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Mice bearing the mutant gene Cat:Fr have dominantly inherited congenital cataracts, which are more extensive in the mutant homozygote than in the heterozygote. The biochemical and ultrastructural properties of these lenses were examined and compared with those of lenses in which cataracts were induced with acetaminophen and bleomycin. The Cat mutation induces a dominant, by inheritance, loss of beta-H crystallins, but this change is also seen in the bleomycin cataracts, and in the presence of 1 M sucrose, or at 4(DEGREES)C. There are codominantly inherited alterations in the relative proportions of crystallin and albuminoid components in the inherited cataracts, and in the presence of 1 M sucrose. Changes in amino acid composition of the lens proteins are dominantly inherited in the Cat mutation. There are also abnormalities of amino acid composition in the proteins from the acetaminophen cataracts, but these are different from those caused by the mutation. As to the ultrastructural changes, the inherited cataracts have a relatively normal anterior epithelium, but show marked degeneration of nuclear and deep cortical fibres. The bleomycin cataracts also show extensive nuclear destruction, but in addition, appear to be completely devoid of capsule, and have degenerating anterior epithelium cells, which are not seen in the inherited cataract. The acetaminophen cataracts, by contrast, retain normal overall structural architecture, but the individual fibres become swollen and flaky, and develop an increased number of interdigitating processes. These abnormal biochemical properties not unique to the Cat:Fr mouse are unlikely to be proximal effects of the mutant gene, and may be general consequences of the presence of a cataract, from whatever cause. The differences between ultrastructural abnormalities seen in the drug induced and inherited cataracts suggest that these etiological agents induce cataracts by different mechanisms, a fact that is not always apparent from