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The object of investigation was to study the reflex from an eye-ground, the character of the disorder of electric activity of retina during the experimental vitreous haemorrhage and the possibility of correction of these alterations by the antioxidants. The research was conducted on 5 month 300 chinchilla rabbits of male sex, weight 2.8-3.2 kg. The phenosan kali, superoxidedismutase (SOD), catalasa, "Hemaza", ditikarbomat natrium (DTKN), mannitol, tocopherol acetate, deferooxamin were used. The rabbits treated with the antioxidants complex and "Hemasa" showed the best dynamic of the restoration of the ophthalmological conditions. It was found that, vitreous haemorrhage considerably damaged the formation of ERG. Separate application of antioxidants: phenosan kali, SOD and mannitol restore the amplitude of ERG retina during intravitreal haemorrhage, not influencing the temporal parameters. The application of antioxidants complex considerably restores the amplitude characteristics, becoming close to the norm, not influencing the time of ERG parameters development.

We studied the prooxidant and cytotoxic action of thiols N-acetylcystein (NAC) and glutathione (GSH) combined with vitamin Bl2b. The synergism of action of the thiols and Bl2b resulted in human carcinoma cell damage was found. It was shown that GSH and NAC in physiological doses combined with Bl2b caused the initiation of apoptosis. It was established that prooxidant action of the thiols combined with vitamin Bl2b, i. e. generation and accumulation of hydrogen peroxide in culture medium, led to intracellular oxidative stress and injury of cell redox system. These effects were completely abolished by nonthiol antioxidants catalase and pyruvate. The chelators of iron phenanthroline and deferoxamine did not suppress the H2O2 accumulation in culture medium but significantly inhibited the cell death induced by the thiols combined with Bl2b. Therefore, the thiols GSH and NAC widely used as antioxidants, in combination with vitamin Bl2b show prooxidant characteristics and induce, with the participation of intracellular iron, apoptotic HEp-2 cell death.