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Nitrogen excretion and oxygen consumption under severe hypoxia in s iluriform fishes from the A mazon

Bernd Pelster; Chris M. Wood; Adalberto Luis Val
Journal of Fish Biology · Vol. 108, Issue 3 · pp. 881-893 · 2026

Abstract

Siluriform fishes collected from the Rio Negro and Rio Solimões proved to be highly resistant to aquatic hypoxia. In all four species analysed in this study, aquatic oxygen consumption significantly decreased from normoxic levels at water PO 2 values near 1 kPa. Air‐breathing activity was observed only in Sturisoma sp. (Rio Negro). In this species, under severe hypoxia, oxygen uptake from the air dominated, but total oxygen uptake was significantly lower than that under normoxic conditions. In Anadoras weddellii (Rio Solimões), aquatic surface respiration was detected. However, the other species ( Tympanopleura atronasus and three members of the family of Sternopygidae; Rio Solimões) showed no attempt to supplement aquatic oxygen uptake, even under severe hypoxia. In all species tested, neither ammonia nor urea‐N excretion was affected by the decreasing water PO 2 . At the lowest water PO 2 levels, the reduction in total oxygen uptake in the face of unchanged nitrogenous waste excretion resulted in extraordinary high nitrogen quotient (NQ) ratios. In normoxia, NQ ratios ranged from 0.16 to 0.34. Urea‐N excretion contributed between 19% and 28% to total nitrogen excretion and appeared to be unrelated to natural diet as indicated by the gut length‐to‐fork length ratio or to plasma urea‐N levels. Overall, our data underline the quantitative importance of urea‐N for nitrogen excretion in siluriform fishes.

Bibliographic Information

JournalJournal of Fish Biology
PublisherWiley
Publication Date2026-03-01
Publication Year2026
Volume108
Issue3
Pages881-893
Document TypeJournal Article
Print ISSN0022-1112
eISSN1095-8649
DOI10.1111/jfb.70022
SubjectGeneral Aquaculture, Fisheries & Fish Science

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NARA Access Coverage1997-01-01~Current
Journal Homepagehttps://onlinelibrary.wiley.com/loi/10958649
Publisher PageOpen Publisher Page
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