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The biosynthesis of eugenol begins with the amino acid tyrosine . L -tyrosine is converted to p -coumaric acid by the enzyme tyrosine ammonia lyase (TAL). [16] From here, p -coumaric acid is converted to caffeic acid by p -coumarate 3-hydroxylase using oxygen and NADPH . S -Adenosyl methionine (SAM) is then used to methylate caffeic acid, forming ferulic acid , which is in turn converted to feruloyl- CoA by the enzyme 4-hydroxycinnamoyl-CoA ligase (4CL). [17] Next, feruloyl-CoA is reduced to coniferaldehyde by cinnamoyl-CoA reductase (CCR). Coniferaldeyhyde is then further reduced to coniferyl alcohol by cinnamyl-alcohol dehydrogenase (CAD) or sinapyl-alcohol dehydrogenase (SAD). Coniferyl alcohol is then converted to an ester in the presence of the substrate CH 3 COSCoA, forming coniferyl acetate. Finally, coniferyl acetate is converted to eugenol via the enzyme eugenol synthase 1 and the use of NADPH.

Androgens are responsible for the growth spurt of adolescence and for the eventual termination of linear growth, which is brought about by fusion of the epiphyseal growth centers. In children, exogenous androgens accelerate linear growth rates but may cause a disproportionate advancement in bone maturation. Use over long periods may result in fusion of the epiphyseal growth centers and termination of growth process. Androgens have been reported to stimulate the production of red blood cells by enhancing the production of erythropoeitic stimulating factor. During exogenous administration of androgens,  endogenous testosterone  release is inhibited through feedback inhibition of pituitary luteinizing hormone (LH).

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