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Ascorbate is a pro-oxidant in chromium-treated human lung cells.
Brooke D Martin1, J Andy Schoenhard, Ji-Mee Hwang
1Department of Chemistry, The University of Montana, 32 Campus Drive, Missoula, MT 59812, USA. brooke.martin@umontana.edu <brooke.martin@umontana.edu>
Mutation Research
|July 22, 2006
Summary
This study investigated chromium toxicity in lung cells. Ascorbic acid (Vitamin C) acts as a pro-oxidant, increasing chromium-induced reactive species, contrary to its antioxidant reputation.
Area of Science:
- Toxicology
- Cell Biology
- Environmental Health
Background:
- Inhalation of hexavalent chromium targets the lungs, necessitating models to study its toxicity.
- Reductive activation of chromium within cells is crucial for its reaction with cellular components.
- Fluorescent dyes like dichlorofluorescein (DCF) and dihydrorhodamine detect chromium activation and reactive species formation.
Purpose of the Study:
- To investigate the roles of glutathione and ascorbic acid (Vitamin C) in generating reactive chromium species (RCS) intracellularly.
- To understand how manipulating these reductants affects chromium-induced oxidative stress in A549 lung cells.
Main Methods:
- Utilized the human A549 lung cell line as a model system.
- Manipulated intracellular glutathione levels using buthionine sulfoximine (BSO).
- Altered ascorbic acid levels by adding ascorbate to culture media.
- Measured intracellular oxidation using fluorescent indicators (DCF, dihydrorhodamine).
Main Results:
- High endogenous glutathione levels in A549 cells reduced basal oxidation.
- Decreasing glutathione with BSO increased both background and chromium-stimulated oxidation.
- Ascorbic acid addition exacerbated chromium-induced oxidative stress, acting as a pro-oxidant.
Conclusions:
- Ascorbic acid functions as a pro-oxidant in chromium-treated lung cells.
- Glutathione plays a significant role in mitigating chromium-induced oxidative damage.
- Understanding these interactions is key to addressing chromium toxicity in lung tissues.