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    The beneficial effect of melatonin on chronic cyclosporin A nephrotoxicity in rats
    (Cambridge Med Publ, 2003) Esrefoglu, M; Kurus, M; Sahna, E
    Cyclosporin A (CsA)-induced nephrotoxicity may be the consequence of oxidative stress. Anti-oxidant agents could be useful in reducing CsA toxicity. In this light microscopy study, tubular dilatation, atrophy, vacuolization and tubulointerstitial fibrosis were observed in rats given CsA, whereas in rats given CsA plus melatonin, no histological changes occurred. It is concluded that melatonin could be useful for reducing the nephrotoxic effects of CsA.
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    Ultrastructural clues for glutamate-induced necrosis in parietal and cerebellar neurons
    (Wiley, 2003) Esrefoglu, M; Gepdiremen, A; Kurus, M
    Glutamate excitotoxicity has been postulated to underlie the neuronal death that occurs after ischemia. The most sensitive tissues to ischemic injury are hippocampus and cerebellum, whereas cerebrum is more resistant. We studied the glutamate-induced ultrastructural alterations in rat parietal and cerebellar neurons comparatively. We observed that glutamate (45 min, 10(-7) M) causes considerable nuclear, mitochondrial and cytoplasmic changes in both the neuron types. Mitochondrial and nuclear changes were particularly more severe in cerebellar granular, than the ones in parietal neurons. It has been concluded that glutamate induces necrotic changes in both parietal and cerebellar neurons. But cerebellar cortex was found to be more sensitive to glutamate excitotoxicity than cerebral cortex. We suggest that mitochondrial damage is, probably, an important factor in neuron necrosis, which is mediated by glutamate excitotoxicity.