Hepatic damage associated with fatal zinc phosphide poisoning in broiler chicks

Abstract

Zinc phosphide (Zn₃P₂) is a widely used rodenticide which has the potential to cause high mortality if ingested. The present study was designed in order to explore the hepatic injury in broiler chicks that were acutely intoxicated with Zn₃P₂. For this purpose, a total number of 12 broiler Saso chicks were divided into two equal groups. Birds of the first group were exposed to 300 ppm Zn₃P₂ via food. Hepatic damage of intoxicated birds was evaluated biochemically and histologically using the transmission electron microscope and subsequently compared with another healthy non-treated controls (second group). The serum activity of aspartate aminotransferase (AST) was significantly higher in those poisoned with Zn₃P₂, While, activities of both Alanine aminotransferase (ALT) and Alkaline phosphatase (ALP), as well as, zinc concentration of hepatic tissue did not represented a significant difference between treated and control birds. Histological examination revealed presence of numerous heterogenic shaped mitochondria in hepatocytes of non-treated birds. Glycogen deposits were also scattered in the form of large electron dense deposits. Kupffer cell was irregular in shape and had numerous pseudopods often projected into sinusoidal lumen. In hepatic cells of intoxicated birds, mitochondrial swelling with cristolysis, few glycogen deposits, vacuoles in the cytoplasm and shrunken darkly stained nuclei are the major ultra-structural changes which were detected. It was concluded that the mitochondria could be one of the main target in hepatocytes for the toxic effect of Zn₃P₂ in broiler chicks.

Keywords: Chicks; Electron microscope; Liver; Zinc phosphide.

Fig. 1

Transmission electron micrograph of the chick’s hepatocyte in control group showing mitochondria (M), rough endoplasmic reticulum (r), glycogen (G), nucleus (N), microvilli (v) and endothelial cell (E). (x2000).

Fig. 2

Higher magnification of control hepatocytes showing several shapes of mitochondria (M), cristae (arrows) rough endoplasmic reticulum (r) and glycogen (G). (×5000).

Fig. 3

Electron micrograph of chick’s liver in control group showing hepatocytes (H), mitochondria (M), glycogen (G), kupffer cell (K), erythrocyte (T), endothelial cell (E), lysosomes (L) and lysosomes with electron dense content (arrows) (×2500).

Fig. 4

Transmission electron micrograph of the hepatocyte of chicks intoxicated by zinc phosphide showing swollen mitochondria (M), vacuoles (O), nucleus (N), eryrhrocytes (arrow), intercalated cell (Int) and kupffer cell (K) (×1000).

Fig. 5

Higher magnification of intoxicated hepatocyte showing swollen mitochondria (M), cristolysis (arrow), flocculant material (asterisk), dilated rough endoplasmic reticulum (r), glycogen (G), vacuoles (O) and nucleus (N) (×3000).

Fig. 6

Another electron micrograph of the hepatocyte of chicks treated with zinc phosphide showing swollen mitochondria (M), vacuoles (O), erythrocyte (T) and shrunken nucleus (N) and absence of microvilli in sinusoids (arrow head) (×2000).