Effects of Naloxone on Sodium- and Potassium-activated and Magnesium-dependent Adenosine-5′-Triphosphatase Activity and Lipid Peroxidation and Early Ultrastructural Findings after Experimental Spinal Cord Injury

Abstract

Endorphins have been implicated in the pathophysiology of spinal cord injury. The effect of naloxone on the sodium- and potassium-activated and magnesium-dependent adenosine-5'-triphosphatase (Na(+)-K+/Mg+2 ATPase, EC.3.6.1.3.) activity, lipid peroxidation, and early ultrastructural findings were studied in rats at the early stage of spinal cord injury, produced with an aneurysm clip on the T2-T7 segments. The rats were divided into four groups. The 10 rats in Group I, which had no injury and received no medication, were used for determining Na(+)-K+/Mg+2 ATPase activity, the extent of lipid peroxidation (by measuring the level of thiobarbituric acid-reactive substances as malondialdehyde), and normal ultrastructural findings. On the 15 rats in Group II, without spinal cord injury, only laminectomy was performed to determine the effect of surgery on the biochemical indices and findings. In the 15 rats in Group III, physiological saline was administered intraperitoneally in an amount equivalent to that of the naloxone administered immediately after spinal cord injury. In the 15 rats in Group IV, 0.5 mg of naloxone was administered intraperitoneally as a single dose immediately after injury and again 60 minutes after injury. The Na(+)-K+/Mg+2 ATPase activity was promptly reduced after spinal cord injury and remained in a lower level than the levels of Groups I and II during 120 minutes after injury. Naloxone treatment, immediately after trauma, attenuated the inactivation of Na(+)-K+/Mg+2 ATPase. On the other hand, there was a significant difference in the malondialdehyde content between animals in Groups I and III. Naloxone treatment reduced the malondialdehyde content in Group IV.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of epidural cooling on lipid peroxidation after experimental spinal cord injury

“…32 Many researchers have shown that agents inhibiting lipid peroxidation enhance functional recovery in experimental CNS injuries. 13,14,33,34 This concept was supported clinically by NASCIS II. 35 The extent of lipid peroxidation is a useful parameter for evaluating the cellular disturbance caused by spinal cord trauma in experimental conditions.…”

“…35 The extent of lipid peroxidation is a useful parameter for evaluating the cellular disturbance caused by spinal cord trauma in experimental conditions. 13,14,33 There are several methods for measuring the degree of lipid peroxidation in tissue. These methods are measurement of thiobarbituric acid reactive substances (TBARS) content, determination Epidural cooling in SCI S Tu Èzgen et al of changes in diene conjugation aliquots of lipid extracts, and measurement of formation of lipid soluble¯uorescent material.…”

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

“…7,24,25 The pathological lesion in the spinal cord injury requires 1 ± 2 h to develop. 24,26 This lag time is necessary to allow a delayed injury process.…”

“…7,24,25 The pathological lesion in the spinal cord injury requires 1 ± 2 h to develop. 24,26 This lag time is necessary to allow a delayed injury process. Secondary injury processes include ischemia, release of excitotoxic neurotransmitters, free radical generation, lipid peroxidation, and in¯ux of calcium ions in to the neurons.…”

“…Experiments have shown that the free-radical-initiated peroxidative procedure occurs in the injured spinal cord. 4,6,8,11,24,29,40 In this study, tissue lipid peroxidation was evaluated by measuring the thiobarbituric acid reactive substances (TBARS). 23 MDA, formed from the breakdown of polyunsaturated fatty acids, serves as a convenient index for determining the extent of lipid peroxidation.…”