# Crude extract of cyanobacterium (Radiocystis fernandoi) triggers primary osmoregulatory impairment in the gills of nile tilapia (Oreochromis niloticus)

## TL;DR

A cyanobacterium extract harms the gills of Nile tilapia by disrupting osmoregulation and causing structural damage, even without liver toxicity.

## Contribution

This study reveals acute gill toxicity from waterborne exposure to a cyanobacterial extract containing MC-RR and MC-YR in Nile tilapia.

## Key findings

- Gill osmoregulation was impaired, with decreased plasma chloride and epithelial disruption.
- Mucous cell proliferation and pillar cell changes occurred after 12 and 96 hours of exposure.
- No hepatotoxicity was observed despite gill structural and functional damage.

## Abstract

Eutrophication, driven by microalgae proliferation, promotes the production of microcystins (MC), posing global risks to the environment and public health. In Brazil, the species Radiocystis fernandoi commonly produces variants such as MC-RR and MC-YR. However, most toxicological studies still emphasize the isolated hepatoxicity of the MC-LR variant, with limited data on the toxicity of other variants or water exposure of the entire cellular contents released during cyanobacterial lysis. This study assessed acute (12 h and 96 h) effects of waterborne exposure to a crude extract (CE) of R. fernandoi R28 containing MC-RR and YR mostly (10 µg MC-LReq L⁻¹) on juvenile Oreochromis niloticus, focusing on gill osmoregulation and gill and liver tissue integrity. Gill alterations included mucous cell proliferation (12 h) and epithelial disruption with pillar cell changes (96 h), increasing the organ index at 96 h. Plasma chloride decreased at both times, accompanied by a transient rise in branchial carbonic anhydrase activity and lamellar ionocyte abundance at 12 h. Hepatic phosphatase PP1/PP2A, plasmatic acid phosphatase, plasmatic alkaline phosphatase and liver histology remained unaffected. These results show that aqueous exposure to R. fernandoi CE induces acute osmoregulatory impairment, potential disturbances in acid–base regulation, and structural damage in the gills of O. niloticus, even without evident hepatotoxicity. This highlights the gills as a relevant target for less-studied MC congeners and emphasizes the toxicological risks associated with waterborne exposure in eutrophic environments.