What is the transport mechanism of lipophilic drugs/agents into a cell? - Cell Membrane & Apoptosis (Mar/27/2006 )
Hi all,
These days lot of anticancer agents(like small molecules inhibitors) are lipophilic and are known to inhibit specific protein interaction in the cell. They trasverse the cell membrane in to the cytoplasmic target, but does this transport mechanism affect the cell in anyway? does the cell is not put into stress and thereby undergo apoptosis?? OR is it totally safe mode of entry?
regards
Raj
hi raj,
it is very questioned you asked. in general lipophilic drugs can enter the cell by sinple3 diffusion through the cellular membrane based on their logP (partiotining coefficient). however, there are also cases when a specific carrier is used by lipophilic drugs.
if you want to know something more specific write again...cheers
it is very questioned you asked. in general lipophilic drugs can enter the cell by sinple3 diffusion through the cellular membrane based on their logP (partiotining coefficient). however, there are also cases when a specific carrier is used by lipophilic drugs.
if you want to know something more specific write again...cheers
Hi Nexuson,
thanks for your reply. i am more keen to know whether the liphophilic drugs can cause extreme stress to the cells when they diffuse into the cells. Strictly speaking, diffusion doesnt require any energy so they should be fine. but can these agents coat the entire cell surface(during diffusion), and thereby provoking stress induced apoptosis.?? maybe my question is fundamental but i am breaking my head on this for a long time.
thx again
hi, i dont have any "solid" info on this but here some hypothesises:
i think it is possible what you are describing. lipophilic drugs can couse somekind of membrane solubilization. there are several toxins that make the mebrane more leaky, permeabilized. moreover anesthetics and ethanol are partially change the fluidity of cell membranes and thus act on changing properties of their targets (changes in alosteric interactions).
as for your compound is there a dose responce corelation? secondly the death of cells due to leaky membrane should be rapid necrosis so you can measure LDH activity, however if you will see more slow effect that mediated mainly by apoptotic factors i think it will answer the question.
one more thing as i see things are always a kind of compromise between two proceses. there may be some leakage of membrane at subdetectable levels.
C U