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Antioxidant protection by β‐selenoamines against thioacetamide‐induced oxidative stress and hepatotoxicity in mice
Author(s) -
Stefanello Sílvio Terra,
Hartmann Diane Duarte,
Amaral Guilherme Pires,
Courtes Aline Alves,
Leite Martim T. B.,
da Silva Thayanara Cruz,
Gonçalves Débora Farina,
Souza Micaela B.,
da Rosa Pâmela Carvalho,
Dornelles Luciano,
Soares Félix Alexandre Antunes
Publication year - 2017
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.21974
Subject(s) - thioacetamide , oxidative stress , hepatotoxin , lipid peroxidation , chemistry , antioxidant , reactive oxygen species , pharmacology , glutathione , oxidative phosphorylation , biochemistry , intraperitoneal injection , enzyme , toxicity , biology , organic chemistry
Thioacetamide (TAA) is a hepatotoxin that rapidly triggers the necrotic process and oxidative stress in the liver. Nevertheless, organic selenium compounds, such as β‐selenoamines, can be used as pharmacological agents to diminish the oxidative damage. Thus, the aim of this study was to investigate the protective effect of the antioxidant β‐selenoamines on TAA‐induced oxidative stress in mice. Here, we observed that a single intraperitoneal injection of TAA (200 mg/kg) dramatically elevated some parameters of oxidative stress, such as lipid peroxidation and reactive oxygen species (ROS) production, as well as depleted cellular antioxidant defenses. In addition, TAA‐induced edema and morphological changes in the liver, which correlate with high serum aspartate and alanine aminotransferase enzyme activities, and a decrease in cell viability. Conversely, a significant reduction in liver lipid peroxidation, ROS production, and edema was observed in animals that received an intraperitoneal injection of β‐selenoamines (15.6 mg/kg) 1 h after TAA administration.