To identify factors responsible for the down-regulation of mitochondrial biosynthetic processes during anoxia in encysted Artemia franciscana embryos, the effects of oxygen limitation and pH on protein synthesis were investigated in isolated mitochondria. At the optimal pH of 7.5, exposure of mitochondria to anoxia decreases the protein synthesis rate by 79%. Rates were suppressed by a further 10% at pH 6.8, the intracellular pH (pHi) measured under anoxia in vivo. Matrix pH, measured under identical conditions, was 8.43±0.01 at an extramitochondrial pH of 7.9 (mean±S.E.M., n = 3), 8.05±0.01 at pH 7.5, and 7.10±0.01 at pH 6.8. The matrix pH did not vary (P ≥0.20) as a function of oxygen availability during the 1 h assays. Intramitochondrial purine nucleotides varied little as a function of pH. In contrast, after 1 h of protein synthesis under anoxia, ATP levels decreased by up to 40%,. whereas AMP, ADP and GDP concentrations increased, and GTP and GMP concentrations remained relatively constant. The addition of 1 mM ATP at the onset of anoxia maintained the ATP/ADP ratio at the aerobic value, but did not stabilize the GTP/GDP ratio or rescue rates of protein synthesis. Thus, at present, we cannot eliminate the possibility that the decrease in the GTP/GDP ratio during anoxia may contribute to the suppression of protein synthesis. The effect of anoxia was reversible; the rate of protein synthesis upon reoxygenation after a 30 min bout of anoxia was comparable (P = 0.14) with the pre-anoxic rate (193±17 and 174±6 pmol of leucine per mg of protein respectively; mean±S.E.M., n = 3). The array of mitochondrial translation products did not differ qualitatively as a function of either oxygen availability or pH. Finally, similar pH profiles for protein synthesis were obtained with either [3H]leucine or [3H]histidine (known to use different transporters). Consequently, it is improbable that the pH-sensitivity of protein synthesis can be explained by a specific protein effect on the import of the radiolabelled amino acid used. In summary, both oxygen limitation and acidic pH suppress rates of mitochondrial protein synthesis and are likely to contribute to the arrest of mitochondrial anabolic processes during anoxia-induced quiescence in A. franciscana embryos.
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January 1996
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Research Article|
January 01 1996
Oxygen and pH regulation of protein synthesis in mitochondria from Artemia franciscana embryos Available to Purchase
Kurt E. KWAST;
Kurt E. KWAST
*Department of Environmental, Population, and Organismic Biology, University of Colorado, Boulder, CO 80309-0334, U.S.A.
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Steven C. HAND
Steven C. HAND
‡
*Department of Environmental, Population, and Organismic Biology, University of Colorado, Boulder, CO 80309-0334, U.S.A.
†Graduate Program in Molecular Biophysics, University of Colorado, Boulder, CO 80309-0334, U.S.A.
‡To whom correspondence should be addressed.
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Publisher: Portland Press Ltd
Received:
July 17 1995
Revision Received:
September 01 1995
Accepted:
September 06 1995
Online ISSN: 1470-8728
Print ISSN: 0264-6021
The Biochemical Society, London © 1996
1996
Biochem J (1996) 313 (1): 207–213.
Article history
Received:
July 17 1995
Revision Received:
September 01 1995
Accepted:
September 06 1995
Citation
Kurt E. KWAST, Steven C. HAND; Oxygen and pH regulation of protein synthesis in mitochondria from Artemia franciscana embryos. Biochem J 1 January 1996; 313 (1): 207–213. doi: https://doi.org/10.1042/bj3130207
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