Efficacy of N ‐acetyl‐ l ‐cysteine against glyphosate induced oxidative stress and apoptosis in testicular germ cells preventing infertility

2021 ◽  
Author(s):  
Jitender K. Bhardwaj ◽  
Vijay Kumar ◽  
Priyanka Saraf ◽  
Harish Panchal ◽  
Vishavjeet Rathee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
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.

Copper-induced apoptosis and autophagy through oxidative stress-mediated mitochondrial dysfunction in male germ cells

2019 ◽  
Vol 61 ◽  
pp. 104639 ◽  
Author(s):  
Zhenlong Kang ◽  
Na Qiao ◽  
Gaoyang Liu ◽  
Hanming Chen ◽  
Zhaoxin Tang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Germ Cells ◽  
Male Germ Cells ◽  
Induced Apoptosis

Germ cells of male mice express genes for peroxisomal metabolic pathways implicated in the regulation of spermatogenesis and the protection against oxidative stress

2011 ◽  
Vol 136 (4) ◽  
pp. 413-425 ◽  
Author(s):  
Sandra Dastig ◽  
Anca Nenicu ◽  
David M. Otte ◽  
Andreas Zimmer ◽  
Jürgen Seitz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Germ Cells ◽  
Metabolic Pathways ◽  
Male Mice

scholarly journals 002.Human spermatozoa: fruits of creation, seed of doubt

2004 ◽  
Vol 16 (9) ◽  
pp. 2
Author(s):  
R. J. Aitken
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Dna Repair ◽  
Germ Cells ◽  
Oxidative Dna Damage ◽  
Germ Line ◽  
Early Embryo ◽  
Human Spermatozoa ◽  
Obstructive Azoospermia ◽  
Male Germ Line

Defective sperm function is the largest defined cause of human infertility, affecting one in twenty Australian males. Despite its prevalence, we are only just beginning to understand the underlying mechanisms. The past decade has seen two major advances in this field: (1) the discovery that Y chromosome deletions play a key role in the aetiology of non-obstructive azoospermia/oligozoospermia; and (2) recognition that oxidative stress can impact upon the functional competence of human spermatozoa through peroxidative damage to the sperm plasma membrane. Oxidative stress has also been found to disrupt the integrity of DNA in the male germ line and may represent an important mechanism by which environmental impacts on human health are mediated. Thus, paternal exposure to various toxicants (cigarette smoke, organic solvents, heavy metals) has been linked with oxidative DNA damage in spermatozoa and developmental defects, including cancer, in the F1 generation. The male germ line becomes particularly vulnerable to such factors during the post meiotic stages of differentiation. Pre-meiotic germ cells always have the option of undergoing apoptosis if DNA damage is severe. However, post meiotic germ cells have lost both the ability to mount an apoptotic response and the capacity for DNA repair. As a result, germ cells are particularly vulnerable to genotoxic agents during spermiogenesis and epididymal maturation. If the fertilizing capacity of the spermatozoa is retained following toxicant exposure, then DNA damage will be transferred to the zygote and must be repaired subsequently by the oocyte and/or early embryo. Aberrant DNA repair at this stage has the potential to create mutations that will compromise embryonic development and, ultimately, the normality of the offspring. Elucidating the causes of oxidative damage in spermatozoa should help resolve the aetiology of conditions such as male infertility, early pregnancy loss and childhood disease, including cancer.

scholarly journals Oxidative Stress in the Male Germline: A Review of Novel Strategies to Reduce 4-Hydroxynonenal Production

Antioxidants ◽  
2018 ◽  
Vol 7 (10) ◽  
pp. 132 ◽  
Author(s):  
Jessica Walters ◽  
Geoffry De Iuliis ◽  
Brett Nixon ◽  
Elizabeth Bromfield
Keyword(s):  
Oxidative Stress ◽  
Germ Cells ◽  
Cell Function ◽  
De Novo ◽  
Protein Translation ◽  
Egg Recognition ◽  
Male Germline ◽  
New Strategy ◽  
Artery Disease ◽  
The Stability

Germline oxidative stress is intimately linked to several reproductive pathologies including a failure of sperm-egg recognition. The lipid aldehyde 4-hydroxynonenal (4HNE) is particularly damaging to the process of sperm-egg recognition as it compromises the function and the stability of several germline proteins. Considering mature spermatozoa do not have the capacity for de novo protein translation, 4HNE modification of proteins in the mature gametes has uniquely severe consequences for protein homeostasis, cell function and cell survival. In somatic cells, 4HNE overproduction has been attributed to the action of lipoxygenase enzymes that facilitate the oxygenation and degradation of ω-6 polyunsaturated fatty acids (PUFAs). Accordingly, the arachidonate 15-lipoxygenase (ALOX15) enzyme has been intrinsically linked with 4HNE production, and resultant pathophysiology in various complex conditions such as coronary artery disease and multiple sclerosis. While ALOX15 has not been well characterized in germ cells, we postulate that ALOX15 inhibition may pose a new strategy to prevent 4HNE-induced protein modifications in the male germline. In this light, this review focuses on (i) 4HNE-induced protein damage in the male germline and its implications for fertility; and (ii) new methods for the prevention of lipid peroxidation in germ cells.

From germ cells to neonates: the beginning of life and the KEAP1–NRF2 system

2019 ◽  
Author(s):  
Daisuke Matsumaru ◽  
Hozumi Motohashi
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Embryonic Development ◽  
Germ Cells ◽  
Target Genes ◽  
Related Factor ◽  
Environmental Stress Response ◽  
Response System ◽  
Response Systems ◽  
Stress Response System

Abstract The Kelch-like ECH-associated protein 1(KEAP1)–NF-E2-related factor 2 (NRF2) system is one of the most studied environmental stress response systems. In the presence of oxidative and electrophilic insults, the thiols of cysteine residues in KEAP1 are modified, and subsequently stabilized NRF2 activates its target genes that are involved in detoxification and cytoprotection. A myriad of recent studies has revealed the broad range of contributions of the KEAP1–NRF2 system to physiological and pathological processes. However, its functions during gametic and embryonic development are still open for investigation. Although oxidative stress is harmful for embryos, Nrf2−/− mice do not show any apparent morphological abnormalities during development, probably because of the compensatory antioxidant functions of NF-E2-related factor 1 (NRF1). It can also be considered that the antioxidant system is essential for protecting germ cells during reproduction. The maturation processes of germ cells in both sexes are affected by Nrf2 mutation. Hence, in this review, we focus on the stress response system related to reproduction and embryonic development through the functions of the KEAP1–NRF2 system.

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