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© 1984 Oxford University Press

other

Aflatoxin B1: effect on the synthesis and degradation of mitochondrial proteins in hepatocyte monolayers

Carol Brookes , Alan Wright 1, Peter J. Evans 2 and R.John Mayer 

Department of Biochemistry, University of Nottingham Medical School, Queen's Medical Centre Nottingham NG7 2UH
1Tunstall Laboratory, Shell Research Ltd., Sittingbourne Laboratories Sittingbourne, Kent ME9 8AG
2Department of Applied Biology, UWIST, King Edward VII Avenue Cardiff CF1 3NU, UK

The effect of aflatoxin B1 (AFB1), a hepatocarcinogen, on mitochondrial and general protein synthesis and degradation has been studied. AFB1 (0.003, 0.03, 0.25 µg ml–1) inhibited total protein synthesis over a 5 h period by 30, 64 and 82%, respectively, measured by incorporation of [3H]leucine. After 24 h in the presence of AFB1 inhibition was 23, 77 and 100%, respectively. AFB1 inhibited total hepatocyte protein degradation in a concentration independent manner by ~ 50% i.e., from 1.4% h –1 to 0.7% h–1. The immediate effect of AFB1 on mitoribosomal and total mitochondrial protein synthesis and mitochondrial degradation has been assessed by two methods. Mitoribosomal synthesis of proteins was inhibited over a 5 h period by AFB1 in a concentration independent manner by ~43%. Total mitochondrial protein synthesis showed a 23 and 45% inhibition by AFB1 (0.003 and 0.03 µg AFB1 ml–1) over a 4 h period and 25 and 72% inhibition, respectively, after 24 h in culture. The rate of mitochondrial protein degradation was not altered. AFB1 inhibits dibutyryl cyclic AMP-induced tyrosine amino transferase (TAT) activity in hepatocytes by 57% at 0.003 ug ml–1 and 100% at 0.03 µg ml–1 over a 24 h period. Dibutyryl cyclic AMP increases the rate of degradation of proteins in hepatocyte monolayers from 1.4% h–1 to 2.7% h–1 and was inhibited at both concentrations of AFB1 used. AFB1 causes a rapid inhibition of total hepatocyte protein synthesis, synthesis of proteins in hepatocyte mitochondria and the synthesis of imported mitochondrial proteins. General hepatocyte and dibutyryl cyclic AMP-induced protein degradation are significantly inhibited by AFB1 whereas the degradation of mitochondrial proteins is unaffected.


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