The Hypoxia Tolerance of the Goldfish (Carassius auratus) Heart: The NOS/NO System and Beyond

The extraordinary capacity of the goldfish (Carassius auratus) to increase its cardiac performance under acute hypoxia is crucial in ensuring adequate oxygen supply to tissues and organs. However, the underlying physiological mechanisms are not yet completely elucidated. By employing an ex vivo work...

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Bibliographic Details
Published in:Antioxidants 2020-06, Vol.9 (6), p.555
Main Authors: Filice, Mariacristina, Mazza, Rosa, Leo, Serena, Gattuso, Alfonsina, Cerra, Maria Carmela, Imbrogno, Sandra
Format: Article
Language:English
Subjects:
1-Phosphatidylinositol 3-kinase
AKT protein
Anoxia
Biotin
Ca2+-transporting ATPase
Calcium (reticular)
Carassius auratus
cGMP
CYBB protein
Cyclic GMP
Endoplasmic reticulum
Enzyme-linked immunosorbent assay
Experiments
Goldfish
Health aspects
Heart
Hypoxia
Kinases
Laboratory animals
Muscle contraction
myocardial performance
NAD(P)H oxidase
Nitration
Nitric oxide
Nitric-oxide synthase
nitrosative signals
Nox2
Physiological aspects
Physiology
Protein S
Proteins
SERCA2a
Thapsigargin
Western blotting
Wortmannin
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Summary:The extraordinary capacity of the goldfish (Carassius auratus) to increase its cardiac performance under acute hypoxia is crucial in ensuring adequate oxygen supply to tissues and organs. However, the underlying physiological mechanisms are not yet completely elucidated. By employing an ex vivo working heart preparation, we observed that the time-dependent enhancement of contractility, distinctive of the hypoxic goldfish heart, is abolished by the Nitric Oxide Synthase (NOS) antagonist L-NMMA, the Nitric Oxide (NO) scavenger PTIO, as well as by the PI3-kinase (PI3-K) and sarco/endoplasmic reticulum Ca2+-ATPase 2a (SERCA2a) pumps’ inhibition by Wortmannin and Thapsigargin, respectively. In goldfish hearts exposed to hypoxia, an ELISA test revealed no changes in cGMP levels, while Western Blotting analysis showed an enhanced expression of the phosphorylated protein kinase B (pAkt) and of the NADPH oxidase catalytic subunit Nox2 (gp91phox). A significant decrease of protein S-nitrosylation was observed by Biotin Switch assay in hypoxic hearts. Results suggest a role for a PI3-K/Akt-mediated activation of the NOS-dependent NO production, and SERCA2a pumps in the mechanisms conferring benefits to the goldfish heart under hypoxia. They also propose protein denitrosylation, and the possibility of nitration, as parallel intracellular events.
ISSN:2076-3921
2076-3921
DOI:10.3390/antiox9060555