Effect of acute magnesium deficiency (MgD) on aortic endothelial cell (EC) oxidant production

Wiles, Marc E.; Wagner, Tammy L.; Weglicki, William B.

doi:10.1016/s0024-3205(96)00619-4

Cited by 41 publications

(32 citation statements)

References 27 publications

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“…Previously, we have used a DCF-DA probe in the cultured endothelial cell model to monitor cellular oxidant stress when subjected to free radical stress (Dickens et al, 1992;Wiles et al, 1997). The probe DCF-DA would be taken up by the cells and deacetylated intracellularly to the nonfluorescent DCF, which reacts semiquantitatively with either oxidative species or peroxides to generate fluorescent 2,7-dichlorofluorescein within the cells.…”

Section: Resultsmentioning

confidence: 99%

“…Intracellular generation of reactive oxygen species was determined by 2Ј,7Ј-dichlorofluorescin (DCF) as described previously (Dickens et al, 1992;Wiles et al, 1997). The iron-loaded endothelial cells with or without drug pretreatment in 24-well plates were labeled for 30 min with DCF-DA probe (30 M) in a balanced salt buffer containing 10 mM glucose, pH 7.2.…”

Section: Measurement Of Intracellular Oxidant Generationmentioning

confidence: 99%

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d-Propranolol Attenuates Lysosomal Iron Accumulation and Oxidative Injury in Endothelial Cells

Mak

Chmielinska²,

Nedelec³

et al. 2006

J Pharmacol Exp Ther

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The influence of selected ␤-receptor blockers on iron overload and oxidative stress in endothelial cells (ECs) was assessed. Confluent bovine ECs were loaded with iron dextran (15 M) for 24 h and then exposed to dihydroxyfumarate (DHF), a source of reactive oxygen species, for up to 2 h. Intracellular oxidant formation, monitored by fluorescence of 2Ј,7Ј-dichlorofluorescin (DCF; 30 M), increased and peaked at 30 min; total glutathione decreased by 52 Ϯ 5% (p Ͻ 0.01) at 60 min. When the ECs were pretreated 30 min before iron loading with 1.25 to 10 M D-propranolol, glutathione losses were attenuated 15 to 80%, with EC 50 ϭ 3.1 M. D-Propranolol partially inhibited the DCF intensity increase, but atenolol up to 10 M was ineffective. At 2 h, caspase 3 activity was elevated 3.2 Ϯ 0.3-fold (p Ͻ 0.01) in the iron-loaded and DHF-treated ECs, and cell survival, determined 24 h later, decreased 47 Ϯ 6% (p Ͻ 0.01). Ten micromoles of D-propranolol suppressed the caspase 3 activation by 63% (p Ͻ 0.05) and preserved cell survival back to 88% of control (p Ͻ 0.01). In separate experiments, 24-h iron loading resulted in a 3.6 Ϯ 0.8-fold increase in total EC iron determined by atomic absorption spectroscopy; D-propranolol at 5 M reduced this increase to 1.5 Ϯ 0.4-fold (p Ͻ 0.01) of controls. Microscopic observation by Perls' staining revealed that the excessive iron accumulated in vesicular endosomal/lysosomal structures, which were substantially diminished by D-propranolol. We previously showed that propranolol could readily concentrate into the lysosomes and raise the intralysosomal pH; it is suggested that the lysosomotropic properties of D-propranolol retarded the EC iron accumulation and thereby conferred the protective effects against iron load-mediated cytotoxicity.

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Section: Resultsmentioning

confidence: 99%

Section: Measurement Of Intracellular Oxidant Generationmentioning

confidence: 99%

d-Propranolol Attenuates Lysosomal Iron Accumulation and Oxidative Injury in Endothelial Cells

Mak

Chmielinska²,

Nedelec³

et al. 2006

J Pharmacol Exp Ther

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“…The study by Rock et al (32) study mentioned that free radical-mediated injury could contribute to skeletal muscle lesions resulting from Mg deficiency. Mg deficiency has been closely associated with production of ROS, cytokines and eicosanoids, along with vascular compromise in vivo (33). The activity center of GSH-Px is selenocysteine, and selenium is a necessary part of GSH-Px (34).…”

Section: Groupmentioning

confidence: 99%

Deep sea water improves exercise and inhibits oxidative stress in a physical fatigue mouse model

Fan¹,

Tan²,

Yue³

et al. 2016

Biomedical Reports

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Abstract. Physical fatigue is extremely common and occurs daily, and is considered to be associated with oxidative stress. The diverse functions of deep sea water (DSW) have recently gained increasing attention. Previous studies have emphasized the anti-fatigue effect of DSW, but the intrinsic mechanism behind the effect remains to be elucidated. In the imprinting control region (ICR) mice model, DSW delayed the exhaustive swimming time. In addition, DSW decreased the area under the blood lactate (BLA) curve, which was associated with the area under the BLA curve of pre-swimming, post-swimming and post-rest. Furthermore, DSW reduced the basal levels of malondialdehyde and the post-swimming concentration of blood urea nitrogen, lactate dehydrogenase and creatine kinase after swimming, along with an increase in the normal level of antioxidant enzyme activity such as superoxide dismutase and glutathione peroxidase. However, no significant effect on body weight, hepatic glycogen and muscle glycogen was observed between any group. In conclusion, DSW can improve the athletic ability and alleviate physical fatigue of ICR mice. This effect is achieved by enhancing the antioxidant capacity.

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“…74 Weglicki and co-workers have identified an early (week 1) induction of oxi/nitrosative stress and depletion of antioxidant defences in PBMC and endothelial cells. [75][76][77][78] The lymphocyte activation featured here includes their production of proinflammatory cytokines and a neurogenic peptide, substance P, together with the expression of its receptors. 79 Cardiac lesions first appear in this model during week 3 and can be prevented by a substance P receptor antagonist.…”

Section: -54mentioning

confidence: 99%

“…84 In cultured aortic endothelial cells, reduced Mg 2+ concentration of culture medium is associated with increased oxidant production and reduced intracellular glutathione, an antioxidant reserve consumed in neutralising oxi/nitrosative stress. 75 Abnormal Mg 2+ homeostasis could represent the underlying pathophysiological basis for endothelial dysfunction seen in either PAL or SAL.…”

Section: Endothelial Cell Dysfunctionmentioning

confidence: 99%

Toward a broader understanding of aldosterone in congestive heart failure

Weber

Sun

Wodi

et al. 2003

J Renin Angiotensin Aldosterone Syst

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Discovered some 50 years ago, aldosterone (ALDO) has come to be recognised as a mineralocorticoid hormone with well-known endocrine properties in epithelial cells that contribute to the pathophysiology of congestive heart failure. This includes Na + in such non-epithelial cells as peripheral blood mononuclear cells; its influence on endothelial cell function; and its central actions that involve regulation of cerebrospinal fluid composition produced by epithelial cells of the choroid plexus, activity of the hypothalamic paraventricular nucleus involved in Na + appetite, Na + and H 2 O excretion and sympathetic nerve activity, and the regulation of TNF-α production from central and/or peripheral sources. Extra-adrenal steroidogenesis and auto/paracrine properties of ALDO generated de novo in the cardiovasculature are now under investigation and preliminary findings suggest they contribute to tissue repair. The past decade has witnessed a revival of interest in this steroid molecule. In years to come, an even broader understanding of ALDO's contribution to the pathophysiology of congestive heart failure will undoubtedly emerge.

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Effect of acute magnesium deficiency (MgD) on aortic endothelial cell (EC) oxidant production

Cited by 41 publications

References 27 publications

d-Propranolol Attenuates Lysosomal Iron Accumulation and Oxidative Injury in Endothelial Cells

d-Propranolol Attenuates Lysosomal Iron Accumulation and Oxidative Injury in Endothelial Cells

Deep sea water improves exercise and inhibits oxidative stress in a physical fatigue mouse model

Toward a broader understanding of aldosterone in congestive heart failure

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