We examined expression of
retinal dehydrogenase (RALDH) types 1 and 2 in liver and lung, and the effect of
vitamin A status on testis expression by in situ hybridization. Liver expressed RALDH1 and RALDH2 only in stellate cells and hepatocytes, respectively. Lung expressed RALDH1 and RALDH2 throughout the epithelia of the airways, from the principal bronchi to the respiratory bronchiole.
Vitamin A-sufficient rats expressed RALDH1 in spermatocytes, with less intense expression in spermatogonia and spermatids, and expressed RALDH2 in interstitial cells, spermatogonia, and spermatocytes. Neither Sertoli nor peritubular cells showed detectable RALDH1 or RALDH2
mRNA.
Vitamin A deficiency produced a sevenfold increase in RALDH1 and a 70-fold decrease in RALDH2
mRNA in testis. In each case, the net change reflected extensive loss of germ cells, increased intensity of expression in residual germ cells, and expression in Sertoli and peritubular cells. Low-dose RA relatively early during
vitamin A depletion supported spermatogenesis and affected expression of both RALDHs, but did not reinstate "
vitamin A normal" expression patterns. These results show that: RALDH1 and RALDH2 have distinct
mRNA expression patterns in multiple cell types in three
vitamin A target tissues; RALDH expression occurs in cell types that express
cellular retinol-binding protein and
retinol dehydrogenase isozymes (except stellate cells, for which
retinol dehydrogenase expression remains unknown);
vitamin A deficiency and RA supplementation affects the loci and intensity of RALDH mRNAs in testis; and low-dose RA does not substitute completely for
retinol. Overall, these data provide insight into the unique functions of RALDH1 and RALDH2 in
retinoid metabolism.