The Impact of Oxidative Stress in Male Infertility

At present infertility is affecting about 15% of couples and male factor is responsible for almost 50% of infertility cases. Oxidative stress, due to enhanced Reactive Oxygen Species (ROS) production and/or decreased antioxidants, has been repeatedly suggested as a new emerging causative factor of this condition. However, the central roles exerted by ROS in sperm physiology cannot be neglected. On these bases, the present review is focused on illustrating both the role of ROS in male infertility and their main sources of production. Oxidative stress assessment, the clinical use of redox biomarkers and the treatment of oxidative stress-related male infertility are also discussed.

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Molecules and Mechanisms to Overcome Oxidative Stress Inducing Cardiovascular Disease in Cancer Patients

Life ◽

10.3390/life11020105 ◽

2021 ◽

Vol 11 (2) ◽

pp. 105

Author(s):

Francesco Sabbatino ◽

Valeria Conti ◽

Luigi Liguori ◽

Giovanna Polcaro ◽

Graziamaria Corbi ◽

...

Keyword(s):

Oxidative Stress ◽

Cardiovascular Disease ◽

Ros Production ◽

Oxygen Species ◽

Physiological Conditions ◽

Cellular Processes ◽

Pathological Conditions ◽

Detoxification Systems ◽

Cancer Diseases

Reactive oxygen species (ROS) are molecules involved in signal transduction pathways with both beneficial and detrimental effects on human cells. ROS are generated by many cellular processes including mitochondrial respiration, metabolism and enzymatic activities. In physiological conditions, ROS levels are well-balanced by antioxidative detoxification systems. In contrast, in pathological conditions such as cardiovascular, neurological and cancer diseases, ROS production exceeds the antioxidative detoxification capacity of cells, leading to cellular damages and death. In this review, we will first describe the biology and mechanisms of ROS mediated oxidative stress in cardiovascular disease. Second, we will review the role of oxidative stress mediated by oncological treatments in inducing cardiovascular disease. Lastly, we will discuss the strategies that potentially counteract the oxidative stress in order to fight the onset and progression of cardiovascular disease, including that induced by oncological treatments.

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Ovariectomy and its Antioxidative Effect on Bone

Volume 2: Biomedical and Biotechnology Engineering ◽

10.1115/imece2010-40581 ◽

2010 ◽

Author(s):

Durg V. Rai ◽

Harcharan Singh Ranu

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Free Radicals ◽

Bone Loss ◽

Wistar Rats ◽

Reactive Oxygen ◽

Oxygen Species ◽

Female Wistar Rats ◽

The Impact

Ovarian hormone deficiency increases the generation of reactive oxygen species. Oxidative stress due to reactive oxygen species (ROS) can cause oxidative damage to cells. Cells have a number of defense mechanisms to protect themselves from the toxicity of ROS. There is increasing evidence of the role of free radicals in bone resorption and bone loss. Ovariectomised female wistar rats had been used as the animal model for the study of osteoporosis. Even though, there are studies portraying the role of free radicals in bone loss, the defense mechanism adapted by bone in ovariectomised animals remains obscure. So, the impact of ovariectomy on the bone antioxidant system in rats was investigated. Twenty female wistar rats were taken and divided into two groups: ovariectomised and control. It had been found that a significant (p<0.001) decrease in the activity of various enzymes like CAT (catalase), SOD (superoxide dismutase) (p<0.001), GST (glutathione-s-transferase). However, an increase in the malondialdehyde levels was found to be 30% in the ovariectomised rats as compared to the controls. Thus the study elucidates the oxidative stress in bone under ovariectomy.

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Mitophagy and Oxidative Stress: The Role of Aging

Antioxidants ◽

10.3390/antiox10050794 ◽

2021 ◽

Vol 10 (5) ◽

pp. 794

Author(s):

Anna De Gaetano ◽

Lara Gibellini ◽

Giada Zanini ◽

Milena Nasi ◽

Andrea Cossarizza ◽

...

Keyword(s):

Oxidative Stress ◽

Mitochondrial Damage ◽

Ros Production ◽

Oxygen Species ◽

Prime Mover ◽

Age Related ◽

Chronic Oxidative Stress ◽

Parkinson’S Diseases ◽

And Oxidative Stress

Mitochondrial dysfunction is a hallmark of aging. Dysfunctional mitochondria are recognized and degraded by a selective type of macroautophagy, named mitophagy. One of the main factors contributing to aging is oxidative stress, and one of the early responses to excessive reactive oxygen species (ROS) production is the induction of mitophagy to remove damaged mitochondria. However, mitochondrial damage caused at least in part by chronic oxidative stress can accumulate, and autophagic and mitophagic pathways can become overwhelmed. The imbalance of the delicate equilibrium among mitophagy, ROS production and mitochondrial damage can start, drive, or accelerate the aging process, either in physiological aging, or in pathological age-related conditions, such as Alzheimer’s and Parkinson’s diseases. It remains to be determined which is the prime mover of this imbalance, i.e., whether it is the mitochondrial damage caused by ROS that initiates the dysregulation of mitophagy, thus activating a vicious circle that leads to the reduced ability to remove damaged mitochondria, or an alteration in the regulation of mitophagy leading to the excessive production of ROS by damaged mitochondria.

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Exercise in the Metabolic Syndrome

Oxidative Medicine and Cellular Longevity ◽

10.1155/2012/349710 ◽

2012 ◽

Vol 2012 ◽

pp. 1-13 ◽

Cited By ~ 48

Author(s):

Saeid Golbidi ◽

Azam Mesdaghinia ◽

Ismail Laher

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Oxygen Species ◽

Induce Insulin Resistance ◽

The Metabolic Syndrome ◽

Pathophysiological Role ◽

The Impact ◽

Global Population ◽

Muscular Metabolism

The metabolic syndrome is a clustering of obesity, diabetes, hyperlipidemia, and hypertension that is occurring in increasing frequency across the global population. Although there is some controversy about its diagnostic criteria, oxidative stress, which is defined as imbalance between the production and inactivation of reactive oxygen species, has a major pathophysiological role in all the components of this disease. Oxidative stress and consequent inflammation induce insulin resistance, which likely links the various components of this disease. We briefly review the role of oxidative stress as a major component of the metabolic syndrome and then discuss the impact of exercise on these pathophysiological pathways. Included in this paper is the effect of exercise in reducing fat-induced inflammation, blood pressure, and improving muscular metabolism.

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Methylglyoxal, oxidative stress, and hypertension

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y06-077 ◽

2006 ◽

Vol 84 (12) ◽

pp. 1229-1238 ◽

Cited By ~ 69

Author(s):

Tuanjie Chang ◽

Lingyun Wu

Keyword(s):

Oxidative Stress ◽

Protein Glycation ◽

Ros Production ◽

Oxygen Species ◽

Advanced Glycation ◽

Chain Reaction ◽

Research Teams ◽

Glycation End Products ◽

End Products

Pathogenic mechanisms for essential hypertension are unclear despite striking efforts from numerous research teams over several decades. Increased production of reactive oxygen species (ROS) has been associated with the development of hypertension and the role of ROS in hypertension has been well documented in recent years. In this context, it is important to better understand pathways and triggering factors for increased ROS production in hypertension. This review draws a causative linkage between elevated methylglyoxal level, methylglyoxal-induced production of ROS, and advanced glycation end products in the development of hypertension. It is proposed that elevated methylglyoxal level and resulting protein glycation and ROS production may be the upstream links in the chain reaction leading to the development of hypertension.

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BRCA1 interacts with Nrf2 to regulate antioxidant signaling and cell survival

Journal of Experimental Medicine ◽

10.1084/jem.20121337 ◽

2013 ◽

Vol 210 (8) ◽

pp. 1529-1544 ◽

Cited By ~ 144

Author(s):

Chiara Gorrini ◽

Pegah S. Baniasadi ◽

Isaac S. Harris ◽

Jennifer Silvester ◽

Satoshi Inoue ◽

...

Keyword(s):

Oxidative Stress ◽

Mammary Epithelial Cells ◽

Antioxidant Response ◽

Mammary Epithelial ◽

Oxygen Species ◽

Nrf2 Activation ◽

The Impact ◽

Low Expression

Oxidative stress plays an important role in cancer development and treatment. Recent data implicate the tumor suppressor BRCA1 in regulating oxidative stress, but the molecular mechanism and the impact in BRCA1-associated tumorigenesis remain unclear. Here, we show that BRCA1 regulates Nrf2-dependent antioxidant signaling by physically interacting with Nrf2 and promoting its stability and activation. BRCA1-deficient mouse primary mammary epithelial cells show low expression of Nrf2-regulated antioxidant enzymes and accumulate reactive oxygen species (ROS) that impair survival in vivo. Increased Nrf2 activation rescues survival and ROS levels in BRCA1-null cells. Interestingly, 53BP1 inactivation, which has been shown to alleviate several defects associated with BRCA1 loss, rescues survival of BRCA1-null cells without restoring ROS levels. We demonstrate that estrogen treatment partially restores Nrf2 levels in the absence of BRCA1. Our data suggest that Nrf2-regulated antioxidant response plays a crucial role in controlling survival downstream of BRCA1 loss. The ability of estrogen to induce Nrf2 posits an involvement of an estrogen-Nrf2 connection in BRCA1 tumor suppression. Lastly, BRCA1-mutated tumors retain a defective antioxidant response that increases the sensitivity to oxidative stress. In conclusion, the role of BRCA1 in regulating Nrf2 activity suggests important implications for both the etiology and treatment of BRCA1-related cancers.

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Assessment of Superoxide Dismutase and Catalase Evolution in Different Stages of an Experimental Endometriosis

Revista de Chimie ◽

10.37358/rc.17.6.5678 ◽

2017 ◽

Vol 68 (6) ◽

pp. 1381-1383

Author(s):

Allia Sindilar ◽

Carmen Lacramioara Zamfir ◽

Eusebiu Viorel Sindilar ◽

Alin Constantin Pinzariu ◽

Eduard Crauciuc ◽

...

Keyword(s):

Oxidative Stress ◽

Superoxide Dismutase ◽

Antioxidant Enzymes ◽

Reproductive Function ◽

Female Rats ◽

Oxygen Species ◽

Efficient Treatment ◽

Endometrial Cells ◽

Gynecological Disorder ◽

The Impact

Endometriosis is described as a gynecological disorder characterized by the presence of endometrial tissue outside the uterus; extensively explored because of its increasing incidency, with an indubitable diagnostic only after invasive surgery, with no efficient treatment, it has still many aspects to be elucidated. A growing body of facts sustain oxidative stress as a crucial factor between the numerous incriminated factors implicated in endometriosis ethiopathogeny. Reactive oxygen species(ROS) act to decline reproductive function. Our study intends to determine if an experimental model of endometriosis may be useful to assess the impact of oxidative stress on endometrial cells; we have used a murine model of 18 adult Wistar female rats. A fragment from their left uterine horn was implanted in the abdominal wall. After 4 weeks, a laparatomy was performed, 5 endometrial implants were removed, followed by biochemical tissue assay of superoxide dismutase(SOD) and catalase(CAT). At the end of the experiment, the rats were sacrificed, the implants were removed for histopathological exam and biochemical assay of antioxidant enzymes. The results revealed decreased levels of antioxidant enzymes, pointing on significant oxidative stress involvement.

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Oxidative Stress in the Tumor Microenvironment and Its Relevance to Cancer Immunotherapy

Cancers ◽

10.3390/cancers13050986 ◽

2021 ◽

Vol 13 (5) ◽

pp. 986

Author(s):

Nada S. Aboelella ◽

Caitlin Brandle ◽

Timothy Kim ◽

Zhi-Chun Ding ◽

Gang Zhou

Keyword(s):

Oxidative Stress ◽

Tumor Microenvironment ◽

Cancer Cells ◽

Redox Homeostasis ◽

Tumor Rejection ◽

Oxygen Species ◽

Antitumor Effects ◽

Key Drivers ◽

Cancer Immunotherapies ◽

The Impact

It has been well-established that cancer cells are under constant oxidative stress, as reflected by elevated basal level of reactive oxygen species (ROS), due to increased metabolism driven by aberrant cell growth. Cancer cells can adapt to maintain redox homeostasis through a variety of mechanisms. The prevalent perception about ROS is that they are one of the key drivers promoting tumor initiation, progression, metastasis, and drug resistance. Based on this notion, numerous antioxidants that aim to mitigate tumor oxidative stress have been tested for cancer prevention or treatment, although the effectiveness of this strategy has yet to be established. In recent years, it has been increasingly appreciated that ROS have a complex, multifaceted role in the tumor microenvironment (TME), and that tumor redox can be targeted to amplify oxidative stress inside the tumor to cause tumor destruction. Accumulating evidence indicates that cancer immunotherapies can alter tumor redox to intensify tumor oxidative stress, resulting in ROS-dependent tumor rejection. Herein we review the recent progresses regarding the impact of ROS on cancer cells and various immune cells in the TME, and discuss the emerging ROS-modulating strategies that can be used in combination with cancer immunotherapies to achieve enhanced antitumor effects.

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Antioxidants Promote Intestinal Tumor Progression in Mice

Antioxidants ◽

10.3390/antiox10020241 ◽

2021 ◽

Vol 10 (2) ◽

pp. 241

Author(s):

Zhiyuan V. Zou ◽

Kristell Le Gal ◽

Ahmed E. El Zowalaty ◽

Lara E. Pehlivanoglu ◽

Viktor Garellick ◽

...

Keyword(s):

Oxidative Stress ◽

Colorectal Cancer ◽

Tumor Progression ◽

Human Subjects ◽

Plasma Concentrations ◽

Intestinal Tumor ◽

Adenomatous Polyposis ◽

Intestinal Tumors ◽

The Impact

Dietary antioxidants and supplements are widely used to protect against cancer, even though it is now clear that antioxidants can promote tumor progression by helping cancer cells to overcome barriers of oxidative stress. Although recent studies have, in great detail, explored the role of antioxidants in lung and skin tumors driven by RAS and RAF mutations, little is known about the impact of antioxidant supplementation on other cancers, including Wnt-driven tumors originating from the gut. Here, we show that supplementation with the antioxidants N-acetylcysteine (NAC) and vitamin E promotes intestinal tumor progression in the ApcMin mouse model for familial adenomatous polyposis, a hereditary form of colorectal cancer, driven by Wnt signaling. Both antioxidants increased tumor size in early neoplasias and tumor grades in more advanced lesions without any impact on tumor initiation. Importantly, NAC treatment accelerated tumor progression at plasma concentrations comparable to those obtained in human subjects after prescription doses of the drug. These results demonstrate that antioxidants play an important role in the progression of intestinal tumors, which may have implications for patients with or predisposed to colorectal cancer.

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Multifunctional Role of Chitosan Edible Coatings on Antioxidant Systems in Fruit Crops: A Review

International Journal of Molecular Sciences ◽

10.3390/ijms22052633 ◽

2021 ◽

Vol 22 (5) ◽

pp. 2633

Author(s):

Giuseppina Adiletta ◽

Marisa Di Matteo ◽

Milena Petriccione

Keyword(s):

State Of The Art ◽

Antioxidant Systems ◽

Edible Coatings ◽

Ros Production ◽

Oxygen Species ◽

Fruit Crops ◽

Oxidative Damages ◽

Film Forming ◽

Anti Oxidant

Chitosan-based edible coatings represent an eco-friendly and biologically safe preservative tool to reduce qualitative decay of fresh and ready-to-eat fruits during post-harvest life due to their lack of toxicity, biodegradability, film-forming properties, and antimicrobial actions. Chitosan-based coatings modulate or control oxidative stress maintaining in different manner the appropriate balance of reactive oxygen species (ROS) in fruit cells, by the interplay of pathways and enzymes involved in ROS production and the scavenging mechanisms which essentially constitute the basic ROS cycle. This review is carried out with the aim to provide comprehensive and updated over-view of the state of the art related to the effects of chitosan-based edible coatings on anti-oxidant systems, enzymatic and non-enzymatic, evaluating the induced oxidative damages during storage in whole and ready-to-eat fruits. All these aspects are broadly reviewed in this review, with particular emphasis on the literature published during the last five years.

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