Document 0133
 DOCN  M9470133
 TI    Mechanistic aspects of ascorbate inhibition of human immunodeficiency
       virus.
 DT    9409
 AU    Harakeh S; Niedzwiecki A; Jariwalla RJ; Viral Carcinogenesis and
       Immunology Program, Linus Pauling; Institute of Science and Medicine,
       Palo Alto, CA 94306.
 SO    Chem Biol Interact. 1994 Jun;91(2-3):207-15. Unique Identifier :
       AIDSLINE MED/94251847
 AB    We have investigated the molecular basis of the inhibitory effect of
       ascorbate (vitamin C) on human immunodeficiency virus (HIV) expression
       in unstimulated chronically infected and reporter cell lines. Comparison
       of intracellular HIV RNA and protein patterns of ascorbate-treated cells
       with corresponding patterns of untreated controls, did not show
       significant differences in the synthesis or processing of individual
       viral RNA and polypeptides, indicating that the inhibitory effect of
       ascorbate is not directed at steps of viral transcription or
       translation. Enzyme assays on cell extracts showed that the activity of
       an HIV LTR-directed reporter protein made in ascorbate-treated cells was
       reduced to approximately 11% relative to that of untreated control.
       These results, combined with previous observations on the suppression of
       HIV RT activity, are consistent with a mechanism of action in which
       ascorbate exerts a posttranslational inhibitory effect on HIV by causing
       impairment of enzymatic activity.
 DE    beta-Galactosidase/BIOSYNTHESIS  Ascorbic Acid/*PHARMACOLOGY  Blotting,
       Northern  Cell Line  Cell Survival/DRUG EFFECTS  Genes, Reporter  Human
       HIV/*DRUG EFFECTS/GENETICS/METABOLISM  HIV Long Terminal Repeat/DRUG
       EFFECTS  Reverse Transcriptase/ANTAGONISTS & INHIB  RNA,
       Viral/BIOSYNTHESIS  Transcription, Genetic/DRUG EFFECTS  Translation,
       Genetic/DRUG EFFECTS  Viral Proteins/BIOSYNTHESIS  JOURNAL ARTICLE

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