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    Melatonin as a free radical scavenger in experimental head trauma
    (Karger, 1999) Cirak, B; Rousan, N; Kocak, A; Palaoglu, O; Palaoglu, S; Kilic, K
    Head trauma causes two kinds of injury in the neural tissue. One is the primary injury which occurs at the time of impact. The other one is a secondary injury and is a progressive process. Free radicals are produced during oxidative reactions formed after trauma. They have been thought to be responsible in the mechanism of the secondary injury. Some studies have been conducted to demonstrate the role of free oxygen radicals in neuronal injury. The alterations in the free radical level during the early posttraumatic period and the effect of a free radical scavenger on these alterations have not been studied as a whole. We aimed to demonstrate the free oxygen radical level changes in the early posttraumatic period and the effect of melatonin, which is a potent free radical scavenger, on the early posttraumatic free radical level. A two-staged experimental head trauma study was designed. In stage one, post-traumatic free radical level changes were determined. In the second stage, the effect of melatonin on the free radical level changes in the post-traumatic period was studied. Two main groups of rats each divided into four subgroups were studied. Rats in one of the main groups underwent severe head trauma, and malondealdehyde (MDA) levels were measured in the contused cerebral tissue at different time points. Rats in the other main group also underwent the same type of trauma, and melatonin was injected intraperitoneally at different time points after trauma. The MDA level alteration in the tissue was determined after the injection of melatonin. The MDA level increased rapidly in the early posttraumatic period. But in time, it decreased in the groups with only trauma. In the melatonin-treated group, the MDA level decreased after the injection of melatonin, when injected in the early posttraumatic period, compared to the control and trauma groups. However, melatonin increased MDA to a higher level than in the groups with only trauma and the control group when injected later than 2 h after trauma. The MDA level increases in the very early posttraumatic period of cerebral trauma and decreases in time. Melatonin, which is the most potent endogenous free radical scavenger, when injected intraperitoneally to the cerebral traumatized rats in the very early posttraumatic period, causes a significant decrease in the MDA level. But, melatonin, when injected more than 2 h after trauma, increases the MDA level in experimental cerebral trauma in rats. Copyright (C) 2000 S. Karger AG, Basel.
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    A new model for tethered cord syndrome: A biochemical, electrophysiological, and electron microscopic study
    (Karger, 1997) Kocak, A; Kilic, A; Nurlu, G; Konan, A; Kilinc, K; Cirak, B; Colak, A
    In order to investigate the pathophysiology of the tethered cord syndrome, a few experimental models have been developed and used previously. In this study, the authors present a new experimental model to investigate the biochemical, electrophysiological, and histopathological changes in the tethered spinal cord syndrome. A model was produced in guinea pigs using an application of cyanoacrylate to fixate the filum terminale and the surrounding tissue to the dorsal aspect of the sacrum following 5-gram stretching of the spinal cord. The experiments were performed on 40 animals divided into two groups. The responses to tethering were evaluated with hypoxanthine and lipid peroxidation, somatosensory and motor evoked potentials, and transmission electron microscope examination. The hypoxanthine and lipid peroxidation levels significantly increased, indicating an ischemic injury (p < 0.01). The average hypoxanthine level in the control group was 478.8 +/- 68.8 nmol/g wet tissue, while ii, was 651.2 +/- 71.5 nmol/g in the tethered cord group, The lipid peroxidation level in group I Nas 64.0 +/- 5.7 nmol/g wet tissue, whereas it Nas 84.0 +/- 4.7 nmol/g in group II. In the tethered cord group, the latencies of the somatosensory and motor evoked potentials significantly increased, and the amplitudes decreased. These changes indicated a defective conduction in the motor and sensorial nerve fibers. In the transmission electron microscopic examinations, besides the reversible changes like edema and destruction in the gray-white matter junction, irreversible changes like scarcity of neurofilaments and destruction in axons and damage in myelin sheaths were observed. We consider that this work can be used as an experimental model for tethered cord syndrome.