The effect of sodium iodate injection on the development of galactose cataract in the rat was investigated clinically and biochemically. Galactose cataracts were induced in animals which had been injected with a single dose of sodium iodate and compared with those given a saline injection. The degeneration of retinal pigment epithelium was observed electron microscopically after sodium iodate injection. A slit lamp examination of the lens showed that, in animals injected with sodium iodate, galactose-associated lens alterations progressed faster, and mature cataract development was achieved earlier than in the saline-injected animals. Biochemical data which indicated a significantly higher concentration of Na+ and lower concentration of K+ in lenses of sodium iodate-injected animals confirmed the above clinical data. The level of galactitol was higher in lenses of sodium iodate-injected than those of saline injected animals. Acceleration of the development of galactose cataract following sodium iodate injection is apparently due to the higher level of galactose entering the aqueous humor because of breakdown of blood-ocular barriers.
Measurement of the membrane potentials in the isolated frog lens fibers was made by means of intracellular microelectrode techniques. In the normal lens fibers, p-chloromercuribenzene sulfonate (PCMBS), an ––SH inhibitor, caused a large depolarization. The depolarizing effect of PCMBS was augmented when the surface membranes were modified by the proteolytic enzyme, papain. In experimental uveitis induced by injection of physiological saline solution or bovine serum albumin into the vitreous body, the depolarizing effect of PCMBS was also found to be augmented. This augmentation was considered to be related to probably membrane damage caused by proteolytic enzymes in the aqueous humor during the process of uveitis. Damage of the fiber membranes was also electronmicroscopically observed in experimental uveitis, using the histochemical technique of ruthenium red staining.
Measurement of membrane potentials in isolated frog lens fibers was made by means of intracellular microelectrode techniques. The membrane potentials of lens fibers were depolarized to various degrees after exposure to diamide, an -SH inhibitor. When the degree of diamide-induced depolarization was less than 20 mV, the membrane potentials almost fully recovered to the control level within 12 h after immersion in a Ringer’s solution containing dithiothreitol (DTT), a -SH protector. A similar tendency was also recognized in some lenses (57%) whose depolarization was 30 mV. When the degree of depolarization was 40 mV, the membrane potentials further depolarized in all cases tested in spite of treatment with DTT. From this study, it is considered that frog lens fibers could not recover their function if the damage was so severe as to produce a membrane depolarization of more 40 mV. Determination of ionic concentrations in lens fibers revealed a highly significant correlation between the degree of diamide-induced depolarization and changes in concentration ratio of Na+/K+.
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