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Intervention of zinc on the male reproductive toxicity caused by phthalates exposure |
SUN Yue, YANG Liu, SHI Hongyi, LI Anqi, DAI Qimeng, JIN Siyi, GAO Haitao |
Department of Preventive Medicine, School of Public Health and Management, Wenzhou Medical University, Wenzhou 325035, China |
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Cite this article: |
SUN Yue,YANG Liu,SHI Hongyi, et al. Intervention of zinc on the male reproductive toxicity caused by phthalates exposure[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2019, 49(9): 649-653,,660.
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Abstract Objective: To study the protective effect of zinc on reproductive toxicity caused by phthalate exposure in mice. Methods: Thirty-six male ICR mice were randomly divided into the control group, MIXPs (the equipotent toxic mixture of butyl benzyl phthalate (BBP), di (n-butyl) phthalate (DBP) and di (2-ethyhexyl) phthalate (DEHP) group, and MIXPs+ZnSO4 group, with 12 mice in each group. Mice in MIXPs group and MIXPs+ZnSO4 group were treated with 160 mg·kg-1·d-1 MIXPs by gavage with or without 50 mg·kg-1·d-1 ZnSO4. Mice in control group were treated with isodose 0.5% CMC-Na. After 90 days’ intervention, orbital vein blood was collected from each anesthetic mouse. Then dissect the mouse and take male reproductive organs such as the testicles and epididymis. Sperm morphology was observed with electron microscope. The levels of testosterone, SOD, MDA and T-AOC were measured with the commercial kits. Results: Compared with the control, the bodyweight, anogenital distance, serum testosterone, SOD and MDA in testicular tissue in MIXPs group were significantly reduced, while the rate of sperm deformation was significantly increased (P<0.05 or P<0.01), but there were no significant changes in MIXPs+ZnSO4 group. Conclusion: Zinc can inhibit the male reproductive toxicity induced by MIXPs exposure, which may be related to the improvement of the antioxidant level of testicular tissue and the increase of serum testosterone level.
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Received: 28 November 2018
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[1] 中华人民共和国国家卫生和计划生育委员会. 《食品安全国家标准食品接触材料及制品用添加剂使用标准》(GB9685-2016)[S]. 北京: 2016.
[2] 高海涛, 李瑞仙, 邸倩南, 等. 我国人群邻苯二甲酸酯类的暴露水平及风险[J]. 癌变·畸变·突变, 2017, 29(6): 471-475.
[3] National Nanotechnology Coordination Office. Quantifying Exposure to Engineered Nanomaterials (QEEN) from Manufactured Products[EB/OL]. (2015-07-07)[2018-11-28].
https://www.cpsc.gov/en/Regulations-Laws--Standards/Statutes/The-Consumer-Product-Safety-Improvement-Act/Phthalates/Chronic-Hazard-Advisory-Panel-CHAP-on-Phthalates.
[4] WANG Y X, ZENG Q, SUN Y, et al. Phthalate exposure in association with serum hormone levels, sperm DNA damage and spermatozoa apoptosis: A cross-sectional study in China [J]. Environ Res, 2015, 150: 557-565.
[5] GAO H T, XU R, CAO W X, et al. Effects of six priority controlled phthalate esters with long-term low dose integrated exposure on male reproductive toxicity in rats[J]. Food Chem Toxicol, 2017, 101: 94-104.
[6] GAO H T, XU R, CAO W X, et al. Combined effects of simultaneous exposure to six phthalates and emulsifier glycerol monosterate on male reproductive system in rats[J]. Toxicol Appl Pharmacol, 2018, 341: 87-97.
[7] 王丽霞, 王雪楠. 男性不育症患者微量元素含量与精液质量关系的研究[J]. 中国医药科学, 2011, 1(16): 14-15.
[8] 梁妍琦, 钱之玉. 缺锌对雄性大鼠生殖系统的影响[J]. 中国药科大学学报, 1999, 30(1): 47-50.
[9] 李艳, 朱静媛, 庄东刚, 等. 锌对氟致雄性大鼠生殖损伤的拮抗作用[J]. 郑州大学学报(医学版), 2007, 42(1): 75-78.
[10] RAWI S M, SEIF AL NASSR F M. Zinc sulphate and vitamin E alleviate reproductive toxicity caused by aluminium sulphate in male albino rats[J]. Toxicol Ind Health, 2015, 31(3): 221-234.
[11] 刘毓谷. 卫生毒理学基础[M]. 北京: 人民卫生出版社, 1994, 215-217.
[12] ZHANG R, ZHANG L, JIANG D, et al. Mouse organ coefficient and abnormal sperm rate analysis with exposure to tap water and source water in Nanjing reach of Yangtze River[J]. Ecotoxicology, 2014, 23(4): 641-646.
[13] CHEMEK M, VENDITTI M, BOUGHAMOURA S, et al. Involvement of testicular DAAM1 expression in zinc protection against cadmium-induced male rat reproductive tox-icity[J]. J Cell Physiol, 2018, 233(1): 630-640.
[14] NORIEGA N C, HOWDESHELL K L, FURR J, et al. Pubertal administration of DEHP delays puberty, suppresses testosterone production, and inhibits reproductive tract development in male Sprague-Dawley and Long-Evans rats[J]. Toxicol Sci, 2009, 111(1): 163-178.
[15] HANNAS B R, LAMBRIGHT C S, FURR J, et al. Dose-response assessment of fetal testosterone production and gene expression levels in rat testes following in utero exposure to diethylhexyl phthalate, diisobutyl phthalate, diisoheptyl phthalate, and diisononyl phthalate[J]. Toxicol Sci, 2011, 123(1): 206-216.
[16] MOTOHASHI M, WEMPE M F, MUTOU T, et al. Male rats exposed in utero to di(n-butyl) phthalate: Age-related changes in Leydig cell smooth endoplasmic reticulum and testicular testosterone-biosynthesis enzymes/proteins[J]. Reprod Toxicol, 2016, 59: 139-146.
[17] LEHMANN K P, PHILLIPS S, SAR M, et al. Dose-dependent alterations in gene expression and testosterone synthesis in the fetal testes of male rats exposed to di (n-butyl) phthalate[J]. Toxicol Sci, 2004, 81(1): 60-68.
[18] ZHOU D, WANG H, ZHANG J. Di-n-butyl phthalate (DBP) exposure induces oxidative stress in epididymis of adult rats [J]. Toxicol Ind Health, 2011, 27(1): 65-71.
[19] NELLI G, PAMANJI S R. Di-n-butyl phthalate prompts interruption of spermatogenesis, steroidogenesis, and fertility associated with increased testicular oxidative stress in adult male rats[J]. Environ Sci Pollut Res Int, 2017, 24(22): 18563-18574.
[20] ZHANG L D, LI H C, CHONG T, et al. Prepubertal exposure to genistein alleviates di-(2-ethylhexyl) phthalate induced testicular oxidative stress in adult rats[J]. Biomed Res Int, 2014, 2014: 598630. |
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