Short-term Exposure of Nile Tilapia (Oreochromis niloticus) to Mercury

Abstract

To investigate effects of short-term mercury (Hg) exposure in tilapia (Oreochromis niloticus) including histopathological changes, Hg bioaccumulation, and protective role of metallothionein (MT) in different exposure routes, adult tilapias were intraperitoneally injected, orally intubated, or semistatically exposed to 0.5, 1, 2, 5 mg/g mercuric chloride. Histopathology, autometallography (AMG), inductive coupled plasma-atomic emission spectrometry (ICP-AES), and MT immunohistochemistry were determined at 0, 3, 6, 9, 12, and 15 days postexposure. Microscopic lesions were observed in the kidney, hepatopancreas, spleen, and intestine. AMG positive grains were found in renal tubule epithelium, melanomacrophage centers (MMCs), and intestinal epithelium of treated tilapias. Hg concentrations measured by ICP-AES in abdominal visceral organs were significantly higher than in other organs. All exposure routes caused lesions of increasing severity and Hg accumulations in a dose-dependent manner. Semistatic groups produced the highest intensity of lesions, AMG positive staining, as well as total Hg concentrations. Positive MT expression in renal tubule epithelium, pancreatic acini, and splenic MMCs was observed only in semistatic groups. The semistatic exposure route demonstrated the most significant microscopic lesions, Hg bioaccumulation, and MT expression.

Pathogenicity of streptococcus agalactiae in oreochromis niloticus

“…A previous study showed that the liver becomes congested and edematous after infection [7]. In the present study, we also found lower fat vacuolation in the cytoplasm of hepatocytes, as observed in the liver after short-term mercury challenge [24]. After GBS infection, the Nile tilapia showed a loss of appetite, gastritis, and enteritis, leading to protein and energy break off.…”

Melanomacrophage centers in Clarias gariepinus as an immunological biomarker for toxicity of silver nanoparticles

“…Those alterations indicated apoptosis and degeneration of hepatocytes caused by the toxic action of NPs [ 26 ]. Alterations in spleen, kidney, and liver of Nile tilapia Oreochromis niloticus after exposure to mercury have been reported [ 27 ]. Kaewamatawong et al [ 27 ] reported similar alterations in kidney, spleen, and liver of O. niloticus after exposure to mercury, where they observed degeneration and massive necrosis in the kidney, degeneration of hepatocytes with vacuolization, and increased number of MMCs in the spleen in experimental fish compared to the controls.…”

“…Increases in the numbers and size of MMCs have been observed after environmental pollution [ 7 34 ], heavy metal contamination in fish [ 27 31 ], water quality [ 13 ], bacterial infection of fish [ 35 ], fish diseases [ 36 37 ], exposure to toxic plant extracts [ 16 ], after starvation [ 9 ], after exposure to potassium dichromate [ 18 ], fish ulcers [ 14 ], and fish parasites [ 38 ]. Usually, the increase in MMCs associated with histopathological alterations, indicating the oxidative stress that leads to aggregation of lymphocytes suggesting the immune response of MMCs [ 9 18 ].…”

A review of mercury pathological effects on organs specific of fishes

“…In the kidney, mercury exposure can cause inflammation [68], interstitial inflammation, bile duct hyperplasia, and necrosis in the kidney tissue [33]. Furthermore, tilapia that exposed to 2 mg/kg of HgCl 2 for 3 days was found with severe tubulonephrosis and the presence of hyaline droplets in the kidney tissue [69]. Changes in the structure of renal and glomerular were observed as glomeruli lesion, tubularnecrosis/hyalinization, interstitial mononuclear infiltrates, and multifocal melanomacrophage centers in goliath grouper exposed to MeHg with the average concentration of 2.87 ± 4.70 mg/kg [27].…”