Glutamine protects rabbit spermatozoa against oxidative stress via glutathione synthesis during cryopreservation

2017 ◽  
Vol 29 (11) ◽  
pp. 2183 ◽  
Author(s):  
Zhendong Zhu ◽  
Xiaoteng Fan ◽  
Yinghua Lv ◽  
Yan Lin ◽  
De Wu ◽  
...  
Keyword(s):  
Potential Role ◽  
Membrane Integrity ◽  
Mitochondrial Activity ◽  
Oxygen Species ◽  
Glutathione Synthesis ◽  
High Doses ◽  
Cysteine Synthetase ◽  
Rabbit Spermatozoa ◽  
Mammalian Spermatozoa

Mammalian spermatozoa are extremely susceptible to high doses of reactive oxygen species (ROS). The aim of the present study was to investigate the potential role of glutamine in protecting rabbit spermatozoa against ROS stress during cryopreservation and post-thaw incubation. Freshly ejaculated semen was diluted with Tris–citrate–glucose extender supplemented with glutamine. The addition of 20 mM glutamine significantly improved sperm motility, acrosome integrity, membrane integrity and mitochondrial activity. Meanwhile, 20 mM glutamine addition decreased lipid peroxidation and DNA damage in frozen–thawed spermatozoa. Interestingly, supplementation with 20 mM glutamine led to increases in glutathione content and γ-glutamyl cysteine synthetase and glutathione peroxidase activity, with concomitant decreases in ROS levels during cryopreservation and post-thaw incubation. In conclusion, the addition of glutamine to extender solutions protects rabbit spermatozoa from ROS attack by enhancing glutathione synthesis.

scholarly journals Towards a Consensus on Alzheimer’s Disease Comorbidity?

2021 ◽  
Vol 10 (19) ◽  
pp. 4360
Author(s):  
Iska Avitan ◽  
Yudit Halperin ◽  
Trishna Saha ◽  
Naamah Bloch ◽  
Dana Atrahimovich ◽  
...  
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Potential Role ◽  
Oxygen Species ◽  
Degenerative Diseases ◽  
Comorbid Diseases

Alzheimer’s disease (AD) is often comorbid with other pathologies. First, we review shortly the diseases most associated with AD in the clinic. Then we query PubMed citations for the co-occurrence of AD with other diseases, using a list of 400 common pathologies. Significantly, AD is found to be associated with schizophrenia and psychosis, sleep insomnia and apnea, type 2 diabetes, atherosclerosis, hypertension, cardiovascular diseases, obesity, fibrillation, osteoporosis, arthritis, glaucoma, metabolic syndrome, pain, herpes, HIV, alcoholism, heart failure, migraine, pneumonia, dyslipidemia, COPD and asthma, hearing loss, and tobacco smoking. Trivially, AD is also found to be associated with several neurodegenerative diseases, which are disregarded. Notably, our predicted results are consistent with the previously published clinical data and correlate nicely with individual publications. Our results emphasize risk factors and promulgate diseases often associated with AD. Interestingly, the comorbid diseases are often degenerative diseases exacerbated by reactive oxygen species, thus underlining the potential role of antioxidants in the treatment of AD and comorbid diseases.

scholarly journals The Role of Oxidative Stress and Autophagy in Atherosclerosis

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Ida Perrotta ◽  
Saveria Aquila
Keyword(s):  
Potential Role ◽  
Menopausal Status ◽  
Oxygen Species ◽  
Artery Wall ◽  
Complex Interplay ◽  
Biological Investigation ◽  
Cellular Events ◽  
Vascular Smcs ◽  
Subendothelial Space

Atherosclerosis is a multifactorial, multistep disorder of large- and medium-sized arteries involving, in addition to age, gender and menopausal status, a complex interplay between lifestyle and genetic risk factors. Atherosclerosis usually begins with the diffusion and retention of atherogenic lipoproteins into the subendothelial space of the artery wall where they become oxidized by local enzymes and accumulate, leading to the formation of a cushion called atheroma or atheromatous or fibrofatty plaque, composed of a mixture of macrophages, lymphocytes, smooth muscle cells (SMCs), cholesterol cleft, necrotic debris, and lipid-laden foam cells. The pathogenesis of atherosclerosis still remains incompletely understood but emerging evidence suggests that it may involve multiple cellular events, including endothelial cell (EC) dysfunction, inflammation, proliferation of vascular SMCs, matrix (ECM) alteration, and neovascularization. Actually, a growing body of evidence indicates that autophagy along with the chronic and acute overproduction of reactive oxygen species (ROS) is integral to the development and progression of the disease and may represent fruitful avenues for biological investigation and for the identification of new therapeutic targets. In this review, we give an overview of ROS and autophagy in atherosclerosis as background to understand their potential role in this vascular disease.

The production of reactive oxygen and nitrogen species by skeletal muscle

2007 ◽  
Vol 102 (4) ◽  
pp. 1664-1670 ◽  
Author(s):  
Malcolm J. Jackson ◽  
Deborah Pye ◽  
Jesus Palomero
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Potential Role ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Nitrogen Species ◽  
Redox Biology ◽  
Controlled Systems ◽  
Potential Source

Skeletal muscle has been recognized as a potential source for generation of reactive oxygen and nitrogen species for more than 20 years. Initial investigations concentrated on the potential role of mitochondria as a major source for generation of superoxide as a “by-product” of normal oxidative metabolism, but recent studies have identified multiple subcellular sites, where superoxide or nitric oxide are generated in regulated and controlled systems in response to cellular stimuli. Full evaluation of the factors regulating these processes and the functions of the reactive oxygen species generated are important in understanding the redox biology of skeletal muscle.

Free radicals, lipid peroxidation and sperm function

1995 ◽  
Vol 7 (4) ◽  
pp. 659 ◽  
Author(s):  
RJ Aitken
Keyword(s):  
Reactive Oxygen Species ◽  
Lipid Peroxidation ◽  
Reactive Oxygen ◽  
Human Spermatozoa ◽  
Sperm Function ◽  
Oxygen Species ◽  
Normal Sperm ◽  
Oxidative Processes ◽  
Mammalian Spermatozoa

The cellular generation of reactive oxygen species was first observed in mammalian spermatozoa in the late 1940s. The field then remained dormant for 30 years until Thaddeus Mann and Roy Jones published a series of landmark papers in the 1970s in which the importance of lipid peroxidation as a mechanism for damaging mammalian spermatozoa was first intimated. The subsequent demonstration that human spermatozoa produce reactive oxygen species and are susceptible to peroxidative damage has triggered intense interest in the role of oxidative stress in the aetiology of male infertility. Moreover, data have recently been obtained to indicate that, although excessive exposure to reactive oxygen species may be harmful to spermatozoa, in physiological amounts these molecules are of importance in the control of normal sperm function. This review considers the dualistic role of reactive oxygen species and sets out the current understanding of the importance of oxidative processes in both the physiology and the pathology of the human spermatozoon. Extra keywords: human spermatozoa, reactive oxygen species.

scholarly journals Functional inactivation of the oestrogen receptor by the antioestrogen, ZM 182780, sensitises tumour cells to reactive oxygen species

1999 ◽  
Vol 161 (2) ◽  
pp. 199-210 ◽  
Author(s):  
CJ Newton ◽  
N Drummond ◽  
CH Burgoyne ◽  
V Speirs ◽  
GK Stalla ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Oestrogen Receptor ◽  
Reactive Oxygen ◽  
Mitochondrial Activity ◽  
Oxygen Species ◽  
Rat Pituitary ◽  
Functional Inactivation ◽  
Mediate Cell

Reactive oxygen species (ROS) play a fundamental role in both apoptotic and necrotic cell death. Their importance is highlighted by studies showing that they mediate cell death in response to radiotherapy and to some forms of chemotherapy. Here we provide the first evidence for a role of ROS in response to an antiendocrine agent currently undergoing clinical trials. Using the oestrogen receptor (ER) containing rat pituitary GH3 cell line, we show that cell death is induced by the pure steroidal antioestrogen, ZM 182780, and that this is blocked by the antioxidant, N-acetyl cysteine (NAC). By flow cytometry, we show that, prior to the onset of DNA breakdown measured by ELISA, ZM 182780 exposure has no significant effect on intracellular oxidant concentrations. In contrast, ZM 182780 exposure greatly increases sensitivity to oxidants generated by blocking cellular antioxidant pathways and from exogenous administration of hydrogen peroxide (H2O2). As both necrosis and apoptosis are controlled by mitochondrial function, further experiments conducted to determine mitochondrial membrane potential (Delta|gWm) have indicated that the ZM 182780-induced loss of ER function increases the ease with which oxidants collapse mitochondrial activity and, as a consequence, cell death.

scholarly journals Deactivation of the JNK Pathway by GSTP1 Is Essential to Maintain Sperm Functionality

2021 ◽  
Vol 9 ◽  
Author(s):  
Marc Llavanera ◽  
Yentel Mateo-Otero ◽  
Ariadna Delgado-Bermúdez ◽  
Sandra Recuero ◽  
Samuel Olives ◽  
...  
Keyword(s):  
Membrane Integrity ◽  
Mitochondrial Activity ◽  
Computer Assisted ◽  
Sperm Function ◽  
Jnk Pathway ◽  
Male Subfertility ◽  
Mammalian Sperm ◽  
Genetic Abnormalities ◽  
Protein Dysfunction

Fifty percent of male subfertility diagnosis is idiopathic and is usually associated with genetic abnormalities or protein dysfunction, which are not detectable through the conventional spermiogram. Glutathione S-transferases (GSTs) are antioxidant enzymes essential for preserving sperm function and maintaining fertilizing ability. However, while the role of GSTP1 in cell signaling regulation via the inhibition of c-Jun N-terminal kinases (JNK) has been enlightened in somatic cells, it has never been investigated in mammalian spermatozoa. In this regard, a comprehensive approach through immunoblotting, immunofluorescence, computer-assisted sperm assessment (CASA), and flow cytometry analysis was used to characterize the molecular role of the GSTP1–JNK heterocomplex in sperm physiology, using the pig as a model. Immunological assessments confirmed the presence and localization of GSTP1 in sperm cells. The pharmacological dissociation of the GSTP1–JNK heterocomplex resulted in the activation of JNK, which led to a significant decrease in sperm viability, motility, mitochondrial activity, and plasma membrane stability, as well as to an increase of intracellular superoxides. No effects in intracellular calcium levels and acrosome membrane integrity were observed. In conclusion, the present work has demonstrated, for the first time, the essential role of GSTP1 in deactivating JNK, which is crucial to maintain sperm function and has also set the grounds to understand the relevance of the GSTP1–JNK heterocomplex for the regulation of mammalian sperm physiology.

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