Polycyclic aromatic hydrocarbons initiate carcinogenesis by forming permanent membrane lesions of increased permeability. Other non-viral carcinogens may also form similar lesions.
Complexes of carcinogenic polycyclic aromatic hydrocarbons (PAH) and cationic Ah receptors, may be attracted to the cell membrane if its surface is exposed to external negative charge. At the membrane they may be trapped by lipophilic bonding. When the negative charge dissipates, the bound complexes create a local transmembrane charge imbalance. Molecules with organic anions are attracted to the outer surface to restore equilibrium. The two charged species form permanent dipoles (lesions) across the membrane. The membrane at the dipoles is more permeable. Similar permanent lesions involving steroid/receptor complexes may form after the local abnormal surface charge has been long-lived.
Beech
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D000818:Animals; D002273:Carcinogens / Q000633:toxicity*; D002462:Cell Membrane / Q000187:drug effects* / Q000378:metabolism; D002463:Cell Membrane Permeability / Q000187:drug effects; D002471:Cell Transformation, Neoplastic; D004563:Electrochemistry; D008563:Membrane Lipids / Q000378:metabolism; D008954:Models, Biological; D011083:Polycyclic Compounds / Q000633:toxicity*; D013256:Steroids / Q000378:metabolism
D002273:Carcinogens; D008563:Membrane Lipids; D011083:Polycyclic Compounds; D013256:Steroids