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[Mitochondrial thiol-disulfide system under acute hypoxia and hypoxic-hyperoxic adaptation].

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The authors investigated the state of mitochondrial glutathione pool (reduced and oxidized glutathione, protein-GSH mixed disulfides), content of carbonyl groups and free sulfhydryl groups of proteins, protein expression of key mitochondrial antioxidant enzymes such as glutathione peroxidase and

Hypoxia increases plasma glutathione disulfide in rats.

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We tested the hypothesis that hypoxia causes cellular oxidative stress by measuring plasma concentrations of glutathione disulfide (GSSG) in rats exposed to acute and subacute hypoxia. In awake, unanesthetized, catheter-implanted rats, exposure to 8% O2 for 10 min caused pulmonary vasoconstriction

Hemoglobin polymerization via disulfide bond formation in the hypoxia-tolerant turtle Trachemys scripta: implications for antioxidant defense and O2 transport.

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The ability of many reptilian hemoglobins (Hbs) to form high-molecular weight polymers, albeit known for decades, has not been investigated in detail. Given that turtle Hbs often contain a high number of cysteine (Cys), potentially contributing to the red blood cell defense against reactive oxygen

Glutathione disulfide as index of oxidant stress in rat liver during hypoxia.

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Formation of glutathione disulfide (GSSG) was used as an index of reactive oxygen generation in the isolated perfused liver of male Fischer rats during normoxia and hypoxia. Low oxygen tension may affect GSSG formation, rereduction, and transport mechanisms. The effect of short-term hypoxia (15 min)

Glutathione disulfide formation occurring during hypoxia and reoxygenation of rat lung.

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To study changes in glutathione redox status as an indicator of oxidant stress during hypoxia and reoxygenation, we perfused isolated rat lungs with a high or low oxygen perfusate and measured the release of total glutathione and glutathione disulfide (GSSG) into the perfusate. Lungs were perfused

Disulfide cytotoxicity under hypoxia.

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The cytotoxicity of the disulfide n-butyl 2-imidazolyl disulfide (III-2) was determined to be the result of a disruption in the cellular redox state and inhibition of critical membrane enzymes. These events cause perturbations in Ca2+ homeostasis, which may affect the cell signalling machinery and

Protein disulfide isomerase increases in myocardial endothelial cells in mice exposed to chronic hypoxia: a stimulatory role in angiogenesis.

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Previous studies have shown that exposure to chronic hypoxia protects against myocardial infarction, but little is known about the cellular and molecular mechanisms involved. Here we observed that chronic hypoxia for 3 wk resulted in improved survival of mice (from 64% to 83%), reduced infarction

Up-regulation of protein-disulfide isomerase in response to hypoxia/brain ischemia and its protective effect against apoptotic cell death.

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We isolated and identified a stress protein that is up-regulated in response to hypoxia in primary-cultured glial cells. Protein-disulfide isomerase (PDI) was up-regulated not only by hypoxia in glia in vitro, but also by transient forebrain ischemia in rats in vivo. To determine whether newly

Ero1-L alpha plays a key role in a HIF-1-mediated pathway to improve disulfide bond formation and VEGF secretion under hypoxia: implication for cancer.

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Oxygen is the ultimate source of oxidizing power for disulfide bond formation, suggesting that under limiting oxygen proper protein folding might be compromised. We show that secretion of vascular endothelial growth factor (VEGF), a protein with multiple disulfide bonds, was indeed impeded under

A new disulfide-linked dimer of a single-chain antibody fragment against human CD47 induces apoptosis in lymphoid malignant cells via the hypoxia inducible factor-1α pathway.

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CD47 belongs to the immunoglobulin superfamily and is associated with β-integrins. Recently it was reported that CD47 ligation rapidly induces apoptosis in B-chronic lymphocytic leukemia (CLL) cells. Chronic lymphocytic leukemia is still an incurable hematological malignancy even with the novel

Carbonic anhydrase inhibitors: Hypoxia-activatable sulfonamides incorporating disulfide bonds that target the tumor-associated isoform IX.

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An approach for designing bioreductive, hypoxia-activatable carbonic anhydrase (CA, EC 4.2.1.1) inhibitors targeting the tumor-associated isoforms is reported. Sulfonamides incorporating 3,3'-dithiodipropionamide/2,2'-dithiodibenzamido moieties were prepared and reduced enzymatically/chemically in

The thioredoxin redox inhibitors 1-methylpropyl 2-imidazolyl disulfide and pleurotin inhibit hypoxia-induced factor 1alpha and vascular endothelial growth factor formation.

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Hypoxia-inducible factor-1 (HIF-1) is a transcription factor that plays a critical role in tumor growth by increasing resistance to apoptosis and the production of angiogenic factors such as vascular endothelial growth factor (VEGF). HIF-1 is a heterodimer comprised of oxygen-regulated HIF-1alpha

Maternal serum thiol/disulfide homeostasis in pregnancies complicated by fetal hypoxia.

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We aimed to evaluate maternal serum thiol/disulphide homeostasis in pregnancies complicated by fetal distress (FD). A total of 100 patients beyond the 34th week of pregnancy were included in this study, and they were divided into two groups. The study group included 50 patients who had been

Intramolecular disulfide bond between catalytic cysteines in an intein precursor.

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Protein splicing is a self-catalyzed and spontaneous post-translational process in which inteins excise themselves out of precursor proteins while the exteins are ligated together. We report the first discovery of an intramolecular disulfide bond between the two active-site cysteines, Cys1 and

A redox-activatable biopolymer-based micelle for sequentially enhanced mitochondria-targeted photodynamic therapy and hypoxia-dependent chemotherapy

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A tumor redox-activatable micellar nanoplatform based on the naturally occurring biomacromolecule hyaluronic acid (HA) was developed for complementary photodynamic/chemotherapy against CD44-positive tumors. Here HA was first conjugated with l-carnitine (Lc)-modified zinc phthalocyanine (ZnPc) via

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