Advanced Search

CN 34-1304/RISSN 1674-3679

Volume 28 Issue 11
Nov.  2024
Turn off MathJax
Article Contents
ZHANG Fuwei, WANG Wenzhuo, CAI Xiaomin, WANG Lu, HE Heng, ZHONG Rong, TIAN Jianbo, ZHU Ying, MIAO Xiaoping. Effect of phenol exposure and single nucleotide polymorphisms interaction on renal function[J]. CHINESE JOURNAL OF DISEASE CONTROL & PREVENTION, 2024, 28(11): 1241-1249. doi: 10.16462/j.cnki.zhjbkz.2024.11.001
Citation: ZHANG Fuwei, WANG Wenzhuo, CAI Xiaomin, WANG Lu, HE Heng, ZHONG Rong, TIAN Jianbo, ZHU Ying, MIAO Xiaoping. Effect of phenol exposure and single nucleotide polymorphisms interaction on renal function[J]. CHINESE JOURNAL OF DISEASE CONTROL & PREVENTION, 2024, 28(11): 1241-1249. doi: 10.16462/j.cnki.zhjbkz.2024.11.001

Effect of phenol exposure and single nucleotide polymorphisms interaction on renal function

doi: 10.16462/j.cnki.zhjbkz.2024.11.001
Funds:

National Key Research and Development Program of China 2022YFA0806601

More Information
  • Corresponding author: MIAO Xiaoping, E-mail: miaoxp@hust.edu.cn
  • Received Date: 2024-01-13
  • Rev Recd Date: 2024-05-10
  • Available Online: 2024-12-23
  • Publish Date: 2024-11-10
  •   Objective  To investigate of the interaction between exposure to bisphenol A (BPA), bisphenol F (BPF), triclosan (TCS) and gene locus polymorphism on renal function.  Methods  A total of 414 adults were recruited as research subjects from the physical examination population of Tongji Hospital affiliated with Tongji Medical College of Huazhong University of Science and Technology between 2016 and 2021. Population information was collected through questionnaires, and urine samples were obtained for analysis. The internal exposure levels of three phenolic compounds, namely BPA, BPF, and TCS, were subsequently measured in the urine samples of the study subjects. Serum creatinine levels were measured to determine renal function, and eGFR was calculated as an indicator. Blood samples were taken from research subjects to extract DNA for high-throughput genotyping, genome filling, and quality control. Genome-wide association studies (GWAS) were then conducted to analyze gene-environment interactions affecting eGFR levels. Finally, the obtained significant and suggestive genetic loci were annotated by location and function to explore their related biological functions.  Results  Following high-throughput genotyping and genotype filling, 414 samples were obtained with genotype data for 4 135 024 single nucleotide polymorphisms (SNPs) loci. During further identification, three SNPs loci (rs60391380, rs56108314, and rs73082740) were found to have a significant interaction with BPA in relation to renal function. These loci were located in the 4p16.3 chromosome segment, close to the ADRA2C gene. The most significant interaction effect was found for rs60391380, with a beta value of -0.042 (-0.057--0.028) and a P-value of 1.565×10-8. Based on epigenetic modifications, it was speculated that this genetic locus might interact with BPA, activate its regulatory elements, and upregulate the expression of ADRA2C, thereby affecting renal function. Additionally, 844 BPA interaction sites were explored, with suggestive results (P < 5×10-6). In the eGFR genome-wide association analysis, 52 loci were found to interact with BPF in a suggestive manner, but no significant loci were identified. For TCS, no significant or suggestive sites of interaction were found.  Conclusions  The interaction between BPA and SNPs had a joint effect on renal function. However, no statistically significant gene-environment interactions affecting renal function were found for BPF and TCS.
  • loading
  • [1]
    Chen TK, Hoenig MP, Nitsch D, et al. Advances in the management of chronic kidney disease [J]. BMJ, 2023, 383: e074216. DOI: 10.1136/bmj-2022-074216.
    [2]
    Stevens LA, Coresh J, Greene T, et al. Assessing kidney function--measured and estimated glomerular filtration rate [J]. N Engl J Med, 2006, 354(23): 2473-2483, DOI: 10.1056/NEJMra054415.
    [3]
    Navaneethan SD, Zoungas S, Caramori ML, et al. Diabetes management in chronic kidney disease: synopsis of the KDIGO 2022 clinical practice guideline update [J]. Ann Intern Med, 2023, 176(3): 381-387. DOI: 10.7326/m22-2904.
    [4]
    Obrador GT, Schultheiss UT, Kretzler M, et al. Genetic and environmental risk factors for chronic kidney disease [J]. Kidney Int Suppl, 2017, 7(2): 88-106. DOI: 10.1016/j.kisu.2017.07.004.
    [5]
    Freedman BI, Divers J, Palmer ND. Population ancestry and genetic risk for diabetes and kidney, cardiovascular, and bone disease: modifiable environmental factors may produce the cures [J]. Am J Kidney Dis, 2013, 62(6): 1165-1175. DOI: 10.1053/j.ajkd.2013.05.024.
    [6]
    Hobson S, Arefin S, Witasp A, et al. Accelerated vascular aging in chronic kidney disease: the potential for novel therapies [J]. Circ Res, 2023, 132(8): 950-969. DOI: 10.1161/circresaha.122.321751.
    [7]
    王璐, 何恒, 蔡晓敏, 等. 氧化应激在环境酚类暴露与估计肾小球滤过率关联中的中介效应[J]. 华中科技大学学报(医学版), 2023, 52(4): 431-438. DOI: 10.3870/j.issn.1672-0741.2023.04.001.

    Wang L, He H, Cai XM, et al. Mediating role of oxidative stress in the association between environmental phenol exposure and estimated glomerular filtration rate [J]. Acta Med Univ Sci Technol Huazhong, 2023, 52(4): 431-438. DOI: 10.3870/j.issn.1672-0741.2023.04.001.
    [8]
    Zhang X, Flaws JA, Spinella MJ, et al. The relationship between typical environmental endocrine disruptors and kidney disease [J]. Toxics, 2022, 11(1): 32. DOI: 10.3390/toxics11010032.
    [9]
    Nie HL, Wang F, Zhang Y, et al. Associations of serum bisphenol A levels with incident chronic kidney disease risk [J]. Sci Total Environ, 2021, 771: 145401. DOI: 10.1016/j.scitotenv.2021.145401.
    [10]
    Kang JH, Asai D, Toita R. Bisphenol A (BPA) and cardiovascular or cardiometabolic diseases [J]. J Xenobiot, 2023, 13(4): 775-810. DOI: 10.3390/jox13040049.
    [11]
    唐中伟, 王慧敏, 张卓, 等. 基于氧化应激与细胞凋亡探究双酚A慢性暴露致小鼠肾毒性作用机制[J]. 生物工程学报, 2023, 39(1): 372-385, DOI: 10.13345/j.cjb.220360.

    Tang ZW, Wang HM, Zhang Z, et al. Mechanism of nephrotoxicity induced by chronic exposure of bisphenol A in mice based on oxidative stress and cell apoptosis [J]. Chin J Biotech, 2023, 39(1): 372-385, DOI: 10.13345/j.cjb.220360.
    [12]
    赫淑铭, 潘文筱, 刘娴, 等. 双酚类化合物的生物代谢机理研究进展[J]. 环境化学, 2024, 43(3): 711-721. DOI: 10.7524/j.issn.0254-6108.2023041401.

    He SM, Pan WX, Liu X, et al. Research progresses of biotransformation mechanisms of bisphenols [J]. Environmental Chemistry, 2024, 43(3): 711-721. DOI: 10.7524/j.issn.0254-6108.2023041401.
    [13]
    Rasouly HM, Groopman EE, Heyman-Kantor R, et al. The burden of candidate pathogenic variants for kidney and genitourinary disorders emerging from exome sequencing [J]. Ann Intern Med, 2019, 170(1): 11-21. DOI: 10.7326/M18-1241.
    [14]
    Köttgen A, Pattaro C, Böger CA, et al. New loci associated with kidney function and chronic kidney disease [J]. Nat Genet, 2010, 42(5): 376-384. DOI: 10.1038/ng.568.
    [15]
    Freedman BI. APOL1 and nephropathy progression in populations of African ancestry [J]. Semin Nephrol, 2013, 33(5): 425-432. DOI: 10.1016/j.semnephrol.2013.07.004.
    [16]
    Stevens LA, Claybon MA, Schmid CH, et al. Evaluation of the Chronic Kidney Disease Epidemiology Collaboration equation for estimating the glomerular filtration rate in multiple ethnicities [J]. Kidney Int, 2011, 79(5): 555-562. DOI: 10.1038/ki.2010.462.
    [17]
    Colorado-Yohar SM, Castillo-González AC, Sánchez-Meca J, et al. Concentrations of bisphenol-a in adults from the general population: a systematic review and meta-analysis [J]. Sci Total Environ, 2021, 775: 145755. DOI: 10.1016/j.scitotenv.2021.145755.
    [18]
    Yang YJ, Guan J, Yin J, et al. Urinary levels of bisphenol analogues in residents living near a manufacturing plant in South China [J]. Chemosphere, 2014, 112: 481-486. DOI: 10.1016/j.chemosphere.2014.05.004.
    [19]
    Guo JQ, Wu CH, Zhang JM, et al. Early life triclosan exposure and neurodevelopment of children at 3 years in a prospective birth cohort [J]. Int J Hyg Environ Health, 2020, 224: 113427. DOI: 10.1016/j.ijheh.2019.113427.
    [20]
    Pollock T, Arbuckle TE, Guth M, et al. Associations among urinary triclosan and bisphenol A concentrations and serum sex steroid hormone measures in the Canadian and U.S. Populations [J]. Environ Int, 2021, 146: 106229. DOI: 10.1016/j.envint.2020.106229.
    [21]
    Kang H, Lee JP, Choi K. Exposure to phthalates and environmental phenols in association with chronic kidney disease (CKD) among the general US population participating in multi-cycle NHANES (2005-2016) [J]. Sci Total Environ, 2021, 791: 148343. DOI: 10.1016/j.scitotenv.2021.148343.
    [22]
    Priego AR, Parra EG, Mas S, et al. Bisphenol A modulates autophagy and exacerbates chronic kidney damage in mice [J]. Int J Mol Sci, 2021, 22(13): 7189. DOI: 10.3390/ijms22137189.
    [23]
    Moreno-Gómez-Toledano R, Arenas MI, Muñoz-Moreno C, et al. Comparison of the renal effects of bisphenol A in mice with and without experimental diabetes. Role of sexual dimorphism [J]. Biochim Biophys Acta Mol Basis Dis, 2022, 1868(1): 166296. DOI: 10.1016/j.bbadis.2021.166296.
    [24]
    Trasande L, Attina TM, Trachtman H. Bisphenol A exposure is associated with low-grade urinary albumin excretion in children of the United States [J]. Kidney Int, 2013, 83(4): 741-748. DOI: 10.1038/ki.2012.422.
    [25]
    Schlosser P, Tin A, Matias-Garcia PR, et al. Meta-analyses identify DNA methylation associated with kidney function and damage [J]. Nat Commun, 2021, 12(1): 7174. DOI: 10.1038/s41467-021-27234-3.
    [26]
    Lee J, Oh S, Kang H, et al. Environment-wide association study of CKD [J]. Clin J Am Soc Nephrol, 2020, 15(6): 766-775. DOI: 10.2215/CJN.06780619.
    [27]
    Kim JO, Jeon YJ, Kim OJ, et al. Association between common genetic variants of α2A-, α2B- and α2C-adrenoceptors and the risk of silent brain infarction [J]. Mol Med Rep, 2014, 9(6): 2459-2466. DOI: 10.3892/mmr.2014.2072.
    [28]
    Ma Y, Liu HH, Wu JX, et al. The adverse health effects of bisphenol A and related toxicity mechanisms [J]. Environ Res, 2019, 176: 108575. DOI: 10.1016/j.envres.2019.108575.
    [29]
    Granata S, Zaza G, Simone S, et al. Mitochondrial dysregulation and oxidative stress in patients with chronic kidney disease [J]. BMC Genomics, 2009, 10: 388. DOI: 10.1186/1471-2164-10-388.
  • 加载中

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Figures(3)  / Tables(3)

    Article Metrics

    Article views (154) PDF downloads(52) Cited by()
    Proportional views
    Related

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return