an adenocarcinomawithout macroscopic evidence of them.The cancers werelocated in the anastomosis in all cases. basal luminescencefrom tumor gastric tissue generated 38.4 ± 6.8 count perminute / mg / x 10 ~ 6 (mean ± SD) and 14.9 ± 4.0 count per minute / mg / × 10 -6, respectively, in group Ⅰ and Ⅱ animals (P <0.05). The Nitrobluetetrazolium method showed intense staining in tumor tissues but not in non neoplasic mucosa. CONCLUSION: The reduction of oxidative stress and gastrictumor incidence in rats were induced by the intake of ascorbic acid. Therefore, it may have a role in the prevention of gastrictric carcinoma