Retinol and its metabolite retinoic acid play a critical role in immunity, reproduction, and development. Retinoids are known to influence renal development, and show beneficial effects in experimental models of renal disease. beta-Carotene (provitamin A) is cleaved to retinal by beta-carotene 15,15'- monooxygenase (BCM), which is an essential enzyme for retinoid biosynthesis. However, the metabolism of retinol and beta-carotene in renal diseases such as nephrosis remains unclear. We studied BCM gene expression and retinol status in rats with nephrotic syndrome induced by puromycin aminonucleoside (PAN). BCM gene expression in the liver and intestines of PAN-treated rats was decreased compared with that in controls, while the expression in the kidney of PAN-treated animals was increased. Plasma retinol and retinol-binding protein levels were decreased in PAN-treated rats, but hepatic retinol level did not differ between PAN-treated and control rats. Up-regulation of BCM gene expression in the kidneys of rats with nephrotic syndrome may result in increased conversion of beta-carotene to retinal, so this change might supply more retinoic acid to the damaged glomeruli. Changes in the metabolism of retinol and beta-carotene might have an important role in protection against the development of nephrosis.
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