On the Mechanism of Induction of Hepatic Adenosine Triphosphate Deficiency by Ethionine

摘要: Abstract A method is described for the quantitative determination of S-adenosylethionine (AEt) in perchloric acid extracts liver. The administration ethionine to female rats followed by rapid accumulation AEt concentration increases with increasing doses up about 0.25 0.35 mg per g body weight. remains at a maximum level least 24 hours after single injection ethionine. free liver and blood sufficiently high account this persistence maximal levels over period time. close inverse relationship has been found between adenosine triphosphate when measured as function time However, discrepancy exists concentrations ATP dose obtained dosage which induces only moderate decrease concentration. continues fall amount administered increased above level. basis studied be progressive inhibition synthesis adenine nucleotides de novo large associated decreasing ATP. data concerning various effects upon hepatic induction biochemical lesions are consistent hypothesis that primary effect trap reacting With low ethionine, trapping largely compensated increase rate monophosphate novo. increasingly larger exceeds resultant including This, turn, further compromises new formation AMP, leading steady state established During state, not stable but continuously broken down resynthesized. methionine several inhibits AEt, thus allowing partial resynthesis from liberated during transethylation AEt. This accounts reversal those resulting such protein ribonucleic excess triglyceride (fatty liver). structural changes induced offer an interesting example primarily lethal synthesis, enunciated Peters.