||Blockade of alpha-1 Adrenergic Receptor Inhibits Hepatic DNA Synthesis Stimulated by Tumor Promoters.
Tsai, W. H. ;
Cruise, J. L. ;
Michalopoulos, G. K. ;
||Duke Univ. Medical Center, Durham, NC. ;College of St. Thomas, St. Paul, MN.;Health Effects Research Lab., Research Triangle Park, NC.;National Institutes of Health, Bethesda, MD.
||EPA-R-814344 ;NIH-CA43632; EPA/600/J-89/201;
Deoxyribonucleic acids ;
Adrenergic alpha receptor blockaders ;
Organ weight ;
||Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy.
Studies with regenerating liver and hepatocyte cultures have shown that the alpha-1 adrenergic receptor (A1AR) is involved in the early events which transmit a mitogenic signal to hepatocytes after 2/3 partial hepatectomy. In the study, the role of A1AR in DNA synthesis associated with the augmentative hyperplasia stimulated by the xenobiotic hepatic tumor promoters phenobarbital (PB) and alpha-hexachlorocyclohexane (alpha-HCH), and the peroxisome proliferator ciprofibrate was investigated. Male F344 rats were treated with each of the three xenobiotics to stimulate hepatic DNA synthesis. These studies suggest that A1AR is involved in generating the mitogenic signal leading to hepatic DNA synthesis induced by xenobiotic hepatic tumor promoters phenobarbital and alpha-HCH. A1AR is not involved in the mitogenic pathway generated by the peroxisome proliferator ciprofibrate.