Metabolomics analysis of human spermatozoa reveals impaired metabolic pathways in asthenozoospermia

IF 4.4 3区 医学 Q1 MEDICINE, GENERAL & INTERNAL European Journal of Clinical Investigation Pub Date : 2024-07-24 DOI:10.1111/eci.14289
Bárbara Guerra-Carvalho, David F. Carrageta, Tatiana Maurício, Sara C. Pereira, Alberto Barros, Rui A. Carvalho, Marco G. Alves, Pedro Domingues, Pedro F. Oliveira
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Abstract

Background

Infertility is a major health issue, affecting 15% of reproductive-age couples with male factors contributing to 50% of cases. Asthenozoospermia (AS), or low sperm motility, is a common cause of male infertility with complex aetiology, involving genetic and metabolic alterations, inflammation and oxidative stress. However, the molecular mechanisms behind low motility are unclear. In this study, we used a metabolomics approach to identify metabolic biomarkers and pathways involved in sperm motility.

Methods

We compared the metabolome and lipidome of spermatozoa of men with normozoospermia (n = 44) and AS (n = 22) using untargeted LC–MS and the metabolome of seminal fluid using 1H-NMR. Additionally, we evaluated the seminal fluid redox status to assess the oxidative stress in the ejaculate.

Results

We identified 112 metabolites and 209 lipids in spermatozoa and 27 metabolites in the seminal fluid of normozoospermic and asthenozoospermic men. PCA analysis of the spermatozoa's metabolomics and lipidomics data showed a clear separation between groups. Spermatozoa of asthenozoospermic men presented lower levels of several amino acids, and increased levels of energetic substrates and lysophospholipids. However, the metabolome and redox status of the seminal fluid was not altered inAS.

Conclusions

Our results indicate impaired metabolic pathways associated with redox homeostasis and amino acid, energy and lipid metabolism in AS. Taken together, these findings suggest that the metabolome and lipidome of human spermatozoa are key factors influencing their motility and that oxidative stress exposure during spermatogenesis or sperm maturation may be in the aetiology of decreased motility in AS.

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人类精子的代谢组学分析揭示了无精子症中受损的代谢途径。
背景:不育症是一个重大的健康问题,影响着15%的育龄夫妇,其中50%的病例由男性因素造成。无精子症(AS)或精子活力低下是导致男性不育的常见原因,其病因复杂,涉及遗传和代谢改变、炎症和氧化应激。然而,精子活力低背后的分子机制尚不清楚。在这项研究中,我们采用代谢组学方法来确定精子活力所涉及的代谢生物标志物和通路:我们使用非靶向 LC-MS 比较了正常无精子症(44 人)和强直性脊柱炎(22 人)男性精子的代谢组和脂质组,并使用 1H-NMR 比较了精液的代谢组。此外,我们还评估了精液的氧化还原状态,以评估射精中的氧化应激:结果:我们在正常无精症和非正常无精症男性的精子和精液中分别发现了112种代谢物和209种脂质,以及27种代谢物。对精子代谢组学和脂质组学数据的 PCA 分析表明,各组之间存在明显的差异。无精子症男性精子中几种氨基酸的含量较低,而能量底物和溶血磷脂的含量较高。然而,无精子症患者精液的代谢组和氧化还原状态没有改变:我们的研究结果表明,强直性脊柱炎患者与氧化还原平衡及氨基酸、能量和脂质代谢相关的代谢途径受损。综上所述,这些研究结果表明,人类精子的代谢组和脂质组是影响其运动能力的关键因素,精子发生或精子成熟过程中的氧化应激暴露可能是导致强直性脊柱炎患者运动能力下降的病因。
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来源期刊
CiteScore
9.50
自引率
3.60%
发文量
192
审稿时长
1 months
期刊介绍: EJCI considers any original contribution from the most sophisticated basic molecular sciences to applied clinical and translational research and evidence-based medicine across a broad range of subspecialties. The EJCI publishes reports of high-quality research that pertain to the genetic, molecular, cellular, or physiological basis of human biology and disease, as well as research that addresses prevalence, diagnosis, course, treatment, and prevention of disease. We are primarily interested in studies directly pertinent to humans, but submission of robust in vitro and animal work is also encouraged. Interdisciplinary work and research using innovative methods and combinations of laboratory, clinical, and epidemiological methodologies and techniques is of great interest to the journal. Several categories of manuscripts (for detailed description see below) are considered: editorials, original articles (also including randomized clinical trials, systematic reviews and meta-analyses), reviews (narrative reviews), opinion articles (including debates, perspectives and commentaries); and letters to the Editor.
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