The double bond of cycloartenol (compound 7 in diagram) is methylated by SAM to give a carbocation that undergoes a hydride shift and loses a proton to yield a compound with a methylene side-chain. Both of these steps are catalyzed by sterol C-24 methyltransferase (Step E1 in diagram). Compound 8 is then catalyzed by sterol C-4 demethylase (E2) and loses a methyl group to produce cycloeucalenol. Subsequent to this, the cyclopropane ring is opened with cycloeucalenol cycloisomerase (E3) to form 10 . Compound 10 loses a methyl group and undergoes an allylic isomerization to form Gramisterol 11 . This step is catalyzed by sterol C-14 demethylase (E4), sterol Δ14-reductase (E5), and sterol Δ8-Δ7-isomerase (E6). The last methyl group is removed by sterol demethylase (E7) to form episterol 12 . Episterol 12 is methylated by SAM to produce a second carbocation, which loses a proton to yield 13 . This step is catalyzed by 24-methylenesterol C-methyltransferase (E8). Compound 13 now undergoes reduction by NADPH and modifications in the β-ring to form β-sitosterol.
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The most obvious benefit that injectable steroids have over their oral cousins is that they are not hepatotoxic. Injectable steroids are safer on the liver and the user does not risk hepatic injury because injectable compounds don’t require specific chemical alterations which allow them to survive passing through the liver without being broken almost entirely down. It’s also worth consider that injectable steroids have a much longer half-life due to the ester attached to the hormone. To get the maximum benefit from oral steroids, most must be administered daily, or sometimes they are spread out throughout the day. The ester present in injectable steroids allows a much more infrequent administration and don’t need to be administered daily. More information about Esters