[The antioxidant system in the dynamic combined treatment of epilepsy patients with traditional anticonvulsant preparations and an antioxidant--alpha-tocopherol].

Examination of 13 patients suffering from generalized epilepsy has shown about 20-25% decreases in the activity of superoxide dismutase (SOD) and glutathione peroxidase (GP) in red blood cells. Out of them 9 patients were treated with the antioxidant alpha-tocopherol (600 mg daily). Prior to alpha-tocopherol treatment all patients showed abnormal electroencephalographic (EEG) changes; 4 weeks later the effects of the antioxidant appeared as positive EEG changes, reduced frequency of epileptic seizures, increased SOD activity and patients' improved general state.

[Antioxidative activity of drugs used in anticonvulsive therapy].

The influence of medicines used in anticonvulsive therapy: phenobarbital, diphenin, phenazepam and Na-valproate at ascorbate-(ASPOL) and NADP H-(PhPOL) depended lipid peroxidation (POL) in pattern systems (homogenates of rat's brain--HRB, lecithin liposomes-LL) has been studied. It has been established that this medicines do not influence at ASPOL in LL in concentration range of 10-10 M. Phenobarbital (10 M) and Na-valproate (10 M) inhibit ASPOL and PhPOL in HRB in 20-25%.

[The radiation modifying properties of carnosine].

The influence of carnosine (beta-alanyl-l-histidine) on the survival rate of albino mice subjected to whole-body X-irradiation has been investigated. Carnosine (50-200 mg/kg/day) administered per os during a period of 20 days before irradiation (5.0 Gy) increased the survival rate by 45-65%, whereas the administration of carnosine within 30 days after irradiation (5.

[The interrelationship of the processes of lipid peroxidation and lipid phospholipase hydrolysis in the synaptosomes].

The influence of Fe2+, alpha-tocopherol, phospholipase A2 and mepacrine on the activity of lipid peroxidation (LPO) and phospholipid hydrolysis (PLH) was studied in synaptosomes. It was established that there is the tight direct interconnection between LPO and PLH in synaptosomes. It is assumed that activation of endogenous phospholipases in neurons is one of the causes of uncompensated LPO-activation during epileptogenesis.