The role of vitamin E in cellular energy metabolism in cultured adrenocortical cells

Peter J. Hornsby

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23 Scopus citations


AC1 cells, a bovine adrenocortical cell clone, are rapidly arrested and killed by 2 mM aminooxyacetate, an inhibitor of transmination reactions. Toxicity of aminooxyacetate to cultured bovine adrenocortical cells was previously linked to a high ratio of capacity for oxidation of glutamine relative to pyruvate and was reversible by adding excess glutamine. The toxic effects of aminooxyacetate were shown in the present study to be completely prevented by the simultaneous addition of low concentrations (<100 nM) of d‐α‐tocopherol (vitamin E) or selenious acid or higher concentration of other tocopherols, antioxidants, and ubiquinones (coenzymes Q6 and Q10). When antioxidant analogs were tested, it was found that structural features of the molecules that increase antioxidant potency increased potency for prevention of aminooxyacetate toxicity. α‐Tocopherol‐supplemented AC1 cells were found to be significantly less sensitive than nonsupplemented cells to growth inhibition by rotenone but not by fluorocitrate or dinitrophenol. Dinitrophenol (100 m̈M) stimulated substrate oxidation fivefold but had relatively slight effects on growth, either with or without α‐tocopherol, indicating that limitation of the maximal activity of the tricarboxylic acid cycle and respiratory chain is probably not responsible for the sensitivity to aminooxyacetate and rotenone in cells not supplemented with α‐tocopherol. Sensitivity to growth inhibition by rotenone and the prevention by ubiquinones of aminooxyacetate toxicity suggest a restriction of electron flow at the NADH‐ubiquinone step. The resultant higher NADH/NAD+ ratio would result in a lowered capacity for metabolism of pyruvate with consequent dependence for tricarboxylic acid cycle function and energy production on 2‐oxoglutarate from glutamine by the transmination pathway. Vitamin E and other antioxidants may restore efficient function of ubiquinone by preventing side reactions involving lipid peroxidation. Selenium may have a similar effect as cofactor for glutathione peroxidase. A high ratio of capacity for oxidation of glutamine relative to pyruvate and accompanying sensitivity to aminooxyacetate may reflect a deficiency of vitamin E and selenium in adrenocortical cells in culture.

Original languageEnglish (US)
Pages (from-to)207-216
Number of pages10
JournalJournal of Cellular Physiology
Issue number2
StatePublished - Aug 1982


ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

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