Maintenance of small molecule redox homeostasis in mitochondria

Jacobs, Lianne J H C; Riemer, Jan

doi:10.1002/1873-3468.14485

Cited by 9 publications

(3 citation statements)

References 178 publications

(235 reference statements)

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“…Retention of intracellular GSH levels may be a critical factor in the ROS scavenging effect of morroniside against H2O2. GSH exists not only in the cytoplasm but also in mitochondria, and protects mitochondria from oxidative stress by scavenging ROS generated during electron transport and oxidative phosphorylation within mitochondria (Jacobs and Riemer, 2023). Recently, Li et al (2023) found that morroniside can reduce ROS production by restoring the mitochondrial respiratory chain in a Parkinson's disease model.…”

Section: Discussionmentioning

confidence: 99%

Morroniside Protects C2C12 Myoblasts from Oxidative Damage Caused by ROS-Mediated Mitochondrial Damage and Induction of Endoplasmic Reticulum Stress

Hwangbo,

Park,

Bang

et al. 2024

Biomol Ther (Seoul)

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Oxidative stress contributes to the onset of chronic diseases in various organs, including muscles. Morroniside, a type of iridoid glycoside contained in Cornus officinalis , is reported to have advantages as a natural compound that prevents various diseases. However, the question of whether this phytochemical exerts any inhibitory effect against oxidative stress in muscle cells has not been well reported. Therefore, the current study aimed to evaluate whether morroniside can protect against oxidative damage induced by hydrogen peroxide (H 2 O 2 ) in murine C2C12 myoblasts. Our results demonstrate that morroniside pretreatment was able to inhibit cytotoxicity while suppressing H 2 O 2 -induced DNA damage and apoptosis. Morroniside also significantly improved the antioxidant capacity in H 2 O 2 -challenged C2C12 cells by blocking the production of cellular reactive oxygen species and mitochondrial superoxide and increasing glutathione production. In addition, H 2 O 2 -induced mitochondrial damage and endoplasmic reticulum (ER) stress were effectively attenuated by morroniside pretreatment, inhibiting cytoplasmic leakage of cytochrome c and expression of ER stress-related proteins. Furthermore, morroniside neutralized H 2 O 2 -mediated calcium (Ca 2+ ) overload in mitochondria and mitigated the expression of calpains, cytosolic Ca 2+ -dependent proteases. Collectively, these findings demonstrate that morroniside protected against mitochondrial impairment and Ca 2+ -mediated ER stress by minimizing oxidative stress, thereby inhibiting H 2 O 2 -induced cytotoxicity in C2C12 myoblasts.

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Section: Discussionmentioning

confidence: 99%

Morroniside Protects C2C12 Myoblasts from Oxidative Damage Caused by ROS-Mediated Mitochondrial Damage and Induction of Endoplasmic Reticulum Stress

Hwangbo,

Park,

Bang

et al. 2024

Biomol Ther (Seoul)

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“…Experimentally, the lack of GPX1 and SOD2 genes affects the tissue mitochondria, leading to oxidative stress in mice [76]. Overall, SOD2 converts oxygen radicals into hydrogen peroxide, causing mitochondrial dysfunctions [77]. The antioxidative enzymes, i.e., superoxide dismutase (SOD2) and glutathione peroxidase (GPX1), produce the first line of defense actions against free radicals and pathogens [78].…”

Section: Discussionmentioning

confidence: 99%

Preventive Action of Beta-Carotene against the Indoxyl Sulfate-Induced Renal Dysfunction in Male Adult Zebrafish via Regulations of Mitochondrial Inflammatory and β-Carotene Oxygenase-2 Actions

Muthuraman,

Sayem,

Meenakshisundaram

et al. 2023

Biomedicines

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Indoxyl sulfate (IS) is a metabolic byproduct of indole metabolism. IS readily interacts with the mitochondrial redox metabolism, leading to altered renal function. The β-carotene oxygenase-2 (BCO2) enzyme converts carotenoids to intermediate products. However, the role of β-carotene (BC) in IS-induced renal dysfunction in zebrafish and their modulatory action on BCO2 and mitochondrial inflammations have not been explored yet. Hence, the present study is designed to investigate the role of BC in the attenuation of IS-induced renal dysfunction via regulations of mitochondrial redox balance by BCO2 actions. Renal dysfunction was induced by exposure to IS (10 mg/L/hour/day) for 4 weeks. BC (50 and 100 mg/L/hour/day) and coenzyme Q10 (CoQ10; 20 mg/L/hour/day) were added before IS exposure. BC attenuated the IS-induced increase in blood urea nitrogen (BUN) and creatinine concentrations, adenosine triphosphate (ATP), and complex I activity levels, and the reduction of renal mitochondrial biomarkers, i.e., BCO2, superoxide dismutase-2 (SOD2), glutathione peroxidase-1 (GPX1), reduced and oxidized glutathione (GSH/GSSG) ratio, and carbonylated proteins. Moreover, renal histopathological changes were analyzed by the eosin and hematoxylin staining method. As a result, the administration of BC attenuated the IS-induced renal damage via the regulation of mitochondrial function.

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“…The mitochondrial NADPH is central to ROS production and the reduction in thiols (-SH). Numerous protein functions are controlled by the reduction in -SH [115]. In line with cancer signaling, NADPH-Thioredoxin-1 (Trx-1) is instrumental in activating Apurinic/apyrimidinic endonuclease 1 (APE-1), which is a key regulator for various cancer signaling junctions such as nuclear factor-κB (NF-κB), NRF2, protein-53 (p53), Redox effector factor-1 (Ref1), estrogen receptor and glucocorticoid receptor [116,117].…”

Section: Mitochondria Regulation Of Redox Balancementioning

confidence: 99%

Cancer Bioenergetics and Tumor Microenvironments—Enhancing Chemotherapeutics and Targeting Resistant Niches through Nanosystems

Farhana

Alsrhani

Khan

et al. 2023

Cancers

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Cancer is an impending bottleneck in the advanced scientific workflow to achieve diagnostic, prognostic, and therapeutic success. Most cancers are refractory to conventional diagnostic and chemotherapeutics due to their limited targetability, specificity, solubility, and side effects. The inherent ability of each cancer to evolve through various genetic and epigenetic transformations and metabolic reprogramming underlies therapeutic limitations. Though tumor microenvironments (TMEs) are quite well understood in some cancers, each microenvironment differs from the other in internal perturbations and metabolic skew thereby impeding the development of appropriate diagnostics, drugs, vaccines, and therapies. Cancer associated bioenergetics modulations regulate TME, angiogenesis, immune evasion, generation of resistant niches and tumor progression, and a thorough understanding is crucial to the development of metabolic therapies. However, this remains a missing element in cancer theranostics, necessitating the development of modalities that can be adapted for targetability, diagnostics and therapeutics. In this challenging scenario, nanomaterials are modular platforms for understanding TME and achieving successful theranostics. Several nanoscale particles have been successfully researched in animal models, quite a few have reached clinical trials, and some have achieved clinical success. Nanoparticles exhibit an intrinsic capability to interact with diverse biomolecules and modulate their functions. Furthermore, nanoparticles can be functionalized with receptors, modulators, and drugs to facilitate specific targeting with reduced toxicity. This review discusses the current understanding of different theranostic nanosystems, their synthesis, functionalization, and targetability for therapeutic modulation of bioenergetics, and metabolic reprogramming of the cancer microenvironment. We highlight the potential of nanosystems for enhanced chemotherapeutic success emphasizing the questions that remain unanswered.

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Maintenance of small molecule redox homeostasis in mitochondria

Cited by 9 publications

References 178 publications

Morroniside Protects C2C12 Myoblasts from Oxidative Damage Caused by ROS-Mediated Mitochondrial Damage and Induction of Endoplasmic Reticulum Stress

Morroniside Protects C2C12 Myoblasts from Oxidative Damage Caused by ROS-Mediated Mitochondrial Damage and Induction of Endoplasmic Reticulum Stress

Preventive Action of Beta-Carotene against the Indoxyl Sulfate-Induced Renal Dysfunction in Male Adult Zebrafish via Regulations of Mitochondrial Inflammatory and β-Carotene Oxygenase-2 Actions

Cancer Bioenergetics and Tumor Microenvironments—Enhancing Chemotherapeutics and Targeting Resistant Niches through Nanosystems

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