Cargando…

The etiologies of DNA abnormalities in male infertility: An assessment and review

The sperm DNA damage may occur in testis, genital ducts, and also after ejaculation. Mechanisms altering chromatin remodeling are abortive apoptosis and oxidative stress resulting from reactive oxygen species. Three classifications of intratesticular, post-testicular, and external factors have been...

Descripción completa

Detalles Bibliográficos
Autores principales: Pourmasumi, Soheila, Sabeti, Parvin, Rahiminia, Tahereh, Mangoli, Esmat, Tabibnejad, Nasim, Talebi, Ali Reza
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Research and Clinical Center for Infertility 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5605854/
https://www.ncbi.nlm.nih.gov/pubmed/29177237
_version_ 1783265055123439616
author Pourmasumi, Soheila
Sabeti, Parvin
Rahiminia, Tahereh
Mangoli, Esmat
Tabibnejad, Nasim
Talebi, Ali Reza
author_facet Pourmasumi, Soheila
Sabeti, Parvin
Rahiminia, Tahereh
Mangoli, Esmat
Tabibnejad, Nasim
Talebi, Ali Reza
author_sort Pourmasumi, Soheila
collection PubMed
description The sperm DNA damage may occur in testis, genital ducts, and also after ejaculation. Mechanisms altering chromatin remodeling are abortive apoptosis and oxidative stress resulting from reactive oxygen species. Three classifications of intratesticular, post-testicular, and external factors have been correlated with increased levels of human sperm DNA damage which can affect the potential of fertility. Lifestyle, environment, medical, and iatrogenic factors might be considered to cause dysmetabolism to make distracting interactions and endocrine disrupting compounds. As a result, these may induce chromatin/DNA alteration in germ cells, which may be transmitted across generations with phenotypic consequences. Alcohol consumption may not increase the rate of sperm residual histones and protamine deficiency; however, it causes an increase in the percentage of spermatozoa with DNA fragmentation and apoptosis. In a medical problem as spinal cord injury, poor semen parameters and sperm DNA damage were reported. Infection induces reactive oxygen species production, decreases the total antioxidant capacity and sperm DNA fragmentation or antigen production that lead to sperm dysfunctions and DNA fragmentation. While reactive oxygen species generation increases with age, oxidative stress may be responsible for the age-dependent sperm DNA damage. The exposing of reproductive organs in older men to oxidative stress for a long time may produce more DNA-damaged spermatozoa than youngers. Examining the sperm chromatin quality in testicular cancer and Hodgkin’s lymphoma patients prior to chemotherapy demonstrated the high incidence of DNA damage and low compaction in spermatozoa at the time of the diagnosis. In chemotherapy cycle with genotoxic agents in cancer patients, an increase in sperm DNA damage was shown after treatment. In overall, those factors occurring during the prenatal or the adult life alter the distribution of proteins associated with sperm chromatin induce changes in germ cells which can be detected in infertile patients.
format Online
Article
Text
id pubmed-5605854
institution National Center for Biotechnology Information
language English
publishDate 2017
publisher Research and Clinical Center for Infertility
record_format MEDLINE/PubMed
spelling pubmed-56058542017-11-24 The etiologies of DNA abnormalities in male infertility: An assessment and review Pourmasumi, Soheila Sabeti, Parvin Rahiminia, Tahereh Mangoli, Esmat Tabibnejad, Nasim Talebi, Ali Reza Int J Reprod Biomed Review Article The sperm DNA damage may occur in testis, genital ducts, and also after ejaculation. Mechanisms altering chromatin remodeling are abortive apoptosis and oxidative stress resulting from reactive oxygen species. Three classifications of intratesticular, post-testicular, and external factors have been correlated with increased levels of human sperm DNA damage which can affect the potential of fertility. Lifestyle, environment, medical, and iatrogenic factors might be considered to cause dysmetabolism to make distracting interactions and endocrine disrupting compounds. As a result, these may induce chromatin/DNA alteration in germ cells, which may be transmitted across generations with phenotypic consequences. Alcohol consumption may not increase the rate of sperm residual histones and protamine deficiency; however, it causes an increase in the percentage of spermatozoa with DNA fragmentation and apoptosis. In a medical problem as spinal cord injury, poor semen parameters and sperm DNA damage were reported. Infection induces reactive oxygen species production, decreases the total antioxidant capacity and sperm DNA fragmentation or antigen production that lead to sperm dysfunctions and DNA fragmentation. While reactive oxygen species generation increases with age, oxidative stress may be responsible for the age-dependent sperm DNA damage. The exposing of reproductive organs in older men to oxidative stress for a long time may produce more DNA-damaged spermatozoa than youngers. Examining the sperm chromatin quality in testicular cancer and Hodgkin’s lymphoma patients prior to chemotherapy demonstrated the high incidence of DNA damage and low compaction in spermatozoa at the time of the diagnosis. In chemotherapy cycle with genotoxic agents in cancer patients, an increase in sperm DNA damage was shown after treatment. In overall, those factors occurring during the prenatal or the adult life alter the distribution of proteins associated with sperm chromatin induce changes in germ cells which can be detected in infertile patients. Research and Clinical Center for Infertility 2017-06 /pmc/articles/PMC5605854/ /pubmed/29177237 Text en This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Pourmasumi, Soheila
Sabeti, Parvin
Rahiminia, Tahereh
Mangoli, Esmat
Tabibnejad, Nasim
Talebi, Ali Reza
The etiologies of DNA abnormalities in male infertility: An assessment and review
title The etiologies of DNA abnormalities in male infertility: An assessment and review
title_full The etiologies of DNA abnormalities in male infertility: An assessment and review
title_fullStr The etiologies of DNA abnormalities in male infertility: An assessment and review
title_full_unstemmed The etiologies of DNA abnormalities in male infertility: An assessment and review
title_short The etiologies of DNA abnormalities in male infertility: An assessment and review
title_sort etiologies of dna abnormalities in male infertility: an assessment and review
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5605854/
https://www.ncbi.nlm.nih.gov/pubmed/29177237
work_keys_str_mv AT pourmasumisoheila theetiologiesofdnaabnormalitiesinmaleinfertilityanassessmentandreview
AT sabetiparvin theetiologiesofdnaabnormalitiesinmaleinfertilityanassessmentandreview
AT rahiminiatahereh theetiologiesofdnaabnormalitiesinmaleinfertilityanassessmentandreview
AT mangoliesmat theetiologiesofdnaabnormalitiesinmaleinfertilityanassessmentandreview
AT tabibnejadnasim theetiologiesofdnaabnormalitiesinmaleinfertilityanassessmentandreview
AT talebialireza theetiologiesofdnaabnormalitiesinmaleinfertilityanassessmentandreview
AT pourmasumisoheila etiologiesofdnaabnormalitiesinmaleinfertilityanassessmentandreview
AT sabetiparvin etiologiesofdnaabnormalitiesinmaleinfertilityanassessmentandreview
AT rahiminiatahereh etiologiesofdnaabnormalitiesinmaleinfertilityanassessmentandreview
AT mangoliesmat etiologiesofdnaabnormalitiesinmaleinfertilityanassessmentandreview
AT tabibnejadnasim etiologiesofdnaabnormalitiesinmaleinfertilityanassessmentandreview
AT talebialireza etiologiesofdnaabnormalitiesinmaleinfertilityanassessmentandreview