Abstract
A link between corticosteroid therapy and the development of cataract has been known for many years. However, the precise underlying molecular mechanism of pathology has not been characterised, although a role for direct deleterious interactions between corticosteroids and lenticular proteins has been investigated. α-Crystallin is a major lens protein that has exhibited chaperone properties in vitro. Catalase is a ubiquitous enzyme that is an important scavenger of hydrogen peroxide in vivo. The corticosteroid prednisolone-21-hemisuccinate was found to inactivate bovine liver catalase, in vitro in a progressive manner. Coincubation of α-crystallin with catalase in a 1:2 molar ratio (one α-crystallin to two catalase molecules) fully protected against this inactivation. The protection was specific. Aspirin-like analgesics, putative anti-cataract drugs offered no such protection.
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