Magnesium Can Protect against Vanadium-Induced Lipid Peroxidation in the Hepatic Tissue

被引:28
作者
Scibior, Agnieszka [1 ,2 ]
Golebiowska, Dorota [1 ]
Niedzwiecka, Irmina [1 ]
机构
[1] John Paul II Catholic Univ Lublin, Dept Zool & Invertebrate Ecol, Lab Physiol & Anim Biochem, PL-20718 Lublin, Poland
[2] John Paul II Catholic Univ Lublin, Interdisciplinary Res Ctr, Lab Oxidat Stress, PL-20718 Lublin, Poland
关键词
OXIDATIVE STRESS; FREE-RADICALS; MG-GLUCONATE; VANADATE; RATS; MECHANISMS; SULFATE; INJURY; BLOOD; HEPATOCARCINOGENESIS;
D O I
10.1155/2013/802734
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
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页数:11
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