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Sex difference in alcohol metabolism; androgenic steroid as an inducer of kidney alcohol dehydrogenase
Author(s) -
Ohno S.,
Stenius C.,
Christian L. C.
Publication year - 1970
Publication title -
clinical genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 102
eISSN - 1399-0004
pISSN - 0009-9163
DOI - 10.1111/j.1399-0004.1970.tb01967.x
Subject(s) - kidney , alcohol dehydrogenase , endocrinology , medicine , biology , locus (genetics) , inducer , isozyme , alcohol , gene , enzyme , genetics , biochemistry
Available genetic evidence on a number of other species shows that alcohol dehydrogenase (ADH: 1.1.1.1) seen in liver and kidney of vertebrates is specified by the same gene locus. Also in the case of man and the mouse, ADH from liver and kidney show identical electrophoretic mobilities. Yet, in development, ADH appears much earlier in liver than in kidney, and a twofold sex difference is seen in the amount of ADH contained in adult kidney of mice and man: Kidney ADH activity of adult females is about one‐fourth and that of adult males is about one‐half of the liver ADH activity. When castrated adult male and female mice are given 10 mg testosterone, kidney ADH activity rises to about the same level as liver ADH. On the basis of the above, we postulate that the ADH locus of kidney but not of liver is under the control of a secondary repressive genetic regulatory mechanism. This genetic block on transcriptional and translational activity of the ADH locus is removed by androgenic steroid which serves as an inducer. As long as this block is completely removed, the ADH locus of kidney functions at about the same innate rate as the ADH locus of liver.