Laboratório de Síntese, Reatividade e Avaliação Farmacológica e Toxicológica de Organocalcogênios, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, CEP 97105-900, RS, Brazil.
Fundam Clin Pharmacol. 2011 Feb;25(1):80-90. doi: 10.1111/j.1472-8206.2010.00813.x.
The in vitro effect of (E)-2-benzylidene-4-phenyl-1,3-diselenole (BPD) was evaluated through iron/EDTA-induced thiobarbituric acid reactive species (TBARS) and reactive species (RS) determinations as well as of the scavenging 2,2'-diphenyl-1-picrylhydrazyl (DPPH) radical quantification. BPD at the concentrations of 10 and 50 μΜ decreased RS and TBARS levels, respectively. The antioxidant activity was not related to the scavenging DPPH radical mechanism. A second objective of this study was to investigate the hepatoprotective action of BPD, administered by oral route, against oxidative damage induced by 2-nitropropane (2-NP) (100 mg/kg of body weight) in liver of rats. At the dose of 50 mg/kg, BPD protected against the increase in aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) activities induced by 2-NP. BPD (10 and 50 mg/kg) protected against the increase in TBARS levels and alkaline phosphatase (ALP) activity. Sections of liver from 2-NP-exposed rats presented intense infiltration of inflammatory cells and loss of cellular architecture. BPD (10 and 50 mg/kg) attenuated 2-NP-induced hepatic histological alterations. The inhibition of δ-aminolevulinic dehydratase (δ-ALA-D), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione S-transferase (GST) activities and the decreased GSH levels caused by 2-NP were protected by BPD (50 mg/kg). Catalase activity and ascorbic acid levels were not altered by 2-NP. These results demonstrated the antioxidant and hepatoprotective effects of BPD in liver of rats.
（E）-2-苄基-4-苯基-1,3-二硒杂环戊烯（BPD）的体外效应通过铁/EDTA 诱导的硫代巴比妥酸反应性物质（TBARS）和反应性物质（RS）测定以及 2,2'-二苯基-1-苦基肼（DPPH）自由基清除定量来评估。BPD 在 10 和 50 μM 的浓度下分别降低 RS 和 TBARS 水平。抗氧化活性与清除 DPPH 自由基机制无关。本研究的第二个目的是研究 BPD 通过口服途径对 2-硝基丙烷（2-NP）（100mg/kg 体重）诱导的大鼠肝脏氧化损伤的保护作用。在 50mg/kg 剂量下，BPD 可防止 2-NP 引起的天冬氨酸氨基转移酶（AST）、丙氨酸氨基转移酶（ALT）和乳酸脱氢酶（LDH）活性的增加。BPD（10 和 50mg/kg）可防止 TBARS 水平和碱性磷酸酶（ALP）活性的增加。暴露于 2-NP 的大鼠肝脏切片显示炎症细胞强烈浸润和细胞结构丧失。BPD（10 和 50mg/kg）减轻了 2-NP 诱导的肝组织学改变。BPD（50mg/kg）可抑制 δ-氨基酮戊酸脱水酶（δ-ALA-D）、谷胱甘肽过氧化物酶（GPx）、谷胱甘肽还原酶（GR）和谷胱甘肽 S-转移酶（GST）活性，并降低由 2-NP 引起的 GSH 水平。2-NP 未改变过氧化氢酶活性和抗坏血酸水平。这些结果表明 BPD 对大鼠肝脏具有抗氧化和保肝作用。
