scholarly journals Roles of nitric oxide, nitrite and myoglobin on myocardial efficiency in trout (Oncorhynchus mykiss) and goldfish (Carassius auratus): implications for hypoxia tolerance

2010 ◽  
Vol 213 (16) ◽  
pp. 2755-2762 ◽  
Author(s):  
C. L. Pedersen ◽  
S. Faggiano ◽  
S. Helbo ◽  
H. Gesser ◽  
A. Fago
Keyword(s):  
Nitric Oxide ◽  
Oncorhynchus Mykiss ◽  
Carassius Auratus ◽  
Hypoxia Tolerance ◽  
Goldfish Carassius Auratus ◽  
Myocardial Efficiency

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

Antioxidants ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 555 ◽  
Author(s):  
Mariacristina Filice ◽  
Rosa Mazza ◽  
Serena Leo ◽  
Alfonsina Gattuso ◽  
Maria Carmela Cerra ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Carassius Auratus ◽  
Ex Vivo ◽  
Acute Hypoxia ◽  
Protein S ◽  
Elisa Test ◽  
Hypoxia Tolerance ◽  
No Production ◽  
Goldfish Carassius Auratus ◽  
Enhanced Expression

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.

Action of adenosine on energetics, protein synthesis and K(+) homeostasis in teleost hepatocytes

2000 ◽  
Vol 203 (17) ◽  
pp. 2657-2665 ◽  
Author(s):  
G. Krumschnabel ◽  
C. Biasi ◽  
W. Wieser
Keyword(s):  
Protein Synthesis ◽  
Oxygen Consumption ◽  
Atpase Activity ◽  
Oncorhynchus Mykiss ◽  
Carassius Auratus ◽  
Goldfish Carassius Auratus ◽  
Inhibition Of Protein Synthesis ◽  
Rate Of Oxygen Consumption ◽  
A1 Receptor ◽  
Lactate Formation

In a comparative study, we analysed the effects of adenosine on the energetics, protein synthesis and K(+)homeostasis of hepatocytes from the anoxia-tolerant goldfish Carassius auratus and the anoxia-intolerant trout Oncorhynchus mykiss. The rate of oxygen consumption did not respond immediately to the addition of adenosine to the cells from either species, but showed a significant decrease in trout hepatocytes after 30 min. The anaerobic rate of lactate formation was not significantly affected by adenosine in goldfish hepatocytes, but was increased in trout cells. We also studied the effects of adenosine on the two most prominent ATP consumers in these cells, protein synthesis and Na(+)/K(+)-ATPase activity. Under aerobic conditions, adenosine inhibited protein synthesis of hepatocytes from goldfish by 51% and of hepatocytes from trout by 32%. During anoxia, the rate of protein synthesis decreased by approximately 50% in goldfish hepatocytes and by 90% in trout hepatocytes, and this decrease was not altered by the presence of adenosine. Adenosine inhibited normoxic Na(+)/K(+)-ATPase activity and K(+)efflux by 20–35% in the cells of both species. An investigation into the mechanism underlying the inhibition of protein synthesis by adenosine indicated that, in the goldfish cells, adenosine acts via a membrane receptor-mediated pathway, i.e. the effect of adenosine was abolished by applying the A1 receptor antagonist 8-phenyltheophylline. In the trout, however, the uptake of adenosine into hepatocytes seems to be required for an effect on protein synthesis. [Ca(2+)](i) does not seem to be involved in the inhibition of protein synthesis by adenosine.

The relationship between responsiveness and elusiveness of heat-shocked goldfish (Carassius auratus) to attacks by rainbow trout (Oncorhynchus mykiss)

1994 ◽  
Vol 72 (3) ◽  
pp. 423-426 ◽  
Author(s):  
Paul W. Webb ◽  
Hongbao Zhang
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Carassius Auratus ◽  
Prey Capture ◽  
Acclimation Temperature ◽  
Escape Velocity ◽  
Reaction Distance ◽  
Goldfish Carassius Auratus ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
The Relationship

We measured reaction distance, escape velocity, and the apparent looming threshold (ALT) of heat-shocked goldfish (Carassius auratus) attacked by trout (Oncorhynchus mykiss). We tested fish at the acclimation temperature of 15 °C after heat-shocking prey for 2 min at temperatures ranging from 34 to 39 °C. Escape speeds were unaffected by heat shock. Reaction distance decreased from about 21 cm for fish shocked at 35 °C to about 6 cm for those shocked at 39 °C. ALT increased from 0.2 rad∙s−1 for controls to 0.4 rad∙s−1 for goldfish heat-shocked at 39 °C. The elusiveness of prey, E, was measured as the number of attacks required per prey capture. E was related to ALT as: E = 1.29 (±0.47)∙ALT−0.82(±0.25) (mean (±2 SE)). Factors that decrease responsiveness of prey have large effects on the ability of prey to avoid predators.

scholarly journals Mitochondrial KATP channels stabilize intracellular Ca2+ during hypoxia in retinal horizontal cells of goldfish (Carassius auratus)

2021 ◽  
Author(s):  
Michael W. Country ◽  
Michael G. Jonz
Keyword(s):  
Carassius Auratus ◽  
Katp Channels ◽  
Horizontal Cells ◽  
Hypoxia Tolerance ◽  
Dependent Manner ◽  
Cellular Mechanisms ◽  
Atp Production ◽  
Goldfish Carassius Auratus ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Mitochondrial Katp Channels

Neurons of the retina require oxygen to survive. In hypoxia, neuronal ATP production is impaired, ATP-dependent ion pumping is reduced, transmembrane ion gradients are dysregulated, and [Ca2+]i increases enough to trigger excitotoxic cell death. Central neurons of the common goldfish (Carassius auratus) are hypoxia-tolerant, but little is known about how goldfish retinas withstand hypoxia. To study the cellular mechanisms of hypoxia tolerance, we isolated retinal interneurons (horizontal cells; HCs), and measured intracellular Ca2+ concentration ([Ca2+]i) with Fura-2. Goldfish HCs maintained [Ca2+]i throughout 1 h of hypoxia, whereas [Ca2+]i increased irreversibly in HCs of the hypoxia-sensitive rainbow trout (Oncorhynchus mykiss) with just 20 min of hypoxia. Our results suggest mitochondrial ATP-dependent K+ channels (mKATP) are necessary to stabilize [Ca2+]i throughout hypoxia. In goldfish HCs, [Ca2+]i increased when mKATP was blocked with glibenclamide or 5-HD, whereas an mKATP agonist (diazoxide) prevented [Ca2+]i from increasing in hypoxia in trout HCs. We showed that hypoxia protects goldfish HCs via mKATP channels. Glycolytic inhibition with 2-deoxyglucose increased [Ca2+]i, which was rescued by hypoxia in an mKATP-dependent manner. We found no evidence of plasmalemmal KATP channels in patch-clamp experiments. Instead, we confirmed the involvement of KATP in mitochondria with TMRE imaging, as hypoxia rapidly (<5 min) depolarized mitochondria in an mKATP-sensitive manner. We conclude that mKATP channels initiate a neuroprotective pathway in goldfish HCs to maintain [Ca2+]i and avoid excitotoxicity in hypoxia. This model provides novel insight into the cellular mechanisms of hypoxia tolerance in the retina.

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