Chitwood, D.J., Insect Physiology Laboratory Beltsville Agricultural Research Center U. S. Dept. of Agriculture Belt, MD 20705, United States
Lusby, W.R., Insect Physiology Laboratory Beltsville Agricultural Research Center U. S. Dept. of Agriculture Belt, MD 20705, United States
Lozano, R., Insect Physiology Laboratory Beltsville Agricultural Research Center U. S. Dept. of Agriculture Belt, MD 20705, United States
Thompson, M.J., Insect Physiology Laboratory Beltsville Agricultural Research Center U. S. Dept. of Agriculture Belt, MD 20705, United States
Svoboda, J.A., Insect Physiology Laboratory Beltsville Agricultural Research Center U. S. Dept. of Agriculture Belt, MD 20705, United States

Caenorhabditis elegans possesses a unique sterol methylation pathway not reported to occur in any other organism and also removes the C-24 ethyl group of sitosterol (a plant sterol). This nematode produced substantial quantities of 4α-methyl-5α-cholest-8(14)-en-3β-ol and smaller amounts of lophenol from dietary cholesterol, desmosterol or sitosterol. When C. elegans was propagated in media containing sitosterol plus 25-azacoprostane hydrochloride (25-aza-5β-cholestane hydrochloride), an inhibitor of Δ24-sterol reductase in insects, its 4α-methylsterol fraction largely consisted of equal amounts of 4α-methyl-5α-cholesta-7,24-dien-3β-ol and 4α-methyl-5α-cholesta-8(14), 24-dien-3β-ol. Thus 25-azacoprostane hydrochloride inhibited both a Δ24-sterol reductase and a Δ7-sterol isomerase in C. elegans. © 1983.