Department of Zoology and Invertebrate Ecology, The John Paul II Catholic University of Lublin, Lublin, Poland.
Oxid Med Cell Longev. 2013;2013:802734. doi: 10.1155/2013/802734. Epub 2013 May 13.
The protective effect of magnesium as magnesium sulfate (MS) on sodium-metavanadate- (SMV-) induced lipid peroxidation (LPO) under in vivo and in vitro conditions was studied. The 18-week SMV intoxication (Group II, 0.125 V(end)/mL) enhanced spontaneous malondialdehyde (MDA) generation in rat liver, compared with the control (Group I) and MS-supplemented animals (Group III, 0.06 Mg(end)/mL). Coadministration of SMV with MS (Group IV, SMV-MS) caused a return of the MDA level to the control value range. The effect seems to result from the Mg(end)-independent action and its antagonistic interaction with V(end). The in vitro treatment of liver supernatants (LS) obtained from all the tested animals groups with selected exogenous concentrations of Fe(exg) or V(exg) exhibited enhanced MDA production, compared with spontaneously formed MDA. It also showed Mg(exg)-stimulating effect on LPO (LS I, Group I) and revealed that the changes in the MDA generation in LS IV (Group IV) might have resulted from the synergistic interactions of V(end) with Fe(exg) and V(exg) and from the antagonistic interactions of Mg(end) with Fe(exg) and V(exg). The findings allow a suggestion that adequate Mg intake for a specific period in the conditions of SMV exposure may prevent V-induced LPO in the liver.
在体内和体外条件下，研究了硫酸镁（MS）作为镁盐对五氧化二钒（SMV）诱导的脂质过氧化（LPO）的保护作用。与对照组（I 组）和补充 MS 的动物（III 组，0.06 Mg（end）/mL）相比，18 周 SMV 中毒（II 组，0.125 V（end）/mL）增强了大鼠肝脏中自发产生的丙二醛（MDA）。SMV 与 MS 共同给药（IV 组，SMV-MS）导致 MDA 水平恢复到对照值范围。这种作用似乎是由于 Mg（end）的非依赖性作用及其与 V（end）的拮抗相互作用所致。用选定的外源性 Fe（exg）或 V（exg）浓度体外处理从所有测试动物组获得的肝上清液（LS）与自发形成的 MDA 相比，MDA 产生增加。它还显示出 Mg（exg）对 LPO 的刺激作用（LS I，I 组），并表明 LS IV（IV 组）中 MDA 生成的变化可能是由于 V（end）与 Fe（exg）和 V（exg）的协同相互作用以及 Mg（end）与 Fe（exg）和 V（exg）的拮抗相互作用所致。这些发现表明，在 SMV 暴露条件下，在特定时期摄入足够的镁可能会防止 V 诱导的肝脏 LPO。
