Osmotic Effects on the Amino Acid-concentrating Mechanism in the Rabbit Lens.

A characteristic feature of the development of sugar cataracts in rats is the occurrence of a depression in the level of amino acids in the lens a few days after the animals are either placed on a high galactose diet or injected with alloxan.’ Kinsey and Reddy (1, 2) have shown by means of experiments in vitro and in vivo that a nonmetabolizable amino acid is not accumulated as rapidly in the lenses of diabetic rabbits as in those of normal animals. Thus, the drop in the amino acids that is observed in the development of sugar cataracts probably reflects a decrease in the efficiency of the amino acid-concentrating mechanism. The finding of van Heyningen (3) that there is an accumulation of polyols in sugar cataracts has led to the proposal of an osmotic theory to explain the development of sugar cataracts (4-7). According to this hypothesis, the increased concentration of sugar in the aqueous humor leads to an enhanced sugar uptake by the lens. The resultant high concentration of sugar accelerates its reduction to an alcohol. Since the lens membranes are relatively impermeable to sugar alcohols, these compounds tend to accumulate as they are formed so that a hypertonic condition is created. Osmotic equilibrium is restored by the movement of water from the aqueous humor into the lens fibers, which are caused to swell and eventually to rupture. If the hypothesis is correct, the depressed level of amino acids in the lens should be related in some way either to the accumulation of sugar alcohols or to the osmotic swelling of the lens. This report deals with a study that indicates that the ability of the lens to concentrate two nonmetabolizable amino acids, a-aminoisobutyric acid and laminocyclopentane-1-carboxylic acid,2 is markedly influenced by osmotic changes in the lens.