Abstract
Topical application of the tumor promoter 12-0-tetradecanoylphorbol-13-acetase to the mouse skin resulted in a significant initial increase (at 2 h) in the activity of epidermal hydroxymethylglutaryl CoA reductase followed by a significant decrease by 24 h. Phorbol and phorbol diacetate, which do not cause hyperplasia or promote skin tumor formation, has no effect on this enzyme. Ethylphenylpropiolate, a strong inducer of hyperplasia but a non-tumor promoter, also showed no effect on the reductase activity. Topical application of the products of hydroxymethylgutaryl CoA reductase viz. mevalanolactone or isopentenyl adenosine caused a decrease while cholesterol produced no change in hydroxymethylglutaryl CoA reductase activity. It is speculated that isopentenyladenosine or a closely related product, formed by the initial increase in hydroxymethylglutaryl CoA reductase activity following TPA application, might exert feedback inhibition.
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