Departamento de Química, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.
Pathol Res Pract. 2011 Sep 15;207(9):554-8. doi: 10.1016/j.prp.2011.06.005.
Sepsis is a potentially deadly complication that can be caused by different factors. Actually, it is known that oxidative stress is involved in the pathogenesis of sepsis. Thus, the aim of this study was to evaluate the effect of diphenyl diselenide (PhSe)(2), an emergent compound, on oxidative stress parameters induced by sepsis in rats. Animals were pre-injected with (PhSe)(2) or vehicle. Twenty-four hours later, sepsis was induced by cecal ligation puncture (CLP). After 12 h, liver was taken for thiobarbituric acid reactive species (TBARS) measurement, δ-aminolevunic acid dehydratase (δ-ALA-D), Cu/Zn superoxide dismutase (Cu/Zn SOD) and catalase (CAT) activities assay. The sepsis increased TBARS, inhibited δ-ALA-D, activated Cu/Zn SOD and had a tendency to decrease CAT activity. However, (PhSe)(2) prevented the TBARS formation, but did not prevent the inhibition of δ-ALA-D activity in the animals with damage. Thus, this study showed that (PhSe)(2) partially prevents the oxidative stress induced by sepsis, indicating the potential of this compound as a treatment for this pathology. Nevertheless, more tests should be performed to confirm the hypothesis suggested here.
败血症是一种潜在的致命并发症，可能由不同的因素引起。实际上，已知氧化应激与败血症的发病机制有关。因此，本研究旨在评估二苯二硒（PhSe）（2），一种新兴化合物，对败血症大鼠氧化应激参数的影响。动物预先注射（PhSe）（2）或载体。24 小时后，通过盲肠结扎穿刺（CLP）诱导败血症。12 小时后，取肝进行硫代巴比妥酸反应性物质（TBARS）测量、δ-氨基酮戊酸脱水酶（δ-ALA-D）、铜/锌超氧化物歧化酶（Cu/Zn SOD）和过氧化氢酶（CAT）活性测定。败血症增加了 TBARS，抑制了 δ-ALA-D，激活了 Cu/Zn SOD，并倾向于降低 CAT 活性。然而，（PhSe）（2）可防止 TBARS 的形成，但不能防止损伤动物中 δ-ALA-D 活性的抑制。因此，本研究表明，（PhSe）（2）部分预防了败血症引起的氧化应激，表明该化合物作为该病理治疗的潜力。然而，应该进行更多的测试来证实这里提出的假设。
