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目的研究维生素E对苯并(a)芘所致小鼠肺癌的干预作用。方法将清洁级昆明种小鼠随机分为9组,每组25只。雌性和雄性B(a)P组灌胃1.8μg/kgB(a)P,每周1次,连续8周。雌性和雄性B(a)P+高剂量VE组和雌性B(a)P+低剂量VE组,在染毒的同时通过食物定量摄入VE,分别为100和50mg/(kg·d)。雌性、雄性对照组和VE组通过灌胃给予橄榄油。计算肺癌发病率和肿瘤数。测定小鼠血清中氧化和抗氧化指标。结果雌性和雄性B(a)P组的肺癌发病率和肿瘤结节数分别明显高于相应的雌性、雄性对照组和VE组,差异有统计学意义(P<0.05)。雌性B(a)P+高剂量VE组和B(a)P+低剂量VE组肺癌发病率和肿瘤数明显高于对照组、VE组和雌性B(a)P组,差异有统计学意义(P<0.05)。雄性B(a)P+高剂量VE组肺癌发病率和肿瘤数高于对照组和VE组,差异有统计学意义(P<0.05);与雄性B(a)P组比较,差异无统计学意义(P>0.05)。与雌性B(a)P组比较,雌性B(a)P+低剂量VE组和雌性B(a)P+高剂量VE组SOD活力明显上升,MDA含量明显减少,ROS明显升高,差异均有统计学意义(均P<0.05);雌性B(a)P+高剂量VE组GSH-Px升高,差异有统计学意义(P<0.05)。结论VE对B(a)P所致肺癌的影响机制与抗氧化作用无关。VE对B(a)P所致小鼠肺癌没有预防作用,对雌性小鼠可能具有促癌作用。
Objective To investigate the intervention of vitamin E on lung cancer induced by benzo (a) pyrene in mice. Methods Clean Kunming mice were randomly divided into 9 groups of 25 rats. Female and male B (a) P groups were dosed with 1.8 μg / kg B (a) P once a week for 8 weeks. The female and male B (a) P + high dose VE group and the female B (a) P + low dose VE group were fed with a dose of VE of 100 and 50 mg / (kg · d), respectively. Female, male control and VE groups were given olive oil by gavage. Calculate the incidence of lung cancer and the number of tumors. Determination of mouse serum oxidation and antioxidant indicators. Results The incidence of lung cancer and the number of tumor nodules in female and male B (a) P groups were significantly higher than those in corresponding female, male and VE groups (P <0.05). The incidence and the number of lung cancer in female B (a) P + high dose VE group and B (a) P + low dose VE group were significantly higher than those in control group, VE group and female B (a) P group, with significant difference <0.05). The incidence and the number of lung cancer in male B (a) P + high dose VE group were higher than those in control group and VE group (P <0.05), but there was no significant difference with male B (a) P group (P> 0.05). Compared with female group B (a), the activity of SOD and the content of MDA in the female B (a) P + low dose VE group and the female B (a) P + high dose VE group increased obviously, while the content of MDA increased obviously (P <0.05). The GSH-Px in female B (a) P + high dose VE group was significantly increased (P <0.05). Conclusion The mechanism of VE on B (a) P-induced lung cancer has nothing to do with anti-oxidation. VE has no preventive effect on lung cancer induced by B (a) P in mice and may have a carcinogenic effect on female mice.