Summary:Purpose: Intracortical injection of iron ion induces recurrent seizures and epileptic discharges in the electrocorticogram. This observation may be used as a model of posttraumatic epilepsy. The involvement of iron-mediated oxygen free radical species and neuronal lipid peroxidation in ironinduced seizure has been suggested. Melatonin exerts free radical scavenging properties. In this study, we examined the protective effect of melatonin against iron-induced seizures.Methods: We examined the protective effect of melatonin against in vitro iron-induced oxidative damage in homogenates from rat cerebral cortex, by measuring the concentration of thiobarbituric acid reactive substances (TBARS), as an index of oxidative damage. We also examined the effect of melatonin on the appearance of epileptic discharges in the EEG following injection of FeC1, into the sensorimotor cortex in anesthetized rats, and by measuring the concentration of TBARS in the brain tissue.Results: FeCI, increased the concentration of TBARS in brain homogenates in a concentration-dependent manner, and melatonin reduced FeC1,-induced rise in TBARS in a doseresponse fashion. Pretreatment with melatonin suppressed or delayed the development of FeC1,-induced epileptic discharges and decreased the concentration of TBARS in brain tissues.Conclusions: Our results suggest that iron ion generates oxygen free radical species that induce neuronal macromolecular peroxidation and seizure, and that melatonin inhibits ironinduced seizures by scavenging free radicals. Key Words: Melatonin-Iron-induced seizures-Perioxidation-Thiobarbituric acid-Reactive substances-TBARS-Free radical.Neurotrauma with extravasation of red blood cells followed by hemolysis and deposition of iron compounds such as hemosiderin within the brain tissue (1) is associated with the development of post-traumatic epilepsy (2). Similarly, intracortical injection of iron salts or heme compounds into the rodent brain induces recurrent seizures and epileptic discharges in the EEGs (3-5). These observations strongly suggest that trauma or hemorrhagic cortical infarction associated with extravasation of blood and decompartmentalization of iron within the brain may induce epileptic discharge (3, although the specific mechanisms of the epileptogenic effect of iron salts remain unknown. It has been proposed that active oxygen free radicals generated by iron-mediated reactions in the brain (6) peroxidize lipids in neural membranes, resulting in cell death and the formation of an epileptic focus (7). In support of this hypothesis, previ-

Measurement of these three urinary oxidative products is non-invasive. Above all, measurement of urinary nitrate may be most useful in the clinical assessment of oxidative stress in both psoriasis and atopic dermatitis patients. There is a possibility that urinary 8-OHdG level may indicate the different pathogenesis between psoriasis and atopic dermatitis.

Purpose Renal ischemia-reperfusion (I/R), an important cause of acute kidney injury, is unavoidable during various types of operations, including renal transplantation, surgical revascularization of the renal artery, partial nephrectomy, and treatment of suprarenal aortic aneurysms. Exacerbation of I/R injury is mediated by reactive oxygen species (ROS). A recent study has shown that hydrogen has antioxidant properties. In this study, we tested the hypothesis that a hydrogen-rich saline solution (HRSS) attenuates renal I/R injury in a rodent model. Methods Rats were treated with an intravenous injection of HRSS or control saline solution followed by renal I/R. After 24 h of treatment, we performed a histological examination and transmission electron microscopy, and measured serum levels of 8-OHdG.

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The auditory sector of the thalamic reticular nucleus (TRN) plays a pivotal role in gain and/or gate control of auditory input relayed from the thalamus to cortex. The TRN is also likely involved in cross-modal sensory processing for attentional gating function. In the present study, we anatomically examined how cortical and thalamic afferents intersect in the auditory TRN with regard to these two functional pathways. Iontophoretic injections of biocytin into subregions of the auditory TRN, which were made with the guidance of electrophysiological recording of auditory response, resulted in retrograde labeling of cortical and thalamic cells, indicating the sources of afferents to the TRN. Cortical afferents from area Te1 (temporal cortex, area 1), which contains the primary and anterior auditory fields, topographically intersected thalamic afferents from the ventral division of the medial geniculate nucleus at the subregions of the auditory TRN, suggesting tonotopically organized convergence of afferents, although they innervated a given small part of the TRN from large parts. In the caudodorsal and rostroventral parts of the auditory TRN, cortical afferents from nonprimary visual and somatosensory areas intersected thalamic afferents from auditory, visual, and somatosensory nuclei. Furthermore, afferents from the caudal insular cortex and the parvicellular part of the ventral posterior thalamic nucleus, which are associated with visceral processing, converged to the rostroventral end of the auditory TRN. The results suggest that the auditory TRN consists of anatomical nodes that mediate tonotopic and/or cross-modal modulation of auditory and other sensory processing in the loop connectivity between the cortex and thalamus.