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    • Keywords

       

      Oral contraceptive agent; phenobarbital; diethylnitrosamine; liver regeneration; nucleic acids; γ-glutamyl transpeptidase; concanavalin A; hepatocytes agglutination

    • Abstract

       

      Short term effects of ovulen-50, a combination type oral contraceptive agent and phenobarbital—an established hepatic tumour promoter, were examined in the livers of diethylnitrosamine-initiated and uninitiated female rats. Liver mitotic activity as judged by liver weight, [3H] thymidine incorporation into DNA and levels of DNA, RNA and protein were measured in non-regenerating and regenerating liver. Hepatic γ-glutamyl transpeptidase activity and hepatocyte agglutination with concanavalin A were examined in diethylnitrosamine- and/or phenobarbital-treated rats.

      The results indicate that diethylnitrosamine or ovulen-50 individually are mitoinhibitory in regenerating liver. Phenobarbital alone has a slight mitostimulatory effects in non-regenerating liver, but no effect on liver regeneration. Administration of ovulen-50 and phenobarbital to diethylnitrosamine initiated rats mitigated the mitoinhibition during regeneration. Contrary to the earlier observation with ovulen-50, neither phenobarbital nor diethylnitrosamine induced hepatocyte agglutination in the presence of concanavalin A. Like ovulen-50, diethylnitrosamine also increased the level of hepatic γ-glutamyl transpeptidase. Phenobarbital produced only insignificant rise and did not substantially exacerbate the effect diethylnitrosamine.

      The data show that though some of the effects of ovulen-50 resemble those of diethylnitrosamine or phenobarbital, the changes observed may not be related to the neoplastic phenomenon since they were not seen in an initiator-promoter combination regimen.

    • Author Affiliations

       

      V V Annapurna1 M A Mukundan1 B Sesikeran1 Mahtab S Bamji1

      1. National Institute of Nutrition, Jamai-Osmania, Hyderabad - 500 007, India
    • Dates

       
  • Journal of Biosciences | News

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