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    The effect of verapamil in the prevention of radiation-induced cataract
    (Elsevier Science Inc, 1999) Cengiz, M; Gürkaynak, M; Atahan, IL; Kilic, K; Totan, Y
    Purpose: Cataract is an unavoidable complication when radiation therapy includes the lens, even in small doses. Alterations in the ion content of the lens were considered to play an essential role in cataract formation. In this experimental study, the effect of verapamil on ion concentrations within the irradiated lenses was investigated in rats. Methods and Materials: Forty female Wistar albino rats, each weighing 180-250 g, were divided into three groups: (a) radiation treated (n = 10); (b) no treatment (n = 10); (c) or a combination of radiation and verapamil (n = 20), Both the radiation group and verapamil-treated group received 5 Gy radiation to the cranium in a single fraction, including the eyes, within the irradiation volume. All animals were sacrificed by bleeding, 7.5 weeks posttreatment. Calcium, sodium, and potassium levels were measured in blood and in lens homogenates, However, for technical reasons, magnesium levels could only be studied in lens homogenates. Results: Potassium and sodium concentrations in lens homogenates did not differ in the control and radiation groups, but both were significantly lower in the verapamil-treated group (p = 0.001, p = 0.009, respectively). Calcium levels were higher in the radiation group and lower in the verapamil-treated group compared to the controls (p < 0.0001); magnesium levels did not differ (p = 0.37). Conclusion: Verapamil effectively decreased the lens calcium concentration, which is accepted as the key element in radiation cataractogenesis, It is therefore concluded that verapamil may reduce the risk of radiation-induced cataract formation. (C) 1999 Elsevier Science Inc.
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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.