scholarly journals Cross-Talk between Mitochondrial Dysfunction-Provoked Oxidative Stress and Aberrant Noncoding RNA Expression in the Pathogenesis and Pathophysiology of SLE

2019 ◽  
Vol 20 (20) ◽  
pp. 5183 ◽  
Author(s):  
Chang-Youh Tsai ◽  
Song-Chou Hsieh ◽  
Cheng-Shiun Lu ◽  
Tsai-Hung Wu ◽  
Hsien-Tzung Liao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Cross Talk ◽  
Noncoding Rna ◽  
Nitrosative Stress ◽  
Noncoding Rnas ◽  
The Body ◽  
Rna Expression ◽  
Epigenetic Regulations ◽  
The Cross

Systemic lupus erythematosus (SLE) is a prototype of systemic autoimmune disease involving almost every organ. Polygenic predisposition and complicated epigenetic regulations are the upstream factors to elicit its development. Mitochondrial dysfunction-provoked oxidative stress may also play a crucial role in it. Classical epigenetic regulations of gene expression may include DNA methylation/acetylation and histone modification. Recent investigations have revealed that intracellular and extracellular (exosomal) noncoding RNAs (ncRNAs), including microRNAs (miRs), and long noncoding RNAs (lncRNAs), are the key molecules for post-transcriptional regulation of messenger (m)RNA expression. Oxidative and nitrosative stresses originating from mitochondrial dysfunctions could become the pathological biosignatures for increased cell apoptosis/necrosis, nonhyperglycemic metabolic syndrome, multiple neoantigen formation, and immune dysregulation in patients with SLE. Recently, many authors noted that the cross-talk between oxidative stress and ncRNAs can trigger and perpetuate autoimmune reactions in patients with SLE. Intracellular interactions between miR and lncRNAs as well as extracellular exosomal ncRNA communication to and fro between remote cells/tissues via plasma or other body fluids also occur in the body. The urinary exosomal ncRNAs can now represent biosignatures for lupus nephritis. Herein, we’ll briefly review and discuss the cross-talk between excessive oxidative/nitrosative stress induced by mitochondrial dysfunction in tissues/cells and ncRNAs, as well as the prospect of antioxidant therapy in patients with SLE.

scholarly journals Power Failure of Mitochondria and Oxidative Stress in Neurodegeneration and Its Computational Models

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 229
Author(s):  
JunHyuk Woo ◽  
Hyesun Cho ◽  
YunHee Seol ◽  
Soon Ho Kim ◽  
Chanhyeok Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Computational Models ◽  
Neuronal Damage ◽  
Living Organism ◽  
The Body ◽  
Mitochondrial Functions ◽  
A Cell ◽  
The Brain ◽  
And Oxidative Stress

The brain needs more energy than other organs in the body. Mitochondria are the generator of vital power in the living organism. Not only do mitochondria sense signals from the outside of a cell, but they also orchestrate the cascade of subcellular events by supplying adenosine-5′-triphosphate (ATP), the biochemical energy. It is known that impaired mitochondrial function and oxidative stress contribute or lead to neuronal damage and degeneration of the brain. This mini-review focuses on addressing how mitochondrial dysfunction and oxidative stress are associated with the pathogenesis of neurodegenerative disorders including Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Parkinson’s disease. In addition, we discuss state-of-the-art computational models of mitochondrial functions in relation to oxidative stress and neurodegeneration. Together, a better understanding of brain disease-specific mitochondrial dysfunction and oxidative stress can pave the way to developing antioxidant therapeutic strategies to ameliorate neuronal activity and prevent neurodegeneration.

scholarly journals Male Infertility: Pathogenetic Significance of Oxidative Stress and Antioxidant Defence (Review)

2021 ◽  
Vol 24 (6) ◽  
pp. 107-116
Author(s):  
Vsevolod Koshevoy ◽  
Svitlana Naumenko ◽  
Pavlo Skliarov ◽  
Serhiy Fedorenko ◽  
Lidia Kostyshyn
Keyword(s):  
Oxidative Stress ◽  
Male Infertility ◽  
Nitrosative Stress ◽  
Antioxidant Properties ◽  
Malonic Dialdehyde ◽  
The Body ◽  
Redox Activity ◽  
Enzymatic System ◽  
Male Body ◽  
Mitochondrial Potential

The basis of the pathogenesis of male infertility is the processes of peroxide oxidation of biological substrates, especially lipids and proteins. By destroying the sperm membrane, toxic peroxidation products reduce its motility and ability to fertilize the egg, which is determined by a decrease in the number of motile sperm in the ejaculate. These changes lead to complete or partial male infertility. The authors of the review found that is accompanied by a damaging effect on the structural and functional activity of the gonads and is manifested, in particular, by an imbalance in the hormonal background of the male body. Similar effects are characteristic of an increase in the content of reactive Nitrogen species and its metabolites, which cause nitrosative stress, which is also the cause of male hypofertility and is inseparable from the state of oxidative stress. In scientific work it is determined that the accumulation of harmful peroxidation products leads to damage and destruction of sperm DNA, reduced activity of acrosomal enzymes and mitochondrial potential of sperm, reduced overall antioxidant activity. This makes it impossible for an adequate response of the body. Multi component antioxidant defense system resists stress. It is represented by enzymatic and non-enzymatic links, which can neutralize harmful radicals and peroxidation products. It contributes to the full manifestation of reproductive function. The presence of powerful antioxidant properties of catalase, superoxide dismutase, and enzymes of the thiol-disulfide system, which form the enzymatic system of antioxidant protection, as well as selenium, zinc, copper, other trace elements, retinol, tocopherol, ascorbic acid, and vitamins as parts of the non-enzymatic system is shown. The efficiency of registration is substantiated thin biochemical shift detectors or complex methods, such as total antioxidant status of sperm or sperm plasma, mitochondrial membrane potential, etc along with simple markers of oxidative stress, such as diene conjugates, malonic dialdehyde, and metabolites of the Nitrogen Oxide cycle. Given the leading role of oxidative stress in the development of male hypofertility, the prospect of further research is the search for modern means for correction, especially among substances with pronounced redox activity

scholarly journals Carvacrol and Thymol Modulate the Cross-Talk between TNF-α and IGF-1 Signaling in Radiotherapy-Induced Ovarian Failure

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Yasmen F. Mahran ◽  
Amira M. Badr ◽  
Alhanouf Aldosari ◽  
Raghad Bin-Zaid ◽  
Hind N. Alotaibi
Keyword(s):  
Oxidative Stress ◽  
Cross Talk ◽  
Ovarian Failure ◽  
Radioprotective Effect ◽  
Whole Body ◽  
Nuclear Antigen ◽  
Hormonal Changes ◽  
Tnf Α ◽  
Ovarian Damage ◽  
The Cross

Premature ovarian failure (POF) is a common cause of infertility in premenopausal women who are unavoidably exposed to cytotoxic therapy. Radiotherapy is one of the most effective cytotoxic treatments. However, the radiosensitivity of ovarian tissues limits its therapeutic outcome and results in the depletion of the primordial follicle and loss of fertility. Therefore, the need for an effective radioprotective therapy is evident especially when none of the current clinically used modalities for radioprotection succeeds efficiently. The present study investigated the potential radioprotective effect of carvacrol (CAR) (80 mg) or thymol (80 mg) on gamma- (γ-) irradiation-induced ovarian damage as well as their role in the cross-talk between IGF-1 and TNF-α signaling and antioxidative activity. In immature female Wister rats, a single dose of whole-body irradiation (3.2 Gy, L D 20 ) produced considerable ovarian damage, which was evident by histopathological findings and hormonal changes. Interestingly, pretreatment with CAR or thymol significantly enhanced the follicular development and restored the anti-Mullerian hormone (AMH), E2, and FSH levels. Both essential oils improved the irradiation-mediated oxidative stress and reduction in proliferating cell nuclear antigen (PCNA) expression. Moreover, irradiated rats exhibited an inverse relationship between IGF-1 and TNF-α levels two days post irradiation, which was further inverted by the pretreatment with CAR and thymol and ought to contribute in their radioprotective mechanisms. In conclusion, CAR and thymol showed a radioprotective effect and rescued the ovarian reserve mainly through counteracting oxidative stress and the dysregulated cross-talk between IGF-1 and TNF-α.

scholarly journals Oral Bisphenol A Worsens Liver Immune-Metabolic and Mitochondrial Dysfunction Induced by High-Fat Diet in Adult Mice: Cross-Talk between Oxidative Stress and Inflammasome Pathway

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1201
Author(s):  
Claudio Pirozzi ◽  
Adriano Lama ◽  
Chiara Annunziata ◽  
Gina Cavaliere ◽  
Clara Ruiz-Fernandez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Bisphenol A ◽  
Mitochondrial Dysfunction ◽  
Cross Talk ◽  
High Fat Diet ◽  
Additional Risk Factor ◽  
High Fat ◽  
Endocrine Disrupting Chemical ◽  
Glucose And Lipid Metabolism

Lines of evidence have shown the embryogenic and transgenerational impact of bisphenol A (BPA), an endocrine-disrupting chemical, on immune-metabolic alterations, inflammation, and oxidative stress, while BPA toxic effects in adult obese mice are still overlooked. Here, we evaluate BPA’s worsening effect on several hepatic maladaptive processes associated to high-fat diet (HFD)-induced obesity in mice. After 12 weeks HFD feeding, C57Bl/6J male mice were exposed daily to BPA (50 μg/kg per os) along with HFD for 3 weeks. Glucose tolerance and lipid metabolism were examined in serum and/or liver. Hepatic oxidative damage (reactive oxygen species, malondialdehyde, antioxidant enzymes), and mitochondrial respiratory capacity were evaluated. Moreover, liver damage progression and inflammatory/immune response were determined by histological and molecular analysis. BPA amplified HFD-induced alteration of key factors involved in glucose and lipid metabolism, liver triglycerides accumulation, and worsened mitochondrial dysfunction by increasing oxidative stress and reducing antioxidant defense. The exacerbation by BPA of hepatic immune-metabolic dysfunction induced by HFD was shown by increased toll-like receptor-4 and its downstream pathways (i.e., NF-kB and NLRP3 inflammasome) amplifying inflammatory cytokine transcription and promoting fibrosis progression. This study evidences that BPA exposure represents an additional risk factor for the progression of fatty liver diseases strictly related to the cross-talk between oxidative stress and immune-metabolic impairment due to obesity.

scholarly journals Proteinopathy, oxidative stress and mitochondrial dysfunction: cross talk in Alzheimer's disease and Parkinson's disease

2017 ◽  
Vol Volume11 ◽  
pp. 797-810 ◽  
Author(s):  
Gargi Ganguly ◽  
Sasanka Chakrabarti ◽  
Uttara Chatterjee ◽  
Luciano Saso
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Cross Talk

scholarly journals Co-Exposure of Cardiomyocytes to IFN-γ and TNF-α Induces Mitochondrial Dysfunction and Nitro-Oxidative Stress: Implications for the Pathogenesis of Chronic Chagas Disease Cardiomyopathy

2021 ◽  
Vol 12 ◽  
Author(s):  
João Paulo Silva Nunes ◽  
Pauline Andrieux ◽  
Pauline Brochet ◽  
Rafael Ribeiro Almeida ◽  
Eduardo Kitano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Mitochondrial Dysfunction ◽  
Chagas Disease ◽  
Nitrosative Stress ◽  
Acid Oxidation ◽  
Oxidative And Nitrosative Stress ◽  
Human Cardiomyocytes ◽  
Tnf Α ◽  
Ifn Γ

Infection by the protozoan Trypanosoma cruzi causes Chagas disease cardiomyopathy (CCC) and can lead to arrhythmia, heart failure and death. Chagas disease affects 8 million people worldwide, and chronic production of the cytokines IFN-γ and TNF-α by T cells together with mitochondrial dysfunction are important players for the poor prognosis of the disease. Mitochondria occupy 40% of the cardiomyocytes volume and produce 95% of cellular ATP that sustain the life-long cycles of heart contraction. As IFN-γ and TNF-α have been described to affect mitochondrial function, we hypothesized that IFN-γ and TNF-α are involved in the myocardial mitochondrial dysfunction observed in CCC patients. In this study, we quantified markers of mitochondrial dysfunction and nitro-oxidative stress in CCC heart tissue and in IFN-γ/TNF-α-stimulated AC-16 human cardiomyocytes. We found that CCC myocardium displayed increased levels of nitro-oxidative stress and reduced mitochondrial DNA as compared with myocardial tissue from patients with dilated cardiomyopathy (DCM). IFN-γ/TNF-α treatment of AC-16 cardiomyocytes induced increased nitro-oxidative stress and decreased the mitochondrial membrane potential (ΔΨm). We found that the STAT1/NF-κB/NOS2 axis is involved in the IFN-γ/TNF-α-induced decrease of ΔΨm in AC-16 cardiomyocytes. Furthermore, treatment with mitochondria-sparing agonists of AMPK, NRF2 and SIRT1 rescues ΔΨm in IFN-γ/TNF-α-stimulated cells. Proteomic and gene expression analyses revealed that IFN-γ/TNF-α-treated cells corroborate mitochondrial dysfunction, transmembrane potential of mitochondria, altered fatty acid metabolism and cardiac necrosis/cell death. Functional assays conducted on Seahorse respirometer showed that cytokine-stimulated cells display decreased glycolytic and mitochondrial ATP production, dependency of fatty acid oxidation as well as increased proton leak and non-mitochondrial oxygen consumption. Together, our results suggest that IFN-γ and TNF-α cause direct damage to cardiomyocytes’ mitochondria by promoting oxidative and nitrosative stress and impairing energy production pathways. We hypothesize that treatment with agonists of AMPK, NRF2 and SIRT1 might be an approach to ameliorate the progression of Chagas disease cardiomyopathy.

The cross-talk between oxidative stress and endocannabinoid system in keratinocytes after UV irradiation

2015 ◽  
Vol 86 ◽  
pp. S28
Author(s):  
Agnieszka Gęgotek ◽  
Wojciech Luczaj ◽  
Ewa Ambrozewicz ◽  
Katarzyna Bielawska ◽  
Elzbieta Skrzydlewska
Keyword(s):  
Oxidative Stress ◽  
Uv Irradiation ◽  
Cross Talk ◽  
Endocannabinoid System ◽  
The Cross
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