scholarly journals Post-Meiotic DNA Damage and Response in Male Germ Cells

DNA Repair ◽  
10.5772/21367 ◽  
2011 ◽  
Author(s):  
Frdric Leduc ◽  
Genevive Acteau ◽  
Marie-Chantal Grgoire ◽  
Olivier Simard ◽  
Jessica Leroux ◽  
...  
Keyword(s):  
Dna Damage ◽  
Germ Cells ◽  
Male Germ Cells

scholarly journals Chronic Exposure to Acrylamide Induces DNA Damage in Male Germ Cells of Mice

2012 ◽  
Vol 129 (1) ◽  
pp. 135-145 ◽  
Author(s):  
Belinda J. Nixon ◽  
Simone J. Stanger ◽  
Brett Nixon ◽  
Shaun D. Roman
Keyword(s):  
Dna Damage ◽  
Germ Cells ◽  
Chronic Exposure ◽  
Male Germ Cells

Aging and oxidative stress alter DNA repair mechanisms in male germ cells of superoxide dismutase-1 null mice

2021 ◽  
Author(s):  
Paulina Nguyen-Powanda ◽  
Bernard Robaire
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Dna Repair ◽  
Superoxide Dismutase ◽  
Germ Cells ◽  
Superoxide Dismutase 1 ◽  
Male Germ Cells ◽  
Dna Repair Mechanisms ◽  
Repair Mechanisms ◽  
And Oxidative Stress

Abstract The efficiency of antioxidant defense system decreases with aging, thus resulting in high levels of reactive oxygen species (ROS) and DNA damage in spermatozoa. This damage can lead to genetic disorders in the offspring. There are limited studies investigating the effects of the total loss of antioxidants, such as superoxide dismutase-1 (SOD1), in male germ cells as they progress through spermatogenesis. In this study, we evaluated the effects of aging and removing SOD1 (in male germ cells of SOD1-null (Sod1−/−) mice) in order to determine the potential mechanism(s) of DNA damage in these cells. Immunohistochemical analysis showed an increase in lipid peroxidation and DNA damage in the germ cells of aged wild-type (WT) and Sod1−/− mice of all age. Immunostaining of OGG1, a marker of base excision repair (BER), increased in aged WT and young Sod1−/− mice. In contrast, immunostaining intensity of LIGIV and RAD51, markers of non-homologous end-joining (NHEJ) and homologous recombination (HR), respectively, decreased in aged and Sod1−/− mice. Gene expression analysis showed similar results with altered mRNA expression of these key DNA repair transcripts in pachytene spermatocytes and round spermatids of aged and Sod1−/− mice. Our study indicates that DNA repair pathway markers of BER, NHEJ, and HR are differentially regulated as a function of aging and oxidative stress in spermatocytes and spermatids, and aging enhances the repair response to increased oxidative DNA damage, whereas impairments in other DNA repair mechanisms may contribute to the increase in DNA damage caused by aging and the loss of SOD1.

scholarly journals Role of HP1β during spermatogenesis and DNA replication

2019 ◽  
Author(s):  
Vijaya Charaka ◽  
Anjana Tiwari ◽  
Raj K Pandita ◽  
Clayton R Hunt ◽  
Tej K. Pandita
Keyword(s):  
Dna Damage ◽  
Dna Replication ◽  
Germ Cells ◽  
Chromatin Condensation ◽  
Genomic Stability ◽  
Replication Forks ◽  
Chromatin Protein ◽  
Male Germ Cells ◽  
Chromatin Compaction

AbstractMaintaining genomic stability in a continually dividing cell population requires accurate DNA repair, especially in male germ cells. Repair and replication protein access to DNA, however, is complicated by chromatin compaction. The HP1β chromatin protein, encoded by Cbx1, is associated with chromatin condensation but its role in meiosis is not clear. To investigate the role of Cbx1 in male germ cells, we generated testis specific Cbx1 deficient transgenic mice by crossing Cbx1flox/flox (Cbx1f/f) mice with Stra8 Cre+/− mice. Loss of Cbx1 in testes adversely affected sperm maturation and Cbx1 deletion increased seminiferous tubule degeneration and basal level DNA damage., We observed that Cbx1−/− MEF cells displayed reduced resolution of stalled DNA replication forks as well as decreased fork restart, indicating defective DNA synthesis. Taken together, these results suggest that loss of Cbx1 in growing cells leads to DNA replication defects and associated DNA damage that impact cell survival.

scholarly journals 180. THE CONSEQUENCES OF ACRYLAMIDE EXPOSURE ON THE MALE GERMLINE

2010 ◽  
Vol 22 (9) ◽  
pp. 98
Author(s):  
B. J. Nixon ◽  
B. Nixon ◽  
S. D. Roman
Keyword(s):  
Gene Expression ◽  
Dna Damage ◽  
Cytochrome P450 ◽  
Germ Cells ◽  
Dietary Exposure ◽  
Cytochrome P450 Enzymes ◽  
Male Germ Cells ◽  
P450 Gene ◽  
Male Germline ◽  
Future Outcomes

Acrylamide is a common industrial compound that has recently been identified in cooked, carbohydrate-rich foods such as potato chips, breads and cereals. Acrylamide has been found to be a reproductive toxin in rodents, eliciting male infertility and transgenerational toxicity through the male germline; thus dietary exposure to the compound may have consequences for male fertility and reproduction in humans. The aim of this project was to elucidate the mechanisms of acrylamide toxicity in male germ cells of mice. Freshly isolated early male germ cells were exposed to acrylamide and assessed for cell viability and aberrant morphology. DNA damage in these cells was also investigated using a modified version of the Comet Assay, which allows for adduct specificity. Significant increases in cell death or aberrant morphology were not observed following acrylamide exposure (1 µM, 18 hours). However, a significant increase in DNA damage (125% increase in mean tail DNA assessed by Comet) was identified; which may originate from either the metabolic conversion of acrylamide to glycidamide, leading to glycidamide adducts, or from oxidative stress. Additionally, the regulation of cytochrome P450 gene expression was measured using real time PCR and early male germ cells were found to upregulate gene expression of cytochrome P450 enzymes in response to acrylamide exposure. Collectively, these results support a genotoxic mode of action of acrylamide toxicity, in addition to potential oxidative damage in male germ cells. However, the mechanism by which acrylamide elicits toxicity in germ cells requires further investigation. Future outcomes of this research may provide insight into factors necessary for the healthy development of offspring and aid in the risk assessment of dietary acrylamide exposure in humans.

Effects of Chemical-Induced DNA Damage on Male Germ Cells

1998 ◽  
pp. 151-160 ◽  
Author(s):  
J. A. Holme ◽  
C. Bjørge ◽  
M. Trbojevic ◽  
A.-K. Olsen ◽  
G. Brunborg ◽  
...  
Keyword(s):  
Dna Damage ◽  
Germ Cells ◽  
Male Germ Cells

Origins and consequences of DNA damage in male germ cells

2007 ◽  
Vol 14 (6) ◽  
pp. 727-733 ◽  
Author(s):  
R John Aitken ◽  
Geoffry N De Iuliis
Keyword(s):  
Dna Damage ◽  
Germ Cells ◽  
Male Germ Cells

How do male germ cells handle DNA damage?

2005 ◽  
Vol 207 (2) ◽  
pp. 521-531 ◽  
Author(s):  
A OLSEN ◽  
B LINDEMAN ◽  
R WIGER ◽  
N DUALE ◽  
G BRUNBORG
Keyword(s):  
Dna Damage ◽  
Germ Cells ◽  
Male Germ Cells

scholarly journals UHRF1 suppresses retrotransposons and cooperates with PRMT5 and PIWI proteins in male germ cells

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Juan Dong ◽  
Xiaoli Wang ◽  
Congcong Cao ◽  
Yujiao Wen ◽  
Akihiko Sakashita ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Dna Damage ◽  
Histone Modification ◽  
Dna Damage Response ◽  
Germ Cells ◽  
Dna Hypomethylation ◽  
Male Germ Cells ◽  
Arginine Methyltransferase ◽  
Male Germline ◽  
Damage Response

Abstract DNA methylation, repressive histone marks, and PIWI-interacting RNA (piRNA) are essential for the control of retrotransposon silencing in the mammalian germline. However, it remains unknown how these repressive epigenetic pathways crosstalk to ensure retrotransposon silencing in the male germline. Here, we show that UHRF1 is responsible for retrotransposon silencing and cooperates with repressive epigenetic pathways in male germ cells. Conditional loss of UHRF1 in postnatal germ cells causes DNA hypomethylation, upregulation of retrotransposons, the activation of a DNA damage response, and switches in the global chromatin status, leading to complete male sterility. Furthermore, we show that UHRF1 interacts with PRMT5, an arginine methyltransferase, to regulate the repressive histone arginine modifications (H4R3me2s and H3R2me2s), and cooperates with the PIWI pathway during spermatogenesis. Collectively, UHRF1 regulates retrotransposon silencing in male germ cells and provides a molecular link between DNA methylation, histone modification, and the PIWI pathway in the germline.

scholarly journals The activated ATM/p53 pathway promotes autophagy in response to oxidative stress-mediated DNA damage induced by Microcystin-LR in male germ cells

2021 ◽  
Vol 227 ◽  
pp. 112919
Author(s):  
Zhihui Tian ◽  
Haohao Liu ◽  
Xinghai Chen ◽  
Michael D. Losiewicz ◽  
Rui Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Germ Cells ◽  
Male Germ Cells ◽  
P53 Pathway
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