摘要
目的观察SD大鼠吸入烹调油烟(cookingoilfumes,COF)后的慢性毒性及其潜在致癌性,探讨COF可能的致癌作用机制。方法以SD大鼠为实验对象,采用动式吸入染毒眼(6.88±0.31)、(15.06±0.35)、(35.33±1.69)mg/m3演,设空白对照组,复制COF慢性动物实验模型;利用免疫组织化学技术研究肺组织突变型p53和脆性组氨酸三联体(FHIT)蛋白表达。结果COF诱发SD大鼠肺癌总发生率为9.42%,雄性6.32%,雌性12.50%,雌雄两组肺癌发生率的差异无统计学意义(P>0.05);突变型p53蛋白在实验组有阳性表达,阳性定位于支气管上皮细胞胞核,对照组呈阴性。肿瘤病例肺组织切片的p53蛋白阳性表达率显著高于对照组(P<0.001);FHIT蛋白在各组均有阳性表达,阳性定位于支气管上皮细胞胞浆,实验组的肿瘤病例与非典型增生病例肺组织切片FHIT蛋白阳性表达率均显著低于对照组(P<0.001,P<0.01)。结论COF为SD大鼠致癌物;COF或(和)其代谢产物致抑癌基因p53、FHIT突变可能是COF致肺癌重要机制之一。
Objective To study the chronic toxicity and the potential carcinogenicity of cooking oil fumes(COF) in SD rats and the mechanism. Methods SD rats were used to make the chronic toxicity model. The rats in experimental groups had been exposed to COF with different concentrations?眼(6.88±0.31) mg/m3, (15.06±0.35) mg/m3 and (35.33±1.69) mg/m3?演 every other day for 12.5 months, exposed for 30 min each time. The rats in control group had inhaled clean air. Immunohistochemistry was used to detect the expression of p53 and FHIT protein in lung tissue. Results Total incidence rate of pulmonary carcinoma in SD rats induced by COF was 9.42%, male 6.32%, female 12.50% respectively. There was not a significant difference between male and female (P>0.05). The pulmonary carcinoma incidence rate of the rats treated at the dosages of (6.88±0.31) mg/m3, (15.06±0.35) mg/m3 and (35.33±1.69) mg/m3 were 6.56%?8.96% and 12.70% respectively. Immunohistochemical staining showed that COF could induce abnormal expression of p53 and FHIT protein in lung tissue. Only in experimental group the positive expression of mutant p53 protein located in bronchi epithelial cell nucleus were found. The positive expression rate of p53 protein in lung tissue section of tumor cases was significantly higher than that of control group(P<0.001). The positive expression rate of FHIT protein of tumor case and atypical hyperplasia's lung tissue section were significantly lower than that of control group (P<0.001, P<0.01). Conclusion COF is carcinogen for Spraque dawley rats. The mutation of anti-oncogene p53 or FHIT plays an important role in the mechanisms of carcinogenesis of COF.
出处
《环境与健康杂志》
CAS
CSCD
北大核心
2005年第2期114-116,共3页
Journal of Environment and Health
