scholarly journals Therapeutic Strategies for Regulating Mitochondrial Oxidative Stress

Biomolecules ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 83 ◽  
Author(s):  
Yuma Yamada ◽  
Yuta Takano ◽  
Satrialdi ◽  
Jiro Abe ◽  
Mitsue Hibino ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Drug Delivery ◽  
Photothermal Therapy ◽  
Therapeutic Strategy ◽  
Therapeutic Strategies ◽  
Clinical Applications ◽  
Mitochondrial Targeting ◽  
Mitochondrial Oxidative Stress ◽  
Anti Oxidant ◽  
The Relationship

There have been many reports on the relationship between mitochondrial oxidative stress and various types of diseases. This review covers mitochondrial targeting photodynamic therapy and photothermal therapy as a therapeutic strategy for inducing mitochondrial oxidative stress. We also discuss other mitochondrial targeting phototherapeutic methods. In addition, we discuss anti-oxidant therapy by a mitochondrial drug delivery system (DDS) as a therapeutic strategy for suppressing oxidative stress. We also describe cell therapy for reducing oxidative stress in mitochondria. Finally, we discuss the possibilities and problems associated with clinical applications of mitochondrial DDS to regulate mitochondrial oxidative stress.

scholarly journals The Essential Element Manganese, Oxidative Stress, and Metabolic Diseases: Links and Interactions

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Longman Li ◽  
Xiaobo Yang
Keyword(s):  
Oxidative Stress ◽  
Metabolic Diseases ◽  
Essential Element ◽  
Ros Generation ◽  
Oxygen Species ◽  
Mitochondrial Oxidative Stress ◽  
Nonalcoholic Fatty Liver ◽  
The Past ◽  
The Relationship

Manganese (Mn) is an essential element that is involved in the synthesis and activation of many enzymes and in the regulation of the metabolism of glucose and lipids in humans. In addition, Mn is one of the required components for Mn superoxide dismutase (MnSOD) that is mainly responsible for scavenging reactive oxygen species (ROS) in mitochondrial oxidative stress. Both Mn deficiency and intoxication are associated with adverse metabolic and neuropsychiatric effects. Over the past few decades, the prevalence of metabolic diseases, including type 2 diabetes mellitus (T2MD), obesity, insulin resistance, atherosclerosis, hyperlipidemia, nonalcoholic fatty liver disease (NAFLD), and hepatic steatosis, has increased dramatically. Previous studies have found that ROS generation, oxidative stress, and inflammation are critical for the pathogenesis of metabolic diseases. In addition, deficiency in dietary Mn as well as excessive Mn exposure could increase ROS generation and result in further oxidative stress. However, the relationship between Mn and metabolic diseases is not clear. In this review, we provide insights into the role Mn plays in the prevention and development of metabolic diseases.

scholarly journals Systemic treatment with a 5HT1a agonist induces anti-oxidant protection and preserves the retina from mitochondrial oxidative stress

2015 ◽  
Vol 140 ◽  
pp. 94-105 ◽  
Author(s):  
Manas R. Biswal ◽  
Chulbul M. Ahmed ◽  
Cristhian J. Ildefonso ◽  
Pingyang Han ◽  
Hong Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Systemic Treatment ◽  
Mitochondrial Oxidative Stress ◽  
5Ht1a Agonist ◽  
Anti Oxidant

scholarly journals Role of Presenilin in Mitochondrial Oxidative Stress and Neurodegeneration in Caenorhabditis elegans

2018 ◽  
Author(s):  
Shaarika Sarasija ◽  
Kenneth R. Norman
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Global Health ◽  
Mitochondrial Function ◽  
Therapeutic Strategies ◽  
Calcium Dysregulation ◽  
Mitochondrial Oxidative Stress ◽  
Health Crisis ◽  
Genes Encoding

Neurodegenerative diseases like Alzheimer’s disease (AD) are poised to become a global health crisis, and therefore understanding the mechanisms underlying the pathogenesis is critical for the development of therapeutic strategies. Mutations in genes encoding presenilin occur in most familial Alzheimer’s disease but the role of PSEN in AD is not fully understood. In this review, the potential modes of pathogenesis of AD are discussed, focusing on calcium homeostasis and mitochondrial function. Moreover, research using Caenorhabditis elegans to explore the effects of calcium dysregulation due to presenilin mutations on mitochondrial function, oxidative stress and neurodegeneration is explored.

scholarly journals An NIR-II Responsive Nanoplatform for Cancer Photothermal and Oxidative Stress Therapy

2021 ◽  
Vol 9 ◽  
Author(s):  
Bin Huang ◽  
Yuanpeng Huang ◽  
Han Han ◽  
Qiuyue Ge ◽  
Dongliang Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Photothermal Therapy ◽  
Antitumor Effect ◽  
Therapeutic Strategy ◽  
Copper Ion ◽  
Oxygen Species ◽  
Intracellular Ros ◽  
Stress Therapy ◽  
Change Material ◽  
And Oxidative Stress

Chemodynamic therapy as an emerging therapeutic strategy has been implemented for oncotherapy. However, the reactive oxygen species can be counteracted by the exorbitant glutathione (GSH) produced by the tumor cells before exerting the antitumor effect. Herein, borneol (NB) serving as a monoterpenoid sensitizer, and copper sulfide (CuS NPs) as an NIR-II photothermal agent were loaded in a thermo-responsive vehicle (NB/CuS@PCM NPs). Under 1,060-nm laser irradiation, the hyperthermia produced by CuS NPs can be used for photothermal therapy and melt the phase change material for drug delivery. In the acidity microenvironment, the CuS NPs released from NB/CuS@PCM NPs could degrade to Cu2+, then Cu2+ was reduced to Cu+ during the depletion of GSH. As Fenton-like catalyst, the copper ion could convert hydrogen peroxide into hydroxyl radicals for chemodynamic therapy. Moreover, the NB originated from NB/CuS@PCM NPs could increase the intracellular ROS content to improve the treatment outcome of chemodynamic therapy. The animal experimental results indicated that the NB/CuS@PCM NPs could accumulate at the tumor site and exhibit an excellent antitumor effect. This work confirmed that the combination of oxidative stress–induced damage and photothermal therapy is a potential therapeutic strategy for cancer treatment.

scholarly journals Metabolic Syndrome and Periodontitis: Is Oxidative Stress a Common Link?

2009 ◽  
Vol 88 (6) ◽  
pp. 503-518 ◽  
Author(s):  
P. Bullon ◽  
J.M. Morillo ◽  
M.C. Ramirez-Tortosa ◽  
J.L. Quiles ◽  
H.N. Newman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Density Lipoprotein ◽  
Serum Levels ◽  
Inflammatory State ◽  
Anti Oxidant ◽  
Obesity Hypertension ◽  
The Relationship

A review of pathological mechanisms that can explain the relationship between periodontitis and cardiovascular disease (CVD) is necessary to improve the management of both conditions. Metabolic syndrome is a combination of obesity, hypertension, impaired glucose tolerance or diabetes, hyperinsulinemia, and dyslipidemia. All these have been examined in recent years in terms of their relationship to periodontitis. Reviewed data indicate an association between some of them (body mass index, high-density lipoprotein-cholesterol [HDL-C], triglycerides, high blood pressure, among others) and periodontitis. Oxidative stress may act as a potential common link to explain relationships between each component of metabolic syndrome and periodontitis. Both conditions show increased serum levels of products derived from oxidative damage, with a pro-inflammatory state likely influencing each other bidirectionally. Adipocytokines might modulate the oxidant/anti-oxidant balance in this relationship.

scholarly journals Analysing the mechanism of mitochondrial oxidation-induced cell death using a multifunctional iridium(III) photosensitiser

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Chaiheon Lee ◽  
Jung Seung Nam ◽  
Chae Gyu Lee ◽  
Mingyu Park ◽  
Chang-Mo Yoo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Mitochondrial Protein ◽  
Cancer Therapeutics ◽  
Potential Mechanism ◽  
Chemical Modifications ◽  
Mitochondrial Oxidative Stress ◽  
Biological Phenomena ◽  
Mitochondrial Oxidation ◽  
The Relationship

AbstractMitochondrial oxidation-induced cell death, a physiological process triggered by various cancer therapeutics to induce oxidative stress on tumours, has been challenging to investigate owing to the difficulties in generating mitochondria-specific oxidative stress and monitoring mitochondrial responses simultaneously. Accordingly, to the best of our knowledge, the relationship between mitochondrial protein oxidation via oxidative stress and the subsequent cell death-related biological phenomena has not been defined. Here, we developed a multifunctional iridium(III) photosensitiser, Ir-OA, capable of inducing substantial mitochondrial oxidative stress and monitoring the corresponding change in viscosity, polarity, and morphology. Photoactivation of Ir-OA triggers chemical modifications in mitochondrial protein-crosslinking and oxidation (i.e., oxidative phosphorylation complexes and channel and translocase proteins), leading to microenvironment changes, such as increased microviscosity and depolarisation. These changes are strongly related to cell death by inducing mitochondrial swelling with excessive fission and fusion. We suggest a potential mechanism from mitochondrial oxidative stress to cell death based on proteomic analyses and phenomenological observations.

scholarly journals Crosstalk between Apoptosis and Autophagy: Molecular Mechanisms and Therapeutic Strategies in Cancer

2013 ◽  
Vol 6 ◽  
pp. JCD.S11034 ◽  
Author(s):  
Abdelouahid El-Khattouti ◽  
Denis Selimovic ◽  
Youssef Haikel ◽  
Mohamed Hassan
Keyword(s):  
Therapeutic Strategy ◽  
Molecular Mechanisms ◽  
Metabolic Stress ◽  
Therapeutic Strategies ◽  
Protective Mechanism ◽  
Tumor Treatment ◽  
Therapeutic Approaches ◽  
Protective Mechanisms ◽  
The Relationship ◽  
Insight Into

Both apoptosis and autophagy are highly conserved processes that besides their role in the maintenance of the organismal and cellular homeostasis serve as a main target of tumor therapeutics. Although their important roles in the modulation of tumor therapeutic strategies have been widely reported, the molecular actions of both apoptosis and autophagy are counteracted by cancer protective mechanisms. While apoptosis is a tightly regulated process that is implicated in the removal of damaged or unwanted cells, autophagy is a cellular catabolic pathway that is involved in lysosomal degradation and recycling of proteins and organelles, and thereby is considered an important survival/protective mechanism for cancer cells in response to metabolic stress or chemotherapy. Although the relationship between autophagy and cell death is very complicated and has not been characterized in detail, the molecular mechanisms that control this relationship are considered to be a relevant target for the development of a therapeutic strategy for tumor treatment. In this review, we focus on the molecular mechanisms of apoptosis, autophagy, and those of the crosstalk between apoptosis and autophagy in order to provide insight into the molecular mechanisms that may be essential for the balance between cell survival and death as well as their role as targets for the development of novel therapeutic approaches.

scholarly journals Oxidative DNA Damage Causes Mitochondrial Genomic Instability in Saccharomyces cerevisiae

2005 ◽  
Vol 25 (12) ◽  
pp. 5196-5204 ◽  
Author(s):  
Nicole A. Doudican ◽  
Binwei Song ◽  
Gerald S. Shadel ◽  
Paul W. Doetsch
Keyword(s):  
Oxidative Stress ◽  
Genomic Instability ◽  
Oxidative Dna Damage ◽  
Excision Repair ◽  
Mitochondrial Oxidative Stress ◽  
Damage Resistance ◽  
Mtdna Damage ◽  
Mitochondrial Superoxide ◽  
Base Excision ◽  
The Relationship

ABSTRACT Mitochondria contain their own genome, the integrity of which is required for normal cellular energy metabolism. Reactive oxygen species (ROS) produced by normal mitochondrial respiration can damage cellular macromolecules, including mitochondrial DNA (mtDNA), and have been implicated in degenerative diseases, cancer, and aging. We developed strategies to elevate mitochondrial oxidative stress by exposure to antimycin and H2O2 or utilizing mutants lacking mitochondrial superoxide dismutase (sod2Δ). Experiments were conducted with strains compromised in mitochondrial base excision repair (ntg1Δ) and oxidative damage resistance (pif1Δ) in order to delineate the relationship between these pathways. We observed enhanced ROS production, resulting in a direct increase in oxidative mtDNA damage and mutagenesis. Repair-deficient mutants exposed to oxidative stress conditions exhibited profound genomic instability. Elimination of Ntg1p and Pif1p resulted in a synergistic corruption of respiratory competency upon exposure to antimycin and H2O2. Mitochondrial genomic integrity was substantially compromised in ntg1Δ pif1Δ sod2Δ strains, since these cells exhibit a total loss of mtDNA. A stable respiration-defective strain, possessing a normal complement of mtDNA damage resistance pathways, exhibited a complete loss of mtDNA upon exposure to antimycin and H2O2. This loss was preventable by Sod2p overexpression. These results provide direct evidence that oxidative mtDNA damage can be a major contributor to mitochondrial genomic instability and demonstrate cooperation of Ntg1p and Pif1p to resist the introduction of lesions into the mitochondrial genome.

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