Avaliação da toxicidade dos metais chumbo e ferro, em zebrafish (Danio rerio), com ênfase em achados clínico-patológicos

Abstract

Anthropogenic activities, such as mining, are associated with increased levels of metals in rivers. Studies have shown that the levels of the metals iron (Fe) and lead (Pb) in the water are elevated after the rupture of mining tailings dams. There is a need for studies on short and long term effects of these metals on fish. In the present study, the acute toxicity of the metals Pb and Fe was assessed in zebrafish (Danio rerio), with an emphasis on clinical and pathological findings. Concentrations of 0 (GCC); 0.46 (GC1); 1.02 (GC2); 2.24 (GC3) and 4.92 (GC4) mg / L of Pb and 0 (GFC); 2.66 (GF1); 5.86 (GF2); 12.88 (GF3) and 28.34 (GF4) mg/L of Fe, diluted in water were used. The experiments were designed as semi-static acute toxicity tests. Evaluations of clinical signs, mortality, anatomopathological lesions and complementary toxicological tests in the water and tissues of the fish were carried out. The clinical signs present in both trials were hypoactivity, abnormal distribution on the surface, sub-reactivity, abnormal distribution on the bottom, demotion behavior and changes in ventilatory functions. In the lead experiment, the 96h mortality was 33.3% in the 0,46 mg/L group, 41.7% in the 1,02 mg/L group, 75% in the 2,24 mg/L group and 91.7% in the 4,92 mg/L group. There were no deaths in the control group. The 96h LC50 in this experiment was 1.1 mg/L of Pb. No macroscopic lesions were observed, but histological lesions were present in the gills of all fish exposed to lead and two predominant patterns of lesions were described. The first pattern (pattern 1) consisted of marked necrosis of the secondary lamellae, with loss of lamellar organization, loss of secondary lamellae and marked accumulation of cellular debris in the interlamellar spaces. Fish with these lesions died spontaneously during the experiment. The other pattern (pattern 2) consisted of fragmentation of cells in the secondary lamella, with lamellar disorganization, epithelial hyperplasia, secondary lamella fusion and accumulation of cell debris between the lining epithelial cells. The fish with these lesions survived the 96h of experimentation, except for some fish from the 4,92 mg/L group that died spontaneously and had both lesion patterns. In the Fe experiment, mortality reached 100% in all experimental groups, except in the control group. Macroscopically, there was orange granular material on the surface of the fish's body and gills. Histologically, there was disorganization of the secondary branchial lamellae, associated with shedding, loss of the lining epithelium and accumulation of cell debris with iron precipitates in the interlamellar spaces. These precipitates were also observed in the oral cavity, stomach, and intestines. In the Prussian Blue reaction (Perls) there was confirmation of the precipitate of iron on the surface of the gills, oral cavity, stomach, and intestines. These findings occurred in all experimental groups, except the control. The present study contributed to the anatomopathological characterization of lead and iron toxicity in fish.