ISSN:
1432-119X
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Medicine
Notes:
Summary Mouse, rat, hamster, guinea pig and sheep kidneys and foetal human, adult male and female human, mouse, rat, hamster and guinea pig livers were examined for hydroxysteroid dehydrogenase activity. 3α-Hydroxysteroids were utilised by all tissues, including neonatal mouse kidney, but the 5α-configuration was a more suitable substrate than the corresponding 5β-steroid. Both N.A.D. and N.A.D.P. were suitable cofactors. Only trace 3β-hydroxysteroid dehydrogenase activity was demonstrable in renal tissue, however liver possessed a higher level of activity and lanosterol, a precurser of cholesterol, was an especially suitable substrate possibly indicating that the liver is capable of synthesising cholesterol. 6β-Hydroxyprogesterone was poorly utilized by renal and hepatic tissue and N.A.D. was found to be the only cofactor suitable for this reaction. All the tissues, possessed 11β-hydroxysteroid dehydrogenase activity. In the kidney, this enzyme occurred in the collecting tubules. It was further noted that in mouse kidney 11β-hydroxysteroid dehydrogenase was absent at birth but appeared within the first fourteen days. Activity with 11β-hydroxysteroids was observed to be more prominent in the liver of male animals and this pattern was also found with 3α-, 3β-, 16α- and 16β-hydroxysteroids, all of which are confirmed by previous biochemical findings. Renal tissue was not capable of utilizing the 16α-hydroxysteroid in contrast to liver which could use this substrate fairly well. 16β- and 17β-hydroxysteroid dehydrogenases were demonstrable in the livers of all species and in all kidneys. The 20β-hydroxysteroid was only poorly utilized by hepatic tissue and not at all by renal tissue. Slight activity was demonstrable with 5α- and 5β-androstans as substrates in liver and the diformazan deposition was presumably due to the action of a steroid reductase.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00306290
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