Urinary Metabolic Biomarkers Link Oxidative Stress Indicators Associated with General Arsenic Exposure to Male Infertility In a Han Chinese Population
Urinary Metabolic Biomarkers Link Oxidative Stress Indicators Associated with General Arsenic Exposure to Male Infertility In a Han Chinese Population
复制标题
尿代谢生物标志物将氧化应激指标与中国汉族人群中一般砷暴露与男性不育联系起来
DOI:
10.1021/es402025n
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发表时间:
2013-08-06
影响因子:
11.4
通讯作者:
Zhu, Yong-Guan
中科院分区:
文献类型:
--
作者:
Shen, Heqing;Xu, Weipan;Zhu, Yong-Guan
To investigate the hypothesis that general environmental arsenic (As) exposure can impair male fertility, we designed a case-control study examining possible correlations between the concentrations of different As species in urine [controls (n = 151) vs cases (n = 140)], urinary metabolic biomarkers [controls (n = 158) vs cases (n = 135)1 and infertility characterized by poor semen quality. Regional participants were recruited sequentially from the affiliated hospitals of Nanjing Medical University. Elevated inorganic arsenate (As-i(V)) exposure was associated with infertility: in comparison with the first quartile, subjects with As-i(V) levels above the median were more likely to exhibit male idiopathic infertility with increasing adjusted odds ratios (AOR) of 4.9 [95% confidence interval (CI), 1.8-13.6] and 13.6 (9596 CI, 4.8-38.6) at the third and fourth quartiles (P = 0.000 for trend), respectively. Other As species did not exhibit a significant dose-dependent correlation with infertility risk. Levels of urinary biomarkers correlated with both male infertility and As-i(V) concentrations [controls (n = 145) vs cases (n = 123)1 the latter correlation was independent of disease. These included acylcarnitines, aspartic acid, and hydroxyestrone, which were negatively associated with infertility, and uridine and methylxanthine, which were positively associated. In conclusion, for the first time we show that elevated urinary concentrations of As-i(V) from general As exposure are significantly associated with male infertility, and As species may exert toxicity via oxidative stress and sexual hormone disrupting mechanisms, as indicated by related biomarkers.