目的通过测定砷暴露人群血液芳香烃受体(aryl hydrocarbon receptor,AhR)和细胞色素P4501A1(cytochrome P4501A1,CYP1A1)mRNA表达,探讨其与慢性砷中毒皮肤改变的关系。方法选取内蒙古巴彦淖尔市杭锦后旗砷暴露地区233位居民,按水砷含量分为〈10μg/L(对照组)、10.〈100μg/L(低剂量组)、100-〈200μg/L(中剂量组)、≥200μg/L(高剂量组),各剂量组分别为55、47、45、86人。运用实时荧光定量PCR技术检测人群血液AhR和CYP1A1mRNA表达水平,mRNA相对表达水平以中位数及四分位数[M(Q1~Q3)]表示,并分析其与皮肤角化、色素脱失的关系。结果高剂量组人群血液AhR和CYP1A1mRNA相对表达水平分别为3.18×10-3(2.42×10-3 - 4.45×10-3)和1.58×10-3(0.80×10-3~2.73×10-3),与对照组[2.30×10-3(1.53×10~~3.20×10-3)和1.00×10-3(0.59×10-3 - 2.09×10-3)]相比较,均明显升高,差异均有统计学意义(P均〈0.05)。各组人群砷中毒、皮肤角化、色素脱失检出率比较,差异均有统计学意义(xz=20.187、15.848、21.595,P均〈0.05)。且砷中毒、皮肤角化、色素脱失检出率随水砷含量的增加而增加(X2=19.012、15.269、16.868,P均〈0.05)。与皮肤正常人群[2.54×100(1.79×10-3—3.43×10-3)、2.57×10-3(1.78×10-3 ~3.52×10-3)]相比较,Ⅲ度皮肤角化、Ⅲ度色素脱失人群血液AhRmRNA表达水平[4.45×10-3(3.47×10-3 - 8.04×10-3)、4.45×10-3(4.02×10-3~6.25×10-3)]均明显升高,差异均有统计学意义(P均〈0.05)。结论长期慢性砷暴露会影响AhR和CYP1A1mRNA表达水平。人群血液AhRmRNA的表达可能与地方性砷中毒人群皮肤改变有关系,而血液中CYP1A1mRNA的表达可能与地方性砷中毒人群皮肤改变无关。
Objective Though measuring the expression levels of blood aryl hydrocarbon receptor (AhR) and cytochrome P-450 1A1 (CYP1A1), to explore the relationship between the expression levels and chronic arsenic poisoning induced skin changes. Methods Totally 233 residents were selected in Hanggin Rear Banner arsenic exposure area of Bayannur City, according to water arsenic concentrations, these people were divided into control ( 〈 10 μg/L, 55 people), low (10 - 〈 100 μg/L, 47), medium (100 - 〈 200 μg/L, 45) and high (≥200 μg/L, 86) arsenic exposure groups. Real-time PCR was used to detect the expression levels of blood AhR and CYP1A1 mRNA, which were presented in median and quartile [M(Q1 - Q3)], and the relationships between their expression levels and keratosis, depigmentation of skin were analyzed. Results The relative expression levels of AhR and CYP1A1 mRNA in high-close groups were 3.18 ×10-3 (2.42 × 10.3 - 4.45 ×10-3) and 1.58 ×10-3 (0.80 ×10-3 - 2.73 ×10-3), which were higher than those in control groups [2.30 ×10-3 (1.53 ×10-3 - 3.20 ×10-3) and 1.00 ×10-3 (0.59 ×10-3 - 2.09 ×10-3)], and the difference were statistically significant (all P 〈 0.05). Compared with control group, the detectable rates of arsenic poisoning, keratosis and depigmentation of skin were higher, and the differences were statistically significant (X2 = 20.187, 15.848, 21.595, all P 〈 0.05). The detectable rates of arsenic poisoning, keratosis and depigmentation of skin were increased with increase of water arsenic concentrations (X2 = 19.012, 15.269, 16.868, all P 〈 0.05). Compared with normal [2.54 × 10-3 (1.79 ×10-3 - 3.43×10-3), 2.57 ×10-3 (1.78 ×10-3 - 3.52 ×10-3)], AhR mRNA relative expression levels [4.45 ×10-3 (3.47 ×10-3 - 8.04 ×10-3), 4.45 ×10-3 (4.02 ×10-3 - 6.25 ×10-3)] of degree Ⅲ keratosis and depigmentation of skin were increased, and the differences were statistically significant (all P 〈 0.05). Conclusion