Prostaglandins and mutagenesis: prevention and/or reversibility of genetic damage induced by benzo (a) pyrene in the bone marrow cells of mice by prostaglandin E1.
Prostaglandin E1 and thromboxane A2 (PGE1 and TXA2) have been proposed to bind to DNA, regulate gene action and prevent mutagenesis. Benzo (a) pyrene (BP) is a known mutagen and tumor promotor. BP-induced damage to the bone marrow cells of mice was prevented and/or reversed by PGE1 and by colchicine, an agent which may enhance PGE1 synthesis and TXA2 synthesis or action. PGF2 alpha did not have any action. Imidazole, a selective TXA2 synthesis inhibitor, enhanced the mutagenic action of benzo (a) pyrene. These results lend support to the concept that an altered PG system may have a role in the pathogenesis of mutagenesis and carcinogenesis.
D000527:Alprostadil; D000818:Animals; D001564:Benzo(a)pyrene / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D001853:Bone Marrow / Q000187:drug effects* / Q000378:metabolism; D003078:Colchicine / Q000494:pharmacology; D015237:Dinoprost; D007093:Imidazoles / Q000494:pharmacology; D008297:Male; D051379:Mice; D009154:Mutation; D011458:Prostaglandins E / Q000494:pharmacology*; D011460:Prostaglandins F / Q000494:pharmacology; D013928:Thromboxane A2 / Q000096:biosynthesis
D007093:Imidazoles; D011458:Prostaglandins E; D011460:Prostaglandins F; D001564:Benzo(a)pyrene; D013928:Thromboxane A2; C029899:imidazole; D015237:Dinoprost; D000527:Alprostadil; D003078:Colchicine