Regulation of dual oxidase hydrogen peroxide synthesis results in an epithelial respiratory burst
| Autor: | Gregory E. Conner |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Medicine (General) Antioxidant QH301-705.5 medicine.medical_treatment Short Communication Cell redox status Clinical Biochemistry Cellular homeostasis Biochemistry Redox NHBE normal human bronchial epithelia 03 medical and health sciences Duox 0302 clinical medicine R5-920 medicine Biology (General) Respiratory Burst Oxidase test NADPH oxidase biology Chemistry Organic Chemistry HRP horseradish peroxidase Peroxiredoxins Hydrogen peroxide Dual Oxidases Cell biology Respiratory burst 030104 developmental biology biology.protein Thioredoxin Peroxiredoxin Oxidation-Reduction 030217 neurology & neurosurgery |
| Zdroj: | Redox Biology, Vol 41, Iss, Pp 101931-(2021) Redox Biology |
| ISSN: | 2213-2317 |
| Popis: | Redox status is a central determinant of cellular activities and redox imbalance is correlated with numerous diseases. NADPH oxidase activity results in formation of H2O2, that, in turn, sets cellular redox status, a key regulator of cellular homeostasis and responses to external stimuli. Hydrogen peroxide metabolism regulates cell redox status by driving changes in protein cysteine oxidation often via cycling of thioredoxin/peroxiredoxin and glutathione; however, regulation of enzymes controlling synthesis and utilization of H2O2 is not understood beyond broad outlines. The data presented here show that calcium-stimulated epithelial Duox H2O2 synthesis is transient, independent of intracellular calcium renormalization, H2O2 scavenging by antioxidant enzymes, or substrate depletion. The data support existence of a separate mechanism that restricts epithelial H2O2 synthesis to a burst and prevents harmful changes in redox tone following continuous stimulation. Elucidation of this H2O2 synthesis tempering mechanism is key to understanding cellular redox regulation and control of downstream effectors, and this observation provides a starting point for investigation of the mechanism that controls H2O2-mediated increases in redox tone. Graphical abstract Image 1 Highlights • DUOX1 and DUOX2 H2O2 synthesis decreases after calcium stimulation even in the continued presence of elevated calcium. • Decreasing DUOX1 and DUOX2 activity in elevated calcium is not due to substrate depletion or assay limitations. • Calcium activation of DUOX1 and DUOX2 H2O2 synthesis results in a respiratory burst independent of calcium renormalization. • The data support a mechanism that limits Duox H2O2 synthesis in the presence of continually elevated calcium stimulation. |
| Databáze: | OpenAIRE |
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