Glutathione-dependent thioredoxin reduction and lipoamide system support in-vitro mammalian ribonucleotide reductase catalysis: a possible antioxidant redundancy

Chatterji, Ajanta; Kumar, Sachin; Sengupta, Rajib

doi:10.1007/s11033-022-07480-4

Cited by 2 publications

(1 citation statement)

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“…Although GSH has the lowest concentration in the nucleus, it plays a crucial role in the cell cycle [20,58,59]. Cells preparing to divide have higher nuclear GSH levels [60,61]. During the early stages of cell proliferation, GSH colocalizes with nuclear DNA.…”

Section: Gsh Biosynthesis and Metabolismmentioning

confidence: 99%

Mitochondrial Glutathione in Cellular Redox Homeostasis and Disease Manifestation

Chen,

Wang,

Chang

et al. 2024

IJMS

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Mitochondria are critical for providing energy to maintain cell viability. Oxidative phosphorylation involves the transfer of electrons from energy substrates to oxygen to produce adenosine triphosphate. Mitochondria also regulate cell proliferation, metastasis, and deterioration. The flow of electrons in the mitochondrial respiratory chain generates reactive oxygen species (ROS), which are harmful to cells at high levels. Oxidative stress caused by ROS accumulation has been associated with an increased risk of cancer, and cardiovascular and liver diseases. Glutathione (GSH) is an abundant cellular antioxidant that is primarily synthesized in the cytoplasm and delivered to the mitochondria. Mitochondrial glutathione (mGSH) metabolizes hydrogen peroxide within the mitochondria. A long-term imbalance in the ratio of mitochondrial ROS to mGSH can cause cell dysfunction, apoptosis, necroptosis, and ferroptosis, which may lead to disease. This study aimed to review the physiological functions, anabolism, variations in organ tissue accumulation, and delivery of GSH to the mitochondria and the relationships between mGSH levels, the GSH/GSH disulfide (GSSG) ratio, programmed cell death, and ferroptosis. We also discuss diseases caused by mGSH deficiency and related therapeutics.

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