目的 观察砷暴露人群血液维A酸受体α(RXRα)mRNA表达水平与砷暴露引起的皮肤损伤之间的关系,探讨砷致皮肤损伤的发生机制.方法 采用分子流行病学方法,以巴彦淖尔市砷中毒病区作为研究现场,抽取在此居住10年以上的居民235人作为研究对象.采集研究对象血样及家中水样,根据饮水砷含量分为对照组(< 10 μg/L)、低砷暴露组(10 ~ < 100 μg/L)、中砷暴露组(100 ~ < 200 μg/L)、高砷暴露组(≥200 μg/L),检查研究对象皮肤角化及色素异常情况;运用实时荧光定量PCR技术,检测血中RXRα mRNA表达水平,分析砷暴露时RXRα mRNA表达与皮肤损伤之间的关系.结果 ①水砷含量与砷中毒皮肤角化、色素异常检出率呈剂量-效应关系(χ2趋势 =14.597、12.825,P均 <0.05).②各组RXRα mRNA 表达比较,差异有统计学意义(F=8.312,P<0.05).其中低砷暴露组[(0.92 ± 0.49)×10-3]与对照组[(1.20 ± 0.53)×10-3]比较显著降低,差异有统计学意义(P < 0.05);高砷暴露组[(1.40 ± 0.45)× 10-3]与中、低砷暴露组[(1.12 ± 0.58、0.92 ± 0.49)×10-3]比较显著升高,差异有统计学意义(P均 <0.05).③不同皮肤损伤程度人群(皮肤角化、色素异常) RXRα mRNA表达比较,(F = 4.206、4.389,P 均 < 0.05),Ⅲ度[(1.98 ± 0.38)× 10-3]角化与Ⅰ度[(1.11 ± 0.52)×10-3]、Ⅱ度[(1.13 ± 0.42)×10-3]比较,差异有统计学意义(P均<0.05);Ⅱ度及以上[(1.61 ± 0.54)×10-3]色素异常与正常组[(1.15 ± 0.52)× 10-3]比较,差异有统计学意义(P < 0.05).结论 慢性砷暴露可以引起RXRα mRNA表达改变,砷中毒所致皮肤损伤与RXRα mRNA的表达异常有关.%Objective To detect retinoid X receptor α (RXRα) mRNA expression in blood of subjects exposed to different concentrations of arsenic via drinking water, to analyze the relationship between RXRα mRNA expression and skin lesion caused by arsenic,and further to explore the skin lesion mechanism of arsenic. Methods Study sites were selected by molecular epidemiology method from high arsenic drinking water area of Bayannur City. Two hundred and thirty-five subjects who had been lived in high arsenic area for more than 10 years were selected;blood samples and water samples were collected from the subjects; according to arsenic concentration in drinking water,they were divided into four groups,<10 μg/L(control group),10-<100 μg/L(low dose group),100- <200 μg/L (middle dose group), and ≥200 μg/L (high dose group). Skin hyperkeratosis and pigment abnormity examination were conducted. The RXRα mRNA expression level in blood samples was detected by real-time quantitative PCR, and then the relationship between expression of RXRα mRNA and different levels of arsenic exposure,and skin lesion induced by arsenic were analyzed. Results ①The results showed that there was a dose-effect relationship between the prevalence of hyperkeratosis, pigment abnormity and arsenic exposure (χ2= 14.597, 12.825, P < 0.05); ②With increasing of arsenic exposure, RXRα mRNA expression in blood decreased firstly and then increased (F = 8.312, P < 0.05), which were significantly different statistically from those of control [(1.20 ±0.53)×10-3]and low dose groups[(0.92 ± 0.49)×10-3,P<0.05];RXRα expression was significantly higher in high dose group[(1.40 ± 0.45)×10-3]than those of middle and low dose groups [(1.12 ± 0.58,0.92 ± 0.49)×10-3,P<0.05]; ③The RXRα mRNA expression in people with different level of skin damage (hyper keratosis and pigment abnormity)were statistically significant(F=4.206,4.389, P< 0.05); degree Ⅲ[(1.98 ± 0.38) × 10-3] hyperkeratosis patients compared with degree Ⅰ [(1.11 ± 0.52) × 10-3] and degree Ⅱ [(1.13 ± 0.42) × 10-3], RXRα mRNA expression was significantly different (P < 0.05), degree Ⅱ and higher degrees [(1.61 ± 0.54) × 10 -3] pigment abnormity patients compared with control [(1.15 ± 0.52)×10-3],RXRα mRNA expression was significantly different (P < 0.05). Conclusions Chronic arsenic exposure has an effect on RXRα mRNA expression in blood. There is a relationship between abnormal expression of RXRα mRNA and skin lesion induced by arsenic.
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