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Method of Direct Segmental Intra-hepatic Delivery Using a Rat Liver Hilar Clamp Model
Published on: April 2, 2017
Magnesium can protect against vanadium-induced lipid peroxidation in the hepatic tissue
Agnieszka Scibior1, Dorota Gołębiowska, Irmina Niedźwiecka
1Department of Zoology and Invertebrate Ecology, The John Paul II Catholic University of Lublin, Lublin, Poland. cellbiol@kul.lublin.pl
Abstract:
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.
Insights
Magnesium sulfate (MS) protects against sodium-metavanadate (SMV) induced liver damage by reducing lipid peroxidation. Adequate magnesium intake may prevent vanadium-induced oxidative stress.
Area of Science:
- Biochemistry
- Toxicology
- Nutritional Science
Background:
- Sodium-metavanadate (SMV) exposure can induce oxidative stress and lipid peroxidation (LPO) in the liver.
- Magnesium (Mg) is an essential mineral with potential protective roles against cellular damage.
Purpose of the Study:
- To investigate the protective effect of magnesium sulfate (MS) against SMV-induced LPO in vivo and in vitro.
- To elucidate the mechanisms underlying the interaction between magnesium and vanadium in the context of oxidative stress.
Main Methods:
- Animal model: Rats were intoxicated with SMV for 18 weeks, with some groups receiving MS co-administration.
- Biochemical assays: Malondialdehyde (MDA) generation was measured as an indicator of LPO in liver tissues and supernatants.
- In vitro experiments: Liver supernatants were treated with exogenous iron (Fe) or vanadium (V) to assess LPO modulation by magnesium.
Main Results:
- SMV intoxication significantly increased MDA generation in rat liver.
- Coadministration of MS with SMV normalized MDA levels to control values.
- In vitro studies indicated synergistic interactions between vanadium and iron/vanadium, and antagonistic interactions with magnesium, on MDA production.
Conclusions:
- Magnesium sulfate demonstrates a protective effect against SMV-induced liver lipid peroxidation.
- Adequate magnesium intake may serve as a preventive strategy against vanadium-induced LPO.
- The protective action of magnesium involves antagonistic interactions with vanadium and potentially other pro-oxidant metals.
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