Simple alcohols are found widely in nature. Ethanol is the most prominent because it is the product of fermentation, a major energy-producing pathway. 24034-73-9, formula is C20H34O, Other simple alcohols, chiefly fusel alcohols, are formed in only trace amounts. More complex alcohols however are pervasive, as manifested in sugars, some amino acids, and fatty acids. , Safety of (2E,6E,10E)-3,7,11,15-Tetramethylhexadeca-2,6,10,14-tetraen-1-ol
Sanvee, Gerda M.;Bouitbir, Jamal;Krahenbuhl, Stephan research published 《 C2C12 myoblasts are more sensitive to the toxic effects of simvastatin than myotubes and show impaired proliferation and myotube formation》, the research content is summarized as follows. Statins reduce cardiovascular complications in patients with high LDL-cholesterol but are associated with myopathy. We compared the toxicity of simvastatin of C2C12 myoblasts and myotubes. Since myoblasts can proliferate and fuse to myotubes, myoblasts can be considered as satellite cells and myotubes as mature muscle fibers. Simvastatin increased plasma membrane permeability and decreased the cellular ATP content in both myoblasts and myotubes, but with a stronger effect on myoblasts. While insulin prevented cytotoxicity up to 8 h after addition of simvastatin to myotubes, prevention in myoblasts required simultaneous addition Mevalonate and geranylgeraniol prevented simvastatin-associated cytotoxicity in both myoblasts and myotubes. Simvastatin impaired the phosphorylation of the insulin receptor (IR β), Akt ser473 and S6rp, and increased phosphorylation of AMPK thr172 in both myotubes and myoblasts, which was prevented by insulin and mevalonate. Simvastatin impaired oxygen consumption and increased superoxide production by myoblasts and myotubes and induced apoptosis via cytochrome c release. In addition, simvastatin impaired proliferation and fusion of myoblasts to myotubes by inhibiting the expression of the nuclear transcription factor MyoD and of the metalloprotease ADAM-12. Decreased expression of the proliferation factor Ki-67 and of ADAM-12 were also observed in gastrocnemius of mice treated with simvastatin. In conclusion, myoblasts were more susceptible to the toxic effects of simvastatin and simvastatin impaired myoblast proliferation and myotube formation. Impaired muscle regeneration may represent a new mechanism of statin myotoxicity.
24034-73-9, Geranylgeraniol is a diterpenoid that is hexadeca-2,6,10,14-tetraene substituted by methyl groups at positions 3, 7, 11 and 15 and a hydroxy group at position 1. It has a role as a plant metabolite, a volatile oil component and an antileishmanial agent. It is a diterpenoid and a polyprenol.
Geranylgeraniol, a precursor to geranylgeranylpyrophosphate, is an intermediate in the mevalonate pathway. Geranylgeraniol has been shown to prevent bone re-absorption, inhibition of osteoclast formation, and kinase activation in vitro. When working with statins, Geranylgeraniol can reduce the toxicity without inhibiting the cholesterol-producing effects. Geranylgeraniol has been documented to counteract the effects of fluvastatin by inhibiting activation of caspase-1 and production of IL-1. Additionally Geranylgeraniol has been found to induce apoptosis in HL-60 cells.
, Safety of (2E,6E,10E)-3,7,11,15-Tetramethylhexadeca-2,6,10,14-tetraen-1-ol
Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts