Publication Date:
2020-06-19
Description:
The free radical nitric oxide (NO) is a powerful metabolic regulator in vertebrates and invertebrates.
At cellular concentrations in the nanomolar range, and simultaneously reduced
internal oxygen partial pressures (pO2), NO completely inhibits cytochrome-c-oxidase
(CytOx) activity and hence mitochondrial- and whole-tissue respiration. The infaunal clam
Arctica islandica regulates pO2 of hemolymph and mantle cavity water to mean values of 〈5
kPa, even in a completely oxygen-saturated environment of 21 kPa. These low internal pO2
values support a longer NO lifespan and NO accumulation in the body fluids and can thus
trigger a depression of metabolic rate in the clams. Measurable amounts of NO formation
were detected in hemocyte cells (~110 pmol NO 100−1 hemocytes h-1 at 6 kPa), which was
not prevented in the presence of the NO synthase inhibitor L-NAME, and in the gill filaments
of A. islandica. Adding a NO donor to intact gills and tissue homogenate significantly inhibited
gill respiration and CytOx activity below 10 kPa. Meanwhile, the addition of the NO-oxidation
product nitrite did not affect metabolic rates. The high nitrite levels found in the
hemolymph of experimental mussels under anoxia do not indicate cellular NO production,
but could be an indication of nitrate reduction by facultative anaerobic bacteria associated
with tissue and/or hemolymph biofilms. Our results suggest that NO plays an important role
in the initiation of metabolic depression during self-induced burrowing and shell closure of A.
islandica. Furthermore, NO appears to reduce mitochondrial oxygen radical formation during
surfacing and cellular reoxygenation after prolonged periods of hypoxia and anoxia.
Repository Name:
EPIC Alfred Wegener Institut
Type:
Article
,
isiRev
,
info:eu-repo/semantics/article
Format:
application/pdf
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