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...
Autores principales: | , , , , , |
---|---|
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 |