One of the most difficult aspects of the problem of the mechanism of action of substances such as iodo-acetic acid (IAA), which have a retinotoxic effect. is that so very few other inhibitors of metabolism have that effect. W e do not know why other inhibitors (of glycolysis as well as of the respiration) which are even more potent than IAA and which in vitro have an even stronger harmful effect, leave the retina unaffected.For instance, the p-chloro-mercurobenzoate of sodium (PCMB), a strong inhibitor of glycolysis and of the respiration, has a pronounced damaging effect on the isolated retina (1); furthermore it suppresses the regeneration of rhodopsin in vitro (2). Nevertheless, all attempts to provoke retinal degeneration in vivo with the aid of this toxic agent have always given a negative result (3, 4), even though in those experiments the doses, administered intravenously, have been quite large (more than 80 O/O of the minimal fatal dose).The faot that it is possible to obtain a high concentration of an injected substance in the retina, and to keep this concentration high for a considerable length of timeby intracarotid injectiongave us the idea to try this method of adminisitration with PCMB, as well. In this preliminary note we report the first results of our experiments (ophthalmoscopical data); in later communications shall report the electro-retinographical, histological and metabolic alterations provoked by this toxic agent.W e have administered the PCMB (Sigma) to pigmented rabbits of an average weight of 2.5 kg; the substance was dissolved in glycyl-glycine buffer, 0.01 M, pH = 8.0, and injected into the right carotid of the animal. From ithe beginning of the experiments we had to take into consideration the fact that this toxic agent cannot be handled easily, in other words, the margin between the efficacious dose and the lethal dose is only slender. It ~ ")
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