Summary:Purpose: Epileptic seizure results from excessive discharge in a population of hyperexcitable neurons. A number of studies help to document the effects of active oxygen free radical scavengers such as α-tocopherol or ascorbic acid (vitamin C). In the present study, we examined the effects of ascorbic acid, at the six different doses, on penicillin-induced epileptiform activity.Methods: A single microinjection of penicillin (2.5 µl, 500 units, intracortically) into the left sensorimotor cortex induced epileptiform activity within 2-5 min, progressing to full seizure activity lasting ∼3-5 h. In the first set of experiments, 30 min after penicillin injection, six different doses of ascorbic acid (25, 50, 100, 200, 400, or 800 mg/kg) were administered intraperitoneally (IP). The other group of animals received the effective dose of ascorbic acid (100 mg/kg, IP) for 7 days. Ascorbic acid administration was stopped 24 h before penicillin treatment. Another group of rats received the effective dose of ascorbic acid (100 mg/kg, IP) 30 min before penicillin treatment. In the second set of experiments, the lipid peroxidation (MDA) and reduced glutathione (GSH) levels of brain were measured in the control, control + ascorbic acid, penicillin, and penicillin + ascorbic acid groups.Results: Ascorbic acid, at the low dose (50, 100 mg/kg, 30 min after penicillin injection), decreased both the frequency and amplitude of penicillin-induced epileptiform activity in rats. Ascorbic acid, at intermediate doses (200, 400 mg/kg, 30 min after penicillin injection), decreased the frequency of epileptiform activity without changing the amplitude. Ascorbic acid, at the lowest dose (25 mg/kg) and highest dose (800 mg/kg) (30 min after penicillin injection), did not change either the frequency or amplitude of epileptiform activity. Ascorbic acid, at the low dose (100 mg/kg) was the most effective dose in changing the frequency and amplitude of penicillin-induced epileptiform activity. Pretreatment with ascorbic acid (100 mg/kg) 30 min before penicillin treatment caused a significant delay in the onset of penicillin-induced epileptiform activity. Pretreatment with ascorbic acid (100 mg/kg) for 7 days did not change the latency of epileptiform activity. The most effective dose of ascorbic acid (100 mg/kg) prevented both the decrease in GSH level and the increase in lipid peroxidation level (MDA) occurring after penicillin-induced epileptiform activity.Conclusions: These data indicate that ascorbic acid has neuroprotective activity against penicillin-induced epileptiform electrocorticogram activity.

Objectives. To investigate the correlation between concentrations of asymmetric dimethylarginine (ADMA) and neopterin (NP) as potential risk factors for cardiovascular diseases in chronic renal failure patients. Method. In this study, 33 patients with renal failure before and after haemodialysis were compared with healthy control subjects. Serum ADMA and NP levels were measured using high performance liquid chromatography (HPLC). Results. When ADMA and NP concentrations in renal failure patients were compared before and after dialysis, before dialysis ADMA and NP concentrations were higher than those in the control group. However, ADMA and NP levels showed a falling mean and clear after dialysis. While there is no correlation between ADMA and NP levels before dialysis, there is a mean and positive correlation between ADMA and NP levels after dialysis. Conclusion. Potential risk factors for cardiovascular diseases include high concentrations of both ADMA and NP levels in chronic renal failure patients. A correlation mean between ADMA and NP levels after dialysis was found, but no correlation between ADMA and NP levels before haemodialysis was discovered. These can be evaluated as two different risk factors independent from each other.

Tryptophan as a circulating precursor of serotonin (5-HT) may suppress food intake and body weight. Tryptophan administration can enhance the generation of reactive oxygen species (ROS) by inducing oxidative pathway in vivo and in vitro. We have examined the effect of repeated tryptophan administration on food consumption, body weight, brain lipid peroxidation and 5-HT immunoreactivity. Tryptophan was given at the dose of 100 mg/kg/24 hr in 0.2 ml saline solution i.p. for 7 days to mice. Control mice received 0.9% NaCL solution at the same manner and volume. Body weights were recorded at the beginning and end of the experiments. Thiobarbituric acid reactive substance (TBARS), the last product of lipid peroxidation, was measured spectrophotometrically. Brain 5-HT levels were determined by the immunohistochemical method. Our findings indicate that the tryptophan suppresses food intake significantly in mice. Body weight decreased and brain TBARS levels increased significantly by repeated tryptophan treatment. Immunohistochemical detection showed that 5-HT levels increased by tryptophan administration. There is a link between increased 5-HT level and oxidative stress by tryptophan administration on brain tissue. Tryptophan at repeated doses should be exercised carefully in clinical practice.

Continuous and intermittent 50 Hz, 1.5 mT magnetic field with the exposure period of 4 h/day for 4 days was used to investigate its possible effect on adult guinea pigs. Tissues and plasma specimens were assessed by biochemical parameters. Malondialdehyde (MDA), glutathione (GSH), nitric oxide (NO) levels and myeloperoxidase activity (MPO) were examined in plasma, liver and brain tissues. All parameters were determined by spectrophotometer. While intermittent magnetic field was effective on plasma lipid peroxidation, continuous magnetic field was found to be effective on plasma MPO activity and NO levels. Augmentation of lipid peroxidation was also observed in liver tissue both intermittent and continuous magnetic field exposures. These results indicate that both the intermittent and continuous magnetic field exposures affect various tissues in a distinct manner because of having different tissue antioxidant status and responses.

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