Summary of project PR002028

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR002028. The data can be accessed directly via it's Project DOI: 10.21228/M8GC01 This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

Project ID: PR002028
Project DOI:doi: 10.21228/M8GC01
Project Title:Metabolomics analysis of human spermatozoa reveals impaired metabolic pathways in asthenozoospermia
Project Summary:Background: Infertility is a major health issue, affecting 15% of reproductive-age couples with male factors contributing to 50% of cases. Asthenozoospermia, or low sperm motility, is a common cause of male infertility with complex etiology, 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 asthenozoospermia (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 in asthenozoospermia. Conclusions: Our results indicate impaired metabolic pathways associated with redox homeostasis and amino acid, energy, and lipid metabolism in asthenozoospermia. 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 etiology of decreased motility in asthenozoospermia.
Institute:University of Aveiro
Department:Department of Chemistry
Last Name:Guerra-Carvalho
First Name:Bárbara
Address:Campus Universitário de Santiago, 3810-193 Aveiro, Portugal
Email:barbaraggcarvalho@gmail.com
Phone:234 370 360
Project Comments:Study part 1 of 2

Summary of all studies in project PR002028

Study IDStudy TitleSpeciesInstituteAnalysis
(* : Contains Untargted data)
Release
Date
VersionSamplesDownload
(* : Contains raw data)
ST003266 Metabolomics analysis of human spermatozoa reveals impaired metabolic pathways in asthenozoospermia (MS data) Homo sapiens University of Aveiro MS 2024-07-25 1 61 Uploaded data (4.7G)*
ST003276 Metabolomics analysis of human spermatozoa reveals impaired metabolic pathways in asthenozoospermia (NMR data) Homo sapiens University of Aveiro NMR 2024-07-25 1 57 Uploaded data (6M)*
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