Increased uptake and accumulation of vitamin C in human immunodeficiency virus 1-infected hematopoietic cell lines
Keywords: oxidation, acid, proteins, transport, resistance, reduction, infections, hiv, glucose, lymphocytes, infection, cells, accumulation, immunodeficiency, proliferation, cell, host, virus, line, humans, division, human, transporter, replication, drug, article, phagocytes, vitamin, hiv-1, uptake, intake, type, controlled, hexoses, study, 1, priority, Reaction, journal, Ascorbic, Monosaccharide, dehydroascorbic, HL-60, hematopoietic
Vitamin C (ascorbic acid) is required for normal host defense and functions importantly in cellular redox systems. To define the interrelationship between human immunodeficiency virus (HIV) infection and vitamin C flux at the cellular level, we analyzed vitamin C uptake and its effects on virus production and cellular proliferation in HIV-infected and uninfected human lymphoid, myeloid, and mononuclear phagocyte cell lines. Chronic or acute infection of these cell lines by HIV-1 led to increased expression of glucose transporter 1, associated with increased transport and accumulation of vitamin C. Infected cells also showed increased transport of glucose analogs. Exposure to vitamin C had a complex effect on cell proliferation and viral production. Low concentrations of vitamin C increased or decreased cell proliferation depending on the cell line and either had no effect or caused increased viral production. Exposure to high concentrations of vitamin C preferentially decreased the proliferation and survival of the HIV-infected cells and caused decreased viral production. These findings indicate that HIV infection in lymphocytic, monocytic, and myeloid cell lines leads to increased expression of glucose transporter 1 and consequent increased cellular vitamin C uptake. High concentrations of vitamin C were preferentially toxic to HIV-infected host defense cell lines in vitro.
|Título de la Revista:||JOURNAL OF BIOLOGICAL CHEMISTRY|
|Fecha de publicación:||1997|
|Página de inicio:||5814|