Mitochondrial Glutathione in Cellular Redox Homeostasis and Disease Manifestation

Chen, Tsung-Hsien; Wang, Hsiang-Chen; Chang, Chia-Jung; Lee, Shih-Yu

doi:10.3390/ijms25021314

Cited by 23 publications

(3 citation statements)

References 214 publications

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“…Localized ROS production not only causes immediate damage to the mitochondria but also modifies the cell's overall oxidative state (Jia et al, 2024a ). Research indicates that increased ROS in the mitochondria generates ferroptosis, which can be impeded by antioxidants or enzymes that target the mitochondria (Chen et al, 2024 ). Secondly, ferroptosis is inhibited partly by certain antioxidant enzymes identified in mitochondria.…”

Section: Organelles Related To Ferroptosismentioning

confidence: 99%

Research progress on ferroptosis in the pathogenesis and treatment of neurodegenerative diseases

Wang,

Fang,

Ling

et al. 2024

Front. Cell. Neurosci.

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Globally, millions of individuals are impacted by neurodegenerative disorders including Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and Alzheimer's disease (AD). Although a great deal of energy and financial resources have been invested in disease-related research, breakthroughs in therapeutic approaches remain elusive. The breakdown of cells usually happens together with the onset of neurodegenerative diseases. However, the mechanism that triggers neuronal loss is unknown. Lipid peroxidation, which is iron-dependent, causes a specific type of cell death called ferroptosis, and there is evidence its involvement in the pathogenic cascade of neurodegenerative diseases. However, the specific mechanisms are still not well known. The present article highlights the basic processes that underlie ferroptosis and the corresponding signaling networks. Furthermore, it provides an overview and discussion of current research on the role of ferroptosis across a variety of neurodegenerative conditions.

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Section: Organelles Related To Ferroptosismentioning

confidence: 99%

Research progress on ferroptosis in the pathogenesis and treatment of neurodegenerative diseases

Wang,

Fang,

Ling

et al. 2024

Front. Cell. Neurosci.

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“…Glutathione (GSH), composed of glycine, cysteine, and glutamic acid, is a prominent intracellular nonenzymatic antioxidant. Given its ability to directly scavenge ROS, the intracellular GSH content serves as a crucial indicator of intracellular oxidative stress and the efficacy of antioxidant defense mechanisms [36]. Under the conditions of oxidative stress, lipids, particularly polyunsaturated fatty acids, are highly susceptible to…”

Section: Intracellular Ros Levels and Antioxidant Enzymes Activities ...mentioning

confidence: 99%

Exploring the Neuroprotective Potential of Desmodium Species: Insights into Radical Scavenging Capacity and Mechanisms against 6-OHDA-Induced Neurotoxicity

Chang,

Lien,

Hsueh

et al. 2024

Plants

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In this study, we collected seven prevalent Taiwanese Desmodium plants, including three species with synonymous characteristics, in order to assess their antioxidant phytoconstituents and radical scavenging capacities. Additionally, we compared their inhibitory activities on monoamine oxidase (MAO) and 6-hydroxydopamine (6-OHDA) auto-oxidation. Subsequently, we evaluated the neuroprotective potential of D. pulchellum on 6-OHDA-induced nerve damage in SH-SY5Y cells and delved into the underlying neuroprotective mechanisms. Among the seven Desmodium species, D. pulchellum exhibited the most robust ABTS radical scavenging capacity and relative reducing power; correspondingly, it had the highest total phenolic and phenylpropanoid contents. Meanwhile, D. motorium showcased the best hydrogen peroxide scavenging capacity and, notably, D. sequax demonstrated remarkable prowess in DPPH radical and superoxide scavenging capacity, along with selective inhibitory activity against MAO-B. Of the aforementioned species, D. pulchellum emerged as the frontrunner in inhibiting 6-OHDA auto-oxidation and conferring neuroprotection against 6-OHDA-induced neuronal damage in the SH-SY5Y cells. Furthermore, D. pulchellum effectively mitigated the increase in intracellular ROS and MDA levels through restoring the activities of the intracellular antioxidant defense system. Therefore, we suggest that D. pulchellum possesses neuroprotective effects against 6-OHDA-induced neurotoxicity due to the radical scavenging capacity of its antioxidant phytoconstituents and its ability to restore intracellular antioxidant activities.

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“…Part of synthesizing ATP inside mitochondria involves the production of ROS [ 52 ], so mitochondria need to be able to manage the ROS effectively. GSH is synthesized in the cytoplasm and brought into the mitochondria, but when mitochondrial levels of GSH are deficient in comparison to mitochondrial ROS levels, cells undergo apoptosis, ferroptosis, necroptosis, and other cellular dysfunction [ 53 ].…”

Section: Brief Overview Of Glutathionementioning

confidence: 99%

Glutathione in HIV-Associated Neurocognitive Disorders

Erdos,

Masuda,

Venketaraman

2024

CIMB

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A large portion of patients with Human Immunodeficiency Virus (HIV) have neurologic sequelae. Those with better-controlled HIV via antiretroviral therapies generally have less severe neurologic symptoms. However, for many patients, antiretrovirals do not adequately resolve symptoms. Since much of the pathogenesis of HIV/AIDS (Autoimmune Deficiency Syndrome) involves oxidative stress either directly, through viral interaction, or indirectly, through inflammatory mechanisms, we have reviewed relevant trials of glutathione supplementation in each of the HIV-associated neurocognitive diseases and have found disease-specific results. For diseases for which trials have not been completed, predicted responses to glutathione supplementation are made based on relevant mechanisms seen in the literature. It is not sufficient to conclude that all HIV-associated neurocognitive disorders (HAND) will benefit from the antioxidant effects of glutathione supplementation. The potential effects of glutathione supplementation in patients with HAND are likely to differ based on the specific HIV-associated neurocognitive disease.

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Mitochondrial Glutathione in Cellular Redox Homeostasis and Disease Manifestation

Cited by 23 publications

References 214 publications

Research progress on ferroptosis in the pathogenesis and treatment of neurodegenerative diseases

Research progress on ferroptosis in the pathogenesis and treatment of neurodegenerative diseases

Exploring the Neuroprotective Potential of Desmodium Species: Insights into Radical Scavenging Capacity and Mechanisms against 6-OHDA-Induced Neurotoxicity

Glutathione in HIV-Associated Neurocognitive Disorders

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