目的: 探讨砷暴露、糖尿病患病和氧化应激损伤之间的关系。方法: 选取218名在巴彦淖尔市杭锦后旗生活20年以上且无明确砷暴露史者为调查对象,按照居民尿砷含量分为低砷组73例(＜13.55 μg/g Cr ),中砷组73例(13.56~36.24 μg/g Cr),高砷组72例(＞36.25 μg/g Cr)。采集研究对象血、尿液,测定尿砷、血清中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和丙二醛(MDA)含量。将研究对象中的25例糖尿病患者纳入病例组;对照组例数采用倾向评分匹配法(PSM)按照1∶5的比例进行匹配,选择125例居民纳入对照组。采用趋势性检验比较尿砷浓度与糖尿病患病率之间的变化趋势;构建中介效应模型探讨氧化应激损伤在不同砷暴露水平与糖尿病患病之间的间接效应。结果: (1)高砷组糖尿病患病率(20.83 %)高于中砷组糖尿病患病率(12.33 %)和低砷组糖尿病患病率(1.37 %),中砷组糖尿病患病率高于低砷组糖尿病患病率,差异具有统计学意义(P＜0.05);尿砷水平与糖尿病患病率呈正相关(P＜0.05);(2)GSH-Px活力、SOD和MDA在尿砷水平与糖尿病患病中起中介作用(P＜0.05)。结论: 砷暴露可能通过影响居民机体氧化应激机制从而导致了糖尿病的发生。
Objective: To explore the relationship between arsenic exposure, diabetes mellitus and oxidative stress injury. Methods: A total of 218 people who had lived in Hangjin Houqi, Bayannur City for more than 20 years and had no clear history of exposure to arsenic were selected as the investigation subjects. According to the urinary arsenic content of residents, they were divided into low arsenic group (73 residents,＜13.55 μg/g Cr) medium arsenic group (73 residents, 13.56~36.24 μg/g Cr), and high arsenic group (72 residents, ＞36.25 μg/g Cr). The blood and urine of the subjects were collected, and the contents of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in urine and serum were determined. Of 25 diabetic mellitus patients in the study were included in the case group. The number of cases in the control group was matched by propensity score matching (PSM) in a ratio of 1∶5, and 125 residents were selected as the control group. Trend test was used to compare the trend between urinary arsenic concentration and the prevalence of diabetes mellitus. A mediating effect model was constructed to explore the indirect effects of oxidative stress injury between different arsenic exposure levels and diabetes mellitus. Results: (1)The prevalence of diabetes mellitus in the high arsenic group (20.83 %) was higher than that in the medium arsenic group (12.33 %) and the low arsenic group (1.37 %), while the prevalence of diabetes mellitus in the medium arsenic group was higher than that in the low arsenic group, and the difference was statistically significant (P＜0.05). Urinary arsenic level was positively correlated with the prevalence of diabetes mellitus (P＜0.05). (2)GSH-Px activity, SOD and MDA played mediating roles between urinary arsenic level and diabetes mellitus (P＜0.05). Conclusion: Arsenic exposure may lead to the occurrence of diabetes mellitus by affecting the mechanism of oxidative stress in residents.
[1] Beck R,Styblo M,Sethupathy P.Arsenic exposure and type 2 diabetes:microRNAs as mechanistic links[J].Curr Diab Rep, 2017,17(3):18.
[2] 孔畅,杨林生,李海蓉,等.内蒙古某饮水型砷中毒病区人群体内砷蓄积与砷代谢的年内变化特征[J].环境化学,2018,37(11):2335-2341.
[3] Bundschuh J,Nlazi NK,Alam MA,et al.Global arsenic dilemma and sustainability[J].J Hazard Mater,2022,436:129197.
[4] Martinez-Castillo M,Garcia-Montalvo EA,Arellano-MendozaM G,et al.Arsenic exposure and non-carcinogenic health effects[J].Hum Exp Toxicol, 2021,40(12_suppl):S826-S850.
[5] Rangel-Moreno K,Gamboa-Loira B,Lopez-Carrillo L,et al.Prevalence of type 2 diabetes mellitus in relation to arsenic exposure and metabolism in Mexican women[J].Environ Res,2022,210:112948.
[6] Navas-Acien A, Silbergeld EK,Pastor-Barriuso R,et al.Arsenic exposure and prevalence of type 2 diabetes in US adults[J].JAMA,2008,300(7):814-822.
[7] 何玲玲.巴彦淖尔市地方性砷中毒分布[J].中国地方病防治杂志,2015,30(3):201.
[8] 安艳,李春春,邓晗依.砷诱发氧化应激研究现状[J].国外医学(医学地理分册),2015,36(3):165-173.
[9] 唐凯,谭薇.氧化应激在糖尿病性视网膜病变早期治疗中的研究进展[J].重庆医学,2023,52(5):787-791.
[10] Zhang PJ,Li T,Wu XY,et al.Oxidative stress and diabetes: antioxidative strategies[J].Front Med, 2020,14(5):583-600.
[11] 中华医学会糖尿病学分会.中国2型糖尿病防治指南(2020年版)(上)[J].中国实用内科杂志,2021,41(8):668-695.
[12] Soza-Ried C, Bustamante E,Caglevic C,et al.Oncogenic role of arsenic exposure in lung cancer:a forgotten risk factor[J].Crit Rev Oncol Hematol,2019,139:128-133.
[13] Saeedi P,Petersohn I,Salpea P,et al.Global and regional diabetes prevalence estimates for 2019 and projections for 2030 and 2045:results from the International Diabetes Federation Diabetes Atlas,9th edition[J].Diabetes Res Clin Pract,2019,157:107843.
[14] Eick SM,Ferreccio C,Acevedo J,et al.Socioeconomic status and the association between arsenic exposure and type 2 diabetes[J].Environ Res,2019,172:578-585.
[15] Idrees M,Batool S.Environmental risk assessment of chronic arsenic in drinking water and prevalence of type-2 diabetes mellitus in Pakistan[J].Environ Technol,2020,41(2):232-237.
[16] 迪力娜尔·买买提,李文波,谢惠芳.饮水型砷暴露与糖尿病关联的meta分析[J/OL].环境与健康杂志,2022:1-5.(2022-10-31).
[17] Jomova K,Jenisova Z,Feszterova M,et al.Arsenic: toxicity,oxidative stress and human disease[J].J Appl Toxicol,2011,31(2):95-107.
[18] Zargari F,Rahaman MS,Kazempour R,et al.Arsenic,oxidative stress and reproductive system[J].J Xenobiot,2022,12(3):214-222.
[19] Miao L,St Clair DK.Regulation of superoxide dismutase genes: implications in disease[J].Free Radic Biol Med, 2009,47(4):344-356.
[20] 刘莹,柳红,孔庆兖.SOD与ROS在As2O3作用于S180肉瘤细胞中的作用研究[J].南京医科大学学报(自然科学版),2005,25(3):180-183,217.
[21] Kumar A,Khushboo,Pandey R,et al.Modulation of superoxide dismutase activity by mercury,lead, and arsenic[J].Biol Trace Elem Res,2020,196(2):654-661.
[22] Handy DE,Loscalzo J.The role of glutathione peroxidase-1 in health and disease[J].Free Radic Biol Med,2022,188:146-161.
[23] 夏荣香,吴军,魏洁群,等.不同价态无机砷染毒对大鼠脏器GSH-Px活力的影响[J].新疆医科大学学报,2010,33(4):337-340.
[24] 袁子薇,袁伟杰,武萌萌,等.通心络胶囊对进展型缺血性脑卒中血清AGE、MDA、SOD、T-AOC水平的影响[J].中华中医药学刊,2023,41(5):235-238.
[25] Jlang XJ,Chen CZ,Liu Y,et al.Critical role of cellular glutathione homeostasis for trivalent inorganic arsenite-induced oxidative damage in human bronchial epithelial cells[J].Mutat Res Genet Toxicol Environ Mutagen, 2014,770:35-45.
[26] Strom A,Kaul K, Bruggemann J, et al.Lower serum extracellular superoxide dismutase levels are associated with polyneuropathy in recent-onset diabetes[J].Exp Mol Med, 2017,49(11):e394.
[27] El-ghoroury EA, Raslan HM, Badawy EA, et al.Malondialdehyde and coenzyme Q10 in platelets and serum in type 2 diabetes mellitus: correlation with glycemic control[J].Blood Coagul Fibrinolysis, 2009,20(4):248-251.
