Toxicological impact of Zinc Nano Particles on tilapia fish (Oreochromis mossambicus)

Abstract

In this study we investigated the acute toxicity of Zinc Nano Particles (ZnO NPs) and bulk ZnO on tilapia fish (Oreochromis mossambicus). Oreochromis mossambicus was exposed to the different concentration of ZnO NPs, ZnO and mixed solution of both ZnO NPs and ZnO (20 ppb, 20 ppb, 20 ppb) respectively for 96 h. A very high impact was recorded in hematological parameters which shows significant increased (p < 0.05) in count of white WBCs and platelets in all the experimental groups compared tocontrol group. The count of RBCs, Hb, hematocrit and MCHC were significantly decreased. The remarkable changes which were recorded during this study were histopathological lesions in the gills of exposed fish including, disorganization of gill lamella, cartilaginous core disruption, lifting of epithelium, loss of secondary gill lamellae, blood congestion, fusion of secondary gills lamellae, shortening of secondary gills lamellae, atrophy and curling. Disassembly were seen in plasma membrane of liver along with blood congestion, pyknosis, necrosis, hyperplasia and formation of vacuoles. Intestinal alterations which were observed include shortening of villi, necrosis, detachment and fusion of villi and extreme goblet cells formation. It is concluded from the present study that high level of ZnO NPs, ZnO and mixed solution has a strong tendency to alter hematological parameters, histological architecture, therefore, the indiscriminate use of ZnO NPs and ZnO can subsidize in reducing the population of Oreochromis mossambicus in natural water bodies.

Keywords: Health parameters; Oreochromis mossambicus; Toxicity; Zinc Nano Particles.

Fig. 1

Hematological parameters of O. mossambicus exposed to ZnO and ZnO NPS. Mean with ** expresses significant difference (p < 0.05).

Fig. 2

Histopathological view of gills of control and experimental group I, II and III fish. A) Microscopic photograph shows the unaltered anatomy of Gill, B) Disruption of cartilaginous core (DC), Epithelial lifting (E), and loss of secondary gill lamellae (L), C) Fusion of secondary gills lamellae (F), Atrophy (A)Disruption of cartilaginous core (DC), Blood congestion (BC), D) Blood congestion (BC), Disruption of cartilaginous core (DC)and Atrophy (A).

Fig. 3

Histopathological view of liver of control and treated group fish. (A) Showing unalteredanatomy of hepatocytes. B) Blood congestion (BC), Pyknosis (P) & Dissolution of biological membrane, (DC), necrosis (N), lymphocytes infiltration (Li) and Vacuolations in the hepatocytes (V), C) Pyknosis (P), Vacuolations in the hepatocytes (V), Blood congestion (BC), necrosis(N) and dissolution of plasma membrane (DP), D)Vacuolations in the hepatocytes (V), Pyknosis (P)necrosis (N)lymphocytes infiltration (LI) and dissolution of plasma membrane (DP).

Fig. 4

Histopathological view of intestine of control and treated group I,II,III, A) Shows unaltered intestinal villi, B) Microscopic photograph shows Shortening of villi (SV), necrosis(N), fusion of villi (FV), Detachment of villi (DV), C) Development of Goblet cells in villi (G), rupturing of villi (RV), fusion of villi (F), necrosis (N), D) Detachment of villi (DV), shortening of villi (SV), appearance of Goblet cells (G) and disintegration of serosa (DS).