scholarly journals Impact of oxidative stress on male and female germ cells: implications for fertility

Reproduction ◽  
2020 ◽  
Vol 159 (4) ◽  
pp. R189-R201 ◽  
Author(s):  
R John Aitken
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Germ Cells ◽  
Germ Line ◽  
Reproductive Function ◽  
Oocyte Quality ◽  
Ros Generation ◽  
Male And Female ◽  
Developmental Capacity ◽  
Lipid Aldehydes

Male and female germ lines are vulnerable to oxidative stress. In spermatozoa, such stress triggers a lipid peroxidation cascade that culminates in the generation of electrophilic lipid aldehydes that bind to DNA and a raft of proteins involved in the delivery of functionally competent cells. One set of targets for these aldehydes are the proteins of the mitochondrial electron transport chain. When this interaction occurs, mitochondrial ROS generation is enhanced leading to the sustained generation of oxidative damage in a self-perpetuating cycle. Such damage affects all aspects of sperm function including motility, sperm-egg recognition, acrosomal exocytosis and sperm-oocyte fusion. Oxidative stress in the male germ line also attacks the integrity of sperm DNA with potential impacts on the developmental capacity of embryos and the health and wellbeing of the offspring. Potential pathways of reactive oxygen species (ROS) generation in male germ cells could involve enhanced lipoxygenase activity, activation of NADPH oxidase and/or electron leakage from mitochondria. Similarly, in the female germ line, both the induction of oocyte senescence following ovulation and the deterioration of oocyte quality with maternal age appear to involve the generation of oxidative damage. In this case, the mitochondria appear to be a particularly important source of ROS compromising the viability and fertilizability of the oocyte and interfering with the normal segregation of chromosomes during meiosis. In light of these considerations, antioxidants should have some role to play in the preservation of reproductive function in both men and women; however, we still await appropriate trials to test this hypothesis.

scholarly journals Reproductive Isolation and Morphogenetic Evolution in Drosophila Analyzed by Breakage of Ethological Barriers

Genetics ◽  
1997 ◽  
Vol 147 (1) ◽  
pp. 231-242 ◽  
Author(s):  
Lucas Sánchez ◽  
Pedro Santamaria
Keyword(s):  
Reproductive Isolation ◽  
Germ Cells ◽  
Morphological Analysis ◽  
Seminal Fluid ◽  
Germ Line ◽  
Regulatory Gene ◽  
Motile Sperm ◽  
Male And Female ◽  
Drosophila Yakuba

Abstract This article reports the breaking of ethological barriers through the constitution of soma-germ line chimeras between species of the melanogaster subgroup of Drosophila, which are ethologically isolated. Female Drosophila yakuba and D. teissieri germ cells in a D. melanogaster ovary produced functional oocytes that, when fertilized by D. melanogaster sperm, gave rise to sterile yakuba-melanogaster andteissieri-melanogaster male and female hybrids. However, the erecta-melanogaster and orena-melanogaster hybrids were lethal, since female D. erecta and D. orena germ cells in a D. melanogaster ovary failed to form oocytes with the capacity to develop normally. This failure appears to be caused by an altered interaction between the melanogaster soma and the erecta and orena germ lines. Germ cells of D. teissieri and D. orena in a D. melanogaster testis produced motile sperm that was not stored in D. melanogaster females. This might be due to incompatibility between the teissieri and orena sperm and the melanogaster seminal fluid. A morphological analysis of the terminalia of yakuba-melanogaster and teissieri-melanogaster hybrids was performed. The effect on the terminalia of teissieri-melanogaster hybrids of a mutation in doublesex, a regulatory gene that controls the development of the terminalia, was also investigated.

scholarly journals Fine-tuning evolution: germ-line epigenetics and inheritance

Reproduction ◽  
2013 ◽  
Vol 146 (1) ◽  
pp. R37-R48 ◽  
Author(s):  
Jessica M Stringer ◽  
Sanna Barrand ◽  
Patrick Western
Keyword(s):  
Germ Cells ◽  
Cell Function ◽  
Germ Line ◽  
Primordial Germ Cells ◽  
Epigenetic Reprogramming ◽  
Fine Tuning ◽  
Male And Female ◽  
Epigenetic Information

In mice, epiblast cells found both the germ-line and somatic lineages in the developing embryo. These epiblast cells carry epigenetic information from both parents that is required for development and cell function in the fetus and during post-natal life. However, germ cells must establish an epigenetic program that supports totipotency and the configuration of parent-specific epigenetic states in the gametes. To achieve this, the epigenetic information inherited by the primordial germ cells at specification is erased and new epigenetic states are established during development of the male and female germ-lines. Errors in this process can lead to transmission of epimutations through the germ-line, which have the potential to affect development and disease in the parent's progeny. This review discusses epigenetic reprogramming in the germ-line and the transmission of epigenetic information to the following generation.

scholarly journals ANTIOXIDATIVE DEFENSE RESPONSE TO APHID-INDUCED OXIDATIVE STRESS IN Glycine max (L.) Merr. cv. “Nam Dan”

2016 ◽  
Vol 54 (6) ◽  
pp. 719 ◽  
Author(s):  
Tran Ngoc Toan ◽  
Tran Thi Van Thanh Huyen ◽  
Mai Van Chung
Keyword(s):  
Oxidative Stress ◽  
Glycine Max ◽  
Oxidative Damage ◽  
Thiobarbituric Acid ◽  
Ros Generation ◽  
Oxygen Species ◽  
Thiobarbituric Acid Reactive Substances ◽  
Aphis Craccivora Koch ◽  
Glycine Max L ◽  
Aphid Feeding

Infestation of cowpea aphid (Aphis craccivora Koch) induced oxidative stress in leaves of soybean (Glycine max (L.) Merr. cv. “Nam Dan”) with a burst in generation of reactive oxygen species (ROS) products such as superoxide anion radical (O2.-) and hydrogen peroxide (H2O2) recorded around 24 hours after aphid feeding. An increase in content of thiobarbituric acid reactive substances (TBARS) in lipid peroxidation and a defined percentage of injury in aphid-infested leaves were resulted from the cellular oxidative damage. The enhanced activity of the antioxidant enzymes such as superoxide dismutase (SOD, EC 1.15.1.1) and catalase (CAT, EC 1.11.1.6) in leaves of soybean “Nam Dan” functions as the antioxidative response that controlled both ROS-generation to be enough levels to play as defensive element and ROS-detoxifying to reduce aphid-induced oxidative damage. The enhancement of SOD and CAT also can improve the tolerance of soybean “Nam Dan” to impact from A. craccivora.

scholarly journals Oxidative Stress and Reproductive Function in the Aging Male

Biology ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 282
Author(s):  
Paulina Nguyen-Powanda ◽  
Bernard Robaire
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Defense ◽  
Structural Integrity ◽  
Germ Line ◽  
Reproductive Function ◽  
Antioxidant Defense System ◽  
Male Reproduction ◽  
Paternal Age ◽  
Theories Of Aging ◽  
The Impact

With the delay of parenthood becoming more common, the age at which men father children is on the rise. While the effects of advanced maternal age have been well documented, only recently have studies started to focus on the impact of advanced paternal age (APA) in the context of male reproduction. As men age, the antioxidant defense system gradually becomes less efficient and elevated levels of reactive oxygen species (ROS) accumulate in spermatozoa; this can impair their functional and structural integrity. In this review, we present an overview of how oxidative stress is implicated in male reproductive aging by providing a summary of the sources and roles of ROS, the theories of aging, and the current animal and human studies that demonstrate the impacts of APA on the male germ line, the health of progeny and fertility, and how treatment with antioxidants may reverse these effects.

523. PLACENTAL ANTIOXIDANT ENZYMES IN RAT PREGNANCY SHOW ZONE- AND STAGE-DEPENDENT VARIATION

2009 ◽  
Vol 21 (9) ◽  
pp. 122
Author(s):  
M. L. Jones ◽  
P. J. Mark ◽  
T. A. Mori ◽  
B. J. Waddell
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Mrna Expression ◽  
Late Pregnancy ◽  
Late Gestation ◽  
Ros Generation ◽  
Dexamethasone Treatment ◽  
Endogenous Protection ◽  
Thioredoxin Reductases

Placental oxidative stress plays a key role in the pathophysiology of placenta-related disorders including preeclampsia. Protection from oxidative stress is provided by antioxidant enzymes which inactivate reactive oxygen species (ROS). The rat placenta consists of two major zones, the junctional (JZ) and labyrinth (LZ), and because only the LZ grows in late gestation we hypothesized it generates more ROS and thus requires greater antioxidant protection. Our previous studies on expression of the antioxidants superoxide dismutase (SOD)-1, SOD-2 and catalase support this hypothesis. Here, we extend these observations to include mRNA expression of SOD-3 and thioredoxin reductases (Txnrd-1, -2, -3) and activities of SOD, hydrogen peroxide (H2O2) scavenging and xanthine oxidase (XO). Placental oxidative damage was assessed by measurement of F2-isoprostanes and TBARS concentrations. We also measured the effects of maternal dexamethasone treatment, since glucocorticoid excess is known to induce oxidative damage in other tissues. Placentas were collected from untreated mothers on days 16 and 22 (term=day 23) and on day 22 after dexamethasone treatment from day 13 (1 μg/ml drinking water). SOD-3, Txnrd-1, -2, and -3 mRNAs were measured in JZ and LZ by qRT-PCR. F2-isoprostanes were measured by GC-MS and kit assays were used to measure TBARS and the activities of SOD, H2O2 scavenging and XO. In both placental zones, expression of SOD-3 and Txnrd-1 mRNAs and H2O2 scavenging activity decreased from day 16 to 22, whereas XO activity increased. Dexamethasone treatment increased H2O2 scavenging in both zones, but had no effect on SOD or XO activities or antioxidant mRNA expression. Despite predicted increases in placental ROS generation in late pregnancy and after dexamethasone, neither F2-isoprostanes nor TBARS were increased. These and our previous data suggest that endogenous protection against oxidative stress is abundant in the rat placenta and provides protection against potential oxidative insults including glucocorticoid excess.

scholarly journals Regulation of Reactive Oxygen Species and Antioxidant Defense in Plants under Salinity

2021 ◽  
Vol 22 (17) ◽  
pp. 9326
Author(s):  
Mirza Hasanuzzaman ◽  
Md. Rakib Hossain Raihan ◽  
Abdul Awal Chowdhury Masud ◽  
Khussboo Rahman ◽  
Farzana Nowroz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Salt Stress ◽  
Oxidative Damage ◽  
Antioxidant Defense ◽  
Reactive Oxygen ◽  
Antioxidant Defense System ◽  
Ros Generation ◽  
Oxygen Species ◽  
Defense System

The generation of oxygen radicals and their derivatives, known as reactive oxygen species, (ROS) is a part of the signaling process in higher plants at lower concentrations, but at higher concentrations, those ROS cause oxidative stress. Salinity-induced osmotic stress and ionic stress trigger the overproduction of ROS and, ultimately, result in oxidative damage to cell organelles and membrane components, and at severe levels, they cause cell and plant death. The antioxidant defense system protects the plant from salt-induced oxidative damage by detoxifying the ROS and also by maintaining the balance of ROS generation under salt stress. Different plant hormones and genes are also associated with the signaling and antioxidant defense system to protect plants when they are exposed to salt stress. Salt-induced ROS overgeneration is one of the major reasons for hampering the morpho-physiological and biochemical activities of plants which can be largely restored through enhancing the antioxidant defense system that detoxifies ROS. In this review, we discuss the salt-induced generation of ROS, oxidative stress and antioxidant defense of plants under salinity.

scholarly journals Reduced mitochondrial ROS, enhanced antioxidant defense, and distinct age-related changes in oxidative damage in muscles of long-lived Peromyscus leucopus

2013 ◽  
Vol 304 (5) ◽  
pp. R343-R355 ◽  
Author(s):  
Yun Shi ◽  
Daniel A. Pulliam ◽  
Yuhong Liu ◽  
Ryan T. Hamilton ◽  
Amanda L. Jernigan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Peromyscus Leucopus ◽  
Laboratory Mouse ◽  
Linear Increase ◽  
Young Age ◽  
Protein Carbonyls ◽  
Ros Generation ◽  
Glutathione Peroxidase 1 ◽  
Age Related

Comparing biological processes in closely related species with divergent life spans is a powerful approach to study mechanisms of aging. The oxidative stress hypothesis of aging predicts that longer-lived species would have lower reactive oxygen species (ROS) generation and/or an increased antioxidant capacity, resulting in reduced oxidative damage with age than in shorter-lived species. In this study, we measured ROS generation in the young adult animals of the long-lived white-footed mouse, Peromyscus leucopus (maximal life span potential, MLSP = 8 yr) and the common laboratory mouse, Mus musculus (C57BL/6J strain; MLSP = 3.5 yr). Consistent with the hypothesis, our results show that skeletal muscle mitochondria from adult P. leucopus produce less ROS (superoxide and hydrogen peroxide) compared with M. musculus. Additionally, P. leucopus has an increase in the activity of antioxidant enzymes superoxide dismutase 1, catalase, and glutathione peroxidase 1 at young age. P. leucopus compared with M. musculus display low levels of lipid peroxidation (isoprostanes) throughout life; however, P. leucopus although having elevated protein carbonyls at a young age, the accrual of protein oxidation with age is minimal in contrast to the linear increase in M. musculus. Altogether, the results from young animals are in agreement with the predictions of the oxidative stress hypothesis of aging with the exception of protein carbonyls. Nonetheless, the age-dependent increase in protein carbonyls is more pronounced in short-lived M. musculus, which supports enhanced protein homeostasis in long-lived P. leucopus.

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 Morroniside protect human granulosa cells against H2O2-induced oxidative damage via regulating Nrf2 and MAPK signaling pathway

2021 ◽  
Author(s):  
Yucong Ma ◽  
Guimin Hao ◽  
Xiaohua Lin ◽  
Zhiming Zhao ◽  
Aimin Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Granulosa Cells ◽  
Caspase 3 ◽  
Nuclear Translocation ◽  
Oocyte Quality ◽  
Mapk Signaling ◽  
Control Group ◽  
Caspase 9 ◽  
Jnk Pathway

Abstract Background Morroniside is the main ingredient of Cornus officinalis, which has an antioxidant effect. Ovarian granulosa cells (GCs) are responsible for regulating the development and atresia of follicles, which are susceptible to oxidative stress. In this study, we investigated whether morroniside could inhibit oxidative stress of GCs induced by hydrogen peroxide (H2O2), thus leading to improve oocyte quality. Methods The study was divided into 5 groups: control group, H2O2 group, morroniside (5 µM) + H2O2, morroniside (10 µM) + H2O2, Morroniside (20 µM) + H2O2. Cell survival rate was determined by CCK-8, ROS fluorescence level was determined by DCFH-DA probe, MDA, 8-OHdG, T-AOC, SOD, NQO1 and caspase-3 were determined by ELISA, SOD, NQO1, Bax, Bcl-2, caspase-3, caspase-9, Nrf2 and MAPKs protein expression were determined by Western blot, and Nrf2 nuclear translocation level was determined by immunofluorescence method. SPSS21.0 was used for statistical data analysis. Results After pretreatment with morroniside, the levels of ROS, MDA and 8-OHdG in ovarian GCs were significantly decreased. Morroniside significantly upregulated the level of p-Nrf2 and promoted the nuclear translocation level of Nrf2, which transcriptionally activated antioxidase SOD and NQO1. In addition, the levels of apoptosis-related proteins Bax, Bcl-2, caspase-3 and caspase-9 were significantly regulated via p38 and JNK pathway by morroniside. Conclusions These results suggested that morroniside could reduce oxidative damage and apoptosis of ovarian GCs induced by H2O2 in multiple ways, which provided a new idea for clinical improvement of oxidative stress in female reproductive system.

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