Synthesis and secretion of albumin in rats during treatment with a carcinogenic dose of N-2-acetylaminofluorene.
The chronic administration of N-2-acetylaminofluorene (N-2-AAF) to rats causes a loss of hepatic cytoplasmic RNA, particularly from the endoplasmic-membrane fractions. At the end of the complete carcinogenic dose, the level of amino-acid incorporation into proalbumin is normal, despite the loss of 35% of membrane-bound RNA. The secretion of albumin, however, is inhibited. This inhibition of secretion is apparently the result of a change in membrane flow and differentiation; transfer of nascent protein from smooth-surfaced vesicles to the Golgi apparatus is blocked. The significance of these findings is discussed.
D015073:2-Acetylaminofluorene / Q000633:toxicity*; D000418:Albumins / Q000096:biosynthesis* / Q000378:metabolism; D000818:Animals; D004721:Endoplasmic Reticulum / Q000187:drug effects; D066298:In Vitro Techniques; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D011228:Prealbumin / Q000096:biosynthesis; D012313:RNA / Q000378:metabolism; D051381:Rats; D012270:Ribosomes / Q000187:drug effects
D000418:Albumins; D011228:Prealbumin; D012313:RNA; D015073:2-Acetylaminofluorene