Decreased chaperone activity of alpha-crystallins in naphthalene-induced cataract possibly results from C-terminal truncation.

Naphthalene-induced cataract has been extensively used to test potential anticataract drugs. Because the morphology as well as the toxic manifestations of naphthalene-induced cataract are reported to be similar to that of age-related cataract, naphthalene cataractogenesis in rats has been used as a valuable animal model to study the aetiology of age-related cataract in humans. This study aimed to determine whether the molecular chaperone activity of the alpha-crystallins was altered in naphthalene-induced cataract, and to clarify the possible mechanism for these changes. The data showed that the chaperone activity of the alpha-crystallins decreased in naphthalene-induced cataract. By mass spectrometry, C-terminal truncation of 16 amino acids and other post-translational modifications such as acetylation, phosphorylation, oxidation and carbamylation of the alpha-crystallins were detected. Furthermore, the results suggested that, at the proteomics level, naphthalene-induced cataract is a valuable animal model for the study of age-related cataract in humans.