Abstract
The cyto-nephrotoxicity in fishes induced by dyes is a global issue. Fluorescein dye has a wide range of applications in industry and biological laboratories. In vivo experiment was planned to assess the sublethal effects of Fluorescein dye, Eosin Y, and Eosin B in Labeo rohita. This freshwater fish was exposed to increasing concentrations (0.0011, 0.0023, and 0.0047 mg/L) of both dyes in the aquarium for definite time intervals. A dye-free trial was set as a control. Fish was anesthetized and dissected by cutting on the ventral side to remove a kidney. Cyto-nephrotoxicity was detected through histopathology. The fish's significant mortality was observed when exposed to 0.0023 mg/L (LC50) and 0.0047 mg/L concentration of Eosin Y dye. These trial groups showed many kidney tissues alterations such as glomerular, tubular epithelial cell's degeneration, a reduced lumen of tubules, vacuolation, absence of bowmen's space, necrosis, glomerulonephritis with increased per tubular space, shrinking of the glomerulus, congestion, clogging, and degeneration of tubules. Eosin B showed less mortality and tissue damage, including glomerular contraction and increased space between glomerulus and capsule. ANOVA showed a highly significant reduction in weight gain of fish at different treatments levels of Eosin Y, but less or none in the case of Eosin B. Increase in fish weight was found to be 66.3 +/- 0.38 g when exposed to Eosin Y at 0.0047 mg/L, but it was 69.05 +/- 0.63 g when exposed to Eosin B while it was almost identical 69.2 +/- 0.23 g for both dye-free trial groups. The pair-wise comparison showed that exposure of the Eosin Y at treatment level 0.0047 mg/L was found to be highly toxic for the kidneys of Labeo rohita. Although both classes of dye are cytotoxic at small concentrations, Eosin Y is acute cyto-nephrotoxic and was found to be involved in growth retardation. To prevent society from fatal consequences, usage of dyes having acute toxicity must be banned or switched to alternates having no effects. (C) 2021 The Author(s). Published by Elsevier B.V. on behalf of King Saud University.