Short-term magnesium deficiency results in decreased levels of serum sphingomyelin, lipid peroxidation, and apoptosis in cardiovascular tissues

2009 ◽  
Vol 297 (1) ◽  
pp. H86-H92 ◽  
Author(s):  
Burton M. Altura ◽  
Nilank C. Shah ◽  
Xian-Cheng Jiang ◽  
Zhiqiang Li ◽  
José Luis Perez-Albela ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Drinking Water ◽  
Dna Fragmentation ◽  
Caspase 3 ◽  
Magnesium Deficiency ◽  
Short Term ◽  
Abdominal Aortic ◽  
Serum Ionized Calcium ◽  
Low Levels ◽  
Dietary Deficiency

The present study tested the hypothesis that short-term dietary deficiency of magnesium (Mg) (21 days) in rats would 1) result in decreased serum(s) [the present study tested the levels of Mg, sphingomyelin (SM), and phosphatidylcholine (PC)]; 2) promote DNA fragmentation, lipid peroxidation (LP), and activation of caspase-3 in cardiac (ventricular and atrial) and vascular(aortic) muscle; and 3) low levels of Mg2+ added to drinking water would either prevent or greatly ameliorate these manifestations. The data indicate that short-term Mg deficiency (10% normal dietary intake) resulted in profound reductions in serum-ionized Mg and total Mg with an elevation in serum-ionized calcium (Ca2+), significant lowering of serum SM and serum PC, with concomitant LP, DNA fragmentation, and activation of caspase-3 in ventricular (right and left chambers), atrial (right and left chambers) and abdominal aortic smooth muscle. The greater the reduction in serum-ionized Mg, the greater the effects on DNA fragmentation, LP, and caspase-3 activity. The intake of water-borne Mg2+ at all levels greatly attenuated or inhibited the reductions in serum SM and serum PC, activation of LP, DNA fragmentation, and the activation of caspase-3; even very low levels of Mg2+ in drinking water (i.e., 15 parts·million−1·day−1) were cardio- and vascular protective. In addition, we demonstrate that short-term dietary deficiency of Mg probably results in a downregulation of SM synthase and a decreased synthesis of PC.

Magnesium deficiency upregulates serine palmitoyl transferase (SPT 1 and SPT 2) in cardiovascular tissues: relationship to serum ionized Mg and cytochrome c

2010 ◽  
Vol 299 (3) ◽  
pp. H932-H938 ◽  
Author(s):  
Burton M. Altura ◽  
Nilank C. Shah ◽  
Zhiqiang Li ◽  
Xian-Cheng Jiang ◽  
Jose Luis Perez-Albela ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Cytochrome C ◽  
Right Ventricular ◽  
Magnesium Deficiency ◽  
Left Ventricular ◽  
Short Term ◽  
Aortic Smooth Muscle ◽  
Cardiovascular Tissues ◽  
Coa Transferase ◽  
Abdominal Aortic

The present work tested the hypothesis that a short-term dietary deficiency of magnesium (Mg) (21 days) in rats would result in the upregulation of the two major subunits of serine palmitoyl-CoA-transferase, serine palmitoyl transferase (SPT 1) and SPT 2 (the rate-limiting enzymes responsible for the de novo biosynthesis of ceramides) in left ventricular, right ventricular, and atrial heart muscle and abdominal aortic smooth muscle, as well as induce a reduction in serum sphingomyelin concomitant with the release of mitochondrial cytochrome c (Cyto c) in these tissues. Our data indicate that short-term Mg deficiency (MgD) resulted in an upregulation of SPT 1 and SPT 2, concomitant with a very significant release of Cyto c in left ventricular, right ventricular, atrial, and abdominal aortic smooth muscle. Short-term MgD also produced a lowering of serum sphingomyelin and ionized Mg. The greater the reduction in serum ionized Mg, the greater the upregulation of SPT 1 and 2 and the more the increase in free Cyto c. The data suggest that MgD, most likely, causes a biosynthesis of ceramides via two pathways in cardiovascular tissues, viz., via the activation of serine palmitoyl-CoA-transferase and sphingomyelinase, which lead to apoptotic events via intrinsic (present study) and extrinsic pathways (previous studies). Low levels of drinking water Mg were cardio- and vasculoprotective.

scholarly journals Short-term magnesium deficiency upregulates sphingomyelin synthase and p53 in cardiovascular tissues and cells: relevance to the de novo synthesis of ceramide

2010 ◽  
Vol 299 (6) ◽  
pp. H2046-H2055 ◽  
Author(s):  
Burton M. Altura ◽  
Nilank C. Shah ◽  
Zhiqiang Li ◽  
Xian-Cheng Jiang ◽  
Aimin Zhang ◽  
...  
Keyword(s):  
De Novo ◽  
Magnesium Deficiency ◽  
Smooth Muscles ◽  
Ceramide Synthase ◽  
De Novo Synthesis ◽  
Short Term ◽  
Sphingomyelin Synthase ◽  
Coa Transferase ◽  
Ceramide Synthesis ◽  
Low Levels

The present study tested the hypotheses that 1) short-term dietary deficiency of magnesium (21 days) in rats would result in the upregulation of sphingomyelin synthase (SMS) and p53 in cardiac and vascular (aortic) smooth muscles, 2) low levels of Mg2+added to drinking water would either prevent or greatly reduce the upregulation of both SMS and p53, 3) exposure of primary cultured vascular smooth muscle cells (VSMCs) to low extracellular Mg2+concentration ([Mg2]o) would lead to the de novo synthesis of ceramide, 4) inhibition of either SMS or p53 in primary culture VSMCs exposed to low [Mg2+]owould lead to reductions in the levels of de novo ceramide synthesis, and 5) inhibition of sphingomyelin palmitoyl-CoA transferase (SPT) or ceramide synthase (CS) in primary cultured VSMCs exposed to low [Mg2+]owould lead to a reduction in the levels of de novo ceramide synthesis. The data indicated that short-term magnesium deficiency (10% normal dietary intake) resulted in the upregulation of SMS and p53 in both ventricular and aortic smooth muscles; even very low levels of water-borne Mg2+(e.g., 15 mg·l−1·day−1) either prevented or ameliorated the upregulation in SMS and p53. Our experiments also showed that VSMCs exposed to low [Mg2+]oresulted in the de novo synthesis of ceramide; the lower the [Mg2+]o, the greater the synthesis of ceramide. In addition, the data indicated that inhibition of either SMS, p53, SPT, or CS in VSMCs exposed to low [Mg2+]oresulted in marked reductions in the de novo synthesis of ceramide.

Endovascular Repair of Ruptured Abdominal Aortic Aneurysms:Logistics and Short-term Results

2003 ◽  
Vol 10 (3) ◽  
pp. 440-446 ◽  
Author(s):  
Timothy Resch ◽  
Martin Malina ◽  
Bengt Lindblad ◽  
Nuno V. Dias ◽  
Björn Sonesson ◽  
...  
Keyword(s):  
Endovascular Repair ◽  
Short Term ◽  
Abdominal Aortic

scholarly journals Possible Role of Peroxynitrite in the Responses Induced by Fusicoccin in Plant Cultured Cells

Plants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 182 ◽  
Author(s):  
Massimo Malerba ◽  
Raffaella Cerana
Keyword(s):  
Cytochrome C ◽  
Dna Fragmentation ◽  
Stress Responses ◽  
Molecular Chaperones ◽  
Caspase 3 ◽  
Cultured Cells ◽  
Acer Pseudoplatanus ◽  
Cytochrome C Release ◽  
Induced Stress

Fusicoccin (FC) is a well-known phytotoxin able to induce in Acer pseudoplatanus L. (sycamore) cultured cells, a set of responses similar to those induced by stress conditions. In this work, the possible involvement of peroxynitrite (ONOO−) in FC-induced stress responses was studied measuring both in the presence and in the absence of 2,6,8-trihydroxypurine (urate), a specific ONOO− scavenger: (1) cell death; (2) specific DNA fragmentation; (3) lipid peroxidation; (4) production of RNS and ROS; (5) activity of caspase-3-like proteases; and (6) release of cytochrome c from mitochondria, variations in the levels of molecular chaperones Hsp90 in the mitochondria and Hsp70 BiP in the endoplasmic reticulum (ER), and of regulatory 14-3-3 proteins in the cytosol. The obtained results indicate a role for ONOO− in the FC-induced responses. In particular, ONOO− seems involved in a PCD form showing apoptotic features such as specific DNA fragmentation, caspase-3-like protease activity, and cytochrome c release from mitochondria.

Effect of various degrees and duration of magnesium deficiency on lipid peroxidation and mineral metabolism in rats

1995 ◽  
Vol 6 (12) ◽  
pp. 681-688 ◽  
Author(s):  
Jürgen Vormann ◽  
Theodor Günther ◽  
Vera Höllriegl ◽  
Klaus Schümann
Keyword(s):  
Lipid Peroxidation ◽  
Magnesium Deficiency ◽  
Mineral Metabolism

DNA Fragmentation: Its Predictivity as a Short Term Test

1982 ◽  
pp. 121-154 ◽  
Author(s):  
Silvio Parodi ◽  
Maurizio Taningher ◽  
Leonardo Santi
Keyword(s):  
Dna Fragmentation ◽  
Short Term ◽  
Short Term Test

scholarly journals Phytic Acid Protects against 6-Hydroxydopamine-Induced Dopaminergic Neuron Apoptosis in Normal and Iron Excess Conditions in a Cell Culture Model

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Qi Xu ◽  
Anumantha G. Kanthasamy ◽  
Manju B. Reddy
Keyword(s):  
Dna Fragmentation ◽  
Phytic Acid ◽  
Caspase 3 ◽  
Fold Increase ◽  
Iron Chelator ◽  
Culture Model ◽  
A Cell ◽  
Induced Apoptosis ◽  
6 Hydroxydopamine ◽  
Stress Dependent

Iron may play an important role in Parkinson's disease (PD) since it can induce oxidative stress-dependent neurodegeneration. The objective of this study was to determine whether the iron chelator, phytic acid (IP6) can protect against 6-hydroxydopamine- (6-OHDA-) induced apoptosis in immortalized rat mesencephalic dopaminergic cells under normal and iron-excess conditions. Caspase-3 activity was increased about 6-fold after 6-OHDA treatment (compared to control; ) and 30 μmol/L IP6 pretreatment decreased it by 38% (). Similarly, a 63% protection () against 6-OHDA induced DNA fragmentation was observed with IP6 pretreatment. Under iron-excess condition, a 6-fold increase in caspase-3 activity () and a 42% increase in DNA fragmentation () with 6-OHDA treatment were decreased by 41% () and 27% (), respectively, with 30 μmol/L IP6. Together, our data suggest that IP6 protects against 6-OHDA-induced cell apoptosis in both normal and iron-excess conditions, and IP6 may offer neuroprotection in PD.

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