Neuroprotective effect of magnesium on lipid peroxidation and axonal function after experimental spinal cord injury

Süzer, Tuncer; Çoşkun, Erdal; İşlekel, Hüray; Tahta, Kadir

doi:10.1038/sj.sc.3100874

Cited by 59 publications

(32 citation statements)

References 21 publications

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“…Magnesium sulfate therapy reduces lipid peroxidation after experimental spinal cord injury (6), long-term hypoxic-ischemic brain damage in 7-d-old rat (7), and the volume of traumatic brain lesions (8). It also facilitates recovery of function following electrolytic cortical injury (9).…”

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Magnesium Sulfate Therapy Is of Mild Benefit to Young Rats with Kaolin-Induced Hydrocephalus

2003

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Hydrocephalus causes damage to periventricular white matter at least in part through chronic ischemia. Magnesium sulfate (MgSO 4 ) has been shown to be protective in various models of neurologic injury. We hypothesized that this agent would ameliorate the effects of experimental childhood-onset hydrocephalus. Hydrocephalus was induced in 3-and 4-wk-old rats by injection of kaolin into the cisterna magna. Tests of cognitive and motor function were performed on a weekly basis. In a blinded and randomized manner, MgSO 4 was administered in two separate experiments (s.c. injection 0.85, 4.1, or 8.2 mM/kg/d), supplemented by osmotic minipump infusion (0.03 mM/d) to prevent low trough levels for 2 wk, beginning 2 wk after induction of hydrocephalus. The brains were then subjected to histopathological and biochemical analyses. With the 4.1 mM/ kg/d dose, serum Mg ϩϩ levels were elevated transiently from 1.3 to~7 mM/L. We observed statistically significant improvement in gait performance and reduced astroglial reaction. There was also a trend to improved memory performance, but no evidence of increased myelin or synaptic protein content. Hydrocephalus is a common neurologic condition characterized by pathologic dilation of the cerebral ventricles. It is usually caused by obstruction of cerebrospinal fluid (CSF) flow. Axon damage in the periventricular white matter is one of the earliest pathologic consequences of ventricular dilation in humans and animals (1). The pathophysiology of hydrocephalus-induced brain damage is multifactorial, with contributions made by gradual physical stretching, compression, ischemia and possible accumulation of metabolic waste products (2). It has been postulated that physical trauma and ischemic injury to axons combine to alter membrane permeability leading to local influx of calcium and activation of calpains, which can cause proteolytic damage to the axonal cytoskeleton (3).Magnesium is a calcium antagonist that blocks NMDA channel receptors in a voltage dependent manner, as well as voltage and receptor-operated calcium channels (4, 5). Magnesium sulfate therapy reduces lipid peroxidation after experimental spinal cord injury (6), long-term hypoxic-ischemic brain damage in 7-d-old rat (7), and the volume of traumatic brain lesions (8). It also facilitates recovery of function following electrolytic cortical injury (9). Magnesium may act as a cerebral vasodilator thereby improving the cerebral circulation (10) and preventing cell damage. Clinically, magnesium sulfate is used for seizure prophylaxis in the management of pregnant women with eclampsia. Some reports suggest that this treatment is associated with reduced incidence of cerebral palsy in low birth weight infants (11).In an experimental model of hydrocephalus induced by injection of kaolin into the cisterna magna of immature rats we have previously demonstrated the presence of abnormal quantities of soluble ionic calcium and activated calpains in the periventricular white matter (3). Diminished blood flow has been demonstrated in ...

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Magnesium Sulfate Therapy Is of Mild Benefit to Young Rats with Kaolin-Induced Hydrocephalus

2003

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“…The concept of dual mechanism in the spinal cord injury was introduced at the beginning of 1900s by Allen who demonstrated that progressive damage occurrs in patients with spinal cord injuries (21). Following SCI, a series of pathological changes occurs in the spinal cord, including bleeding, edema, demyelinization, axonal and neuronal necrosis, and cavity.…”

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confidence: 99%

Effects of individual or combined use of alpha-lipoic acid and methylprednisolone on malondialdehyde, superoxide dismutase, and catalase levels in acute spinal cord injury in rats

Birgul

Canaz

Uğur

et al. 2016

JHSCI

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“…Suzer et al [29] have shown with somatosensoryevoked potentials that magnesium has dose-dependent neuroprotective properties and attenuates lipid peroxidation in an acute traumatic spinal cord injury model. In the traumatic spinal cord injury model in rats, Demediuk et al [30] and Lemke et al [31] have reported that following trauma, the tissue level of magnesium falls to a critical value, reaches its initial level in 7 days, and that this fall in the level of magnesium is proportional to the severity of trauma.…”

Section: Discussionmentioning

confidence: 99%

Effect of Mg<sub>2</sub>SO<sub>4</sub> Usage on Spinal Cord Ischemia-Reperfusion Injury: Electron Microscopic and Functional Evaluation

et al. 2004

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Objectives: To evaluate the effects of intravenous magnesium sulfate (Mg₂SO₄) administration on ischemia-reperfusion injury of the spinal cord. Material and Methods: Sixteen rabbits were randomly assigned to the control (group I, 8 rabbits) and the study group (group II, 8 rabbits). The abdominal aorta was clamped for a period of 30 min followed by a reperfusion period of 60 min. The animals in group II received 0.25 ml/kg/h Mg₂SO₄ intravenous infusion (15% Mg₂SO₄) throughout this procedure. The animals were then observed for 24 h after which their neurological states were evaluated and tissue samples obtained from the spinal cord were examined with electron microscopy. Results: Aortic pressure distal to the cross-clamp during the occlusion period was 9 ± 3 mm Hg in group I and 19 ± 6 mm Hg in group II. All animals in group I were paraplegic at the end of the study. In group II the neurological outcome of 1 animal was poor while the other 7 animals were neurologically in a good condition. Electron microscopic examinations of the spinal cord tissues of group I revealed severe injury but the ultrastructure was well preserved in group II. Conclusions: Intravenous Mg₂SO₄ administration may have protective effects on the ischemia-reperfusion injury of the spinal cord. We propose that Mg₂SO₄ may be an additional protective pharmacological agent in thoracal and thoracoabdominal aortic surgery.

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Neuroprotective effect of magnesium on lipid peroxidation and axonal function after experimental spinal cord injury

Cited by 59 publications

References 21 publications

Magnesium Sulfate Therapy Is of Mild Benefit to Young Rats with Kaolin-Induced Hydrocephalus

Magnesium Sulfate Therapy Is of Mild Benefit to Young Rats with Kaolin-Induced Hydrocephalus

Effects of individual or combined use of alpha-lipoic acid and methylprednisolone on malondialdehyde, superoxide dismutase, and catalase levels in acute spinal cord injury in rats

Effect of Mg<sub>2</sub>SO<sub>4</sub> Usage on Spinal Cord Ischemia-Reperfusion Injury: Electron Microscopic and Functional Evaluation

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