Low concentrations of sodium arsenite induce hepatotoxicity in prepubertal male rats

Arsenic (As) can contaminate air, soil, water, and organisms through mobilization of natural mineralogical deposits or anthropogenic actions. Inorganic‐As compounds are more toxic and widely available in aquatic environments, including drinking water reservoir catchments. Since little is known about...

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Veröffentlicht in:Environmental toxicology 2020-05, Vol.35 (5), p.553-560
Hauptverfasser: Samelo, Ricardo R., Cunha de Medeiros, Paloma, Carvalho Cavalcante, Deborah N., Aranha, Maria L. G., Duarte, Fabio A., Castro, Ítalo B., Ribeiro, Daniel A., Perobelli, Juliana E.
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Sprache:eng
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Zusammenfassung:Arsenic (As) can contaminate air, soil, water, and organisms through mobilization of natural mineralogical deposits or anthropogenic actions. Inorganic‐As compounds are more toxic and widely available in aquatic environments, including drinking water reservoir catchments. Since little is known about its effects on prepubertal mammals, the present study focused on it. Hence, As was administered through drinking water to male Wistar rats from postnatal day 23 to 53. Negative control group received vehicle only (filtered water); As 1 group received AsNaO2 at 0.01 mg L−1 and As2 group received AsNaO2 at 10 mg L−1. It was investigated hepatic and renal toxicity of AsNaO2 (ie, histopathology and apoptosis analysis), as well as its mutagenicity (ie, micronucleus test in liver and bone marrow), cytotoxicity (ie, frequency and type of erythrocytes in blood), and genotoxicity (ie, comet assay in blood). Also, As determination was performed in hepatic and renal tissues. Data obtained revealed that immature organisms present a pattern of arsenic accumulation similar to that observed in adults, suggesting similarity in metabolic processes. In addition, liver showed to be an important target tissue for As toxicity in these experimental conditions, exhibiting infiltrate of defense cells, DNA damages, and increased apoptosis rates.
ISSN:1520-4081
1522-7278
DOI:10.1002/tox.22890