Ferrous Iron Overload Evokes Thyroidal and Interrenal Activation, Shifts Metabolite Pattern and Reverses Hepatic Ion Transporter Activities in Salinity-Acclimated Air-Breathing Fish (Anabas testudineus) Bloch

Aquatic ecosystems are vulnerable to excess iron load as it can cause direct or indirect effect on lotic organisms by disturbing the normal metabolism and osmoregulation. Furthermore, higher iron availability in water could also lead to endocrine disruption in fishes. However, the impact of iron ove...

Full description

Saved in:
Bibliographic Details
Published in:Proceedings of the Zoological Society Vol. 74; no. 4; pp. 605 - 616
Main Authors: Gayathry, R., Peter, Valsa S., Peter, M. C. Subhash
Format: Journal Article Conference Proceeding
Language:English
Published: New Delhi Springer India 01-12-2021
Springer Nature B.V
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Aquatic ecosystems are vulnerable to excess iron load as it can cause direct or indirect effect on lotic organisms by disturbing the normal metabolism and osmoregulation. Furthermore, higher iron availability in water could also lead to endocrine disruption in fishes. However, the impact of iron overload on thyroidal and interrenal axes has not yet known in fishes particularly in salinity-acclimated fishes. We thus investigated the effects of in vivo ferrous iron on thyroid hormone and cortisol dynamics, metabolite pattern and hepatic ion transport status in Freshwater (FW) and Salinity-acclimated (SA) climbing perch, Anabas testudineus Bloch to identify the impact of iron overload on thyroidal and internal axes in salinity-acclimated fish. Exposure of Fe (II) iron exposure (FeSO 4 of 10 3 and 10 4  µg L −1 for 48 h) disrupted thyroid and interrenal axes in fish kept in dilute seawater (20 ppt for three weeks) as evident in the rise of T 4 and cortisol, though Fe(II) iron exposure had little influence on these hormones in FW fish. Both FW and SA fish, which were kept for 24 h and 96 h recovery after a pre-exposure of Fe (II) iron for 48 h, produced little impact on plasma T 3 , T 4 and cortisol levels except a rise in T 4 that occurred in SA fish after a recovery of 24 h. A shift in metabolite pattern occurred in SA fish after 24 and 96 h recovery due to reversal of plasma glucose, lactate and urea levels. Iron exposure lowered Na + /K + -ATPase and Mg 2+ -ATPase activities in the liver of SA fish but showed reversed activities when kept for 96 h recovery. Further, we found a differential sensitivity of FW and SA fish to Fe(II) iron exposure as evident in the activity pattern of H + /K + -ATPase, mCa 2+ ATPase and vH + -ATPase in the liver. Overall, our data indicate that Fe (II) iron loading can activate thyroid and interrenal axes, shift plasma metabolite pattern and reverse hepatic ion transporter function in salinity-acclimated climbing perch, thus presenting evidence for an iron-induced endocrine disruption in salinity-acclimated fish.
ISSN:0373-5893
0974-6919
DOI:10.1007/s12595-021-00420-3