Rhodamine-B induces amyotrophic lateral sclerosis symptoms like -behaviours in zebrafish.

Rhodamine B (RhB), often misused as a food adulterant, accumulates in the brain, causing oxidative stress and neurodegeneration. However, its detrimental effects on molecular mechanisms still require further investigation. The zebrafish is a model organism for studying neurodegeneration and neuropathology. We aimed to investigate the impacts of RhB on neuro-molecular and behaviours in Adult male zebrafish. Zebrafish were exposed to varying RhB concentrations of 0.25, 0.5, 1.0 μM and Rotenone (RoT) of 0.5 μM for 21 days. Behavioural assessments, including the mirror test, shoal preference test, T-maze and Y-maze tests, and novel tank test, were conducted to evaluate the impact of RhB on zebrafish behaviour. Furthermore, biochemical, neurochemical, and histopathological changes in the zebrafish brains were analysed. The neuronal behaviour patterns, such as reduced anxiety-like behaviour, time spent near or interacting with the mirror image, and cognitive dysfunction, were significantly affected by RhB in a time-dose-dependent manner when compared to those of control zebrafish. The glutathione reductase, catalase, lipid peroxidation, and reactive oxygen species levels were significantly increased, and acetylcholinesterase, glutathione peroxidase, superoxide dismutase, butyrylcholinesterase, serotonin, dopamine, and monoamine oxidase A and B were significantly reduced when exposed to RhB, when compared to those of control zebrafish. The C9orf72, btg2, fus, cfos, vgf, drd1b, npas4a, egr1, pax6a, vgf, ubb, atxn2, ier2a, tradbpa, tuba812 and grin1a mRNA levels were significantly upregulated. At the same time, sod1, bdnf, gabra1, and gabra2a were significantly down-regulated in the brain of RhB-exposed zebrafish compared to the control fish. These results suggested that RhB exposure can induce neurodegeneration in zebrafish mimicking Amyotrophic Lateral Sclerosis (ALS).