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Cellular metabolism of arsenic studied in mammalian cellsin vitro
A B Fischer1, J P Buchet, R R Lauwerys
1Institute of Hygiene, Justus-Liebig University, Giessen, Federal Republic of Germany.
Abstract:
The cytotoxicity of trivalent and pentavalent inorganic arsenic was studied in cultured mouse fibroblasts. Concentrations of As(III) in the μM range and approximately 10-fold higher concentrations of As(V) led to a reduction of cellular proliferation and viability with a concomitant increase of LDH release and stimulation of lactate production. Cells pretreated with a low As(III) concentration were less sensitive to toxic doses of As(III) or As(V).Uptake of As(III) by the cells was greater than that of As(V). Both forms of inorganic arsenic were converted intracellularly to monomethylarsonic (MMA) and dimethylarsinic (DMA) acids, which were subsequently released into the culture medium. In As-pretreated cells, which proved more resistant to As toxicity, biotransformation of inorganic to MMA and DMA was increased.
Insights
Trivalent and pentavalent inorganic arsenic exhibit cytotoxicity in mouse fibroblasts. Pretreatment with low arsenic concentrations enhances cellular resistance by increasing arsenic biotransformation.
Area of Science:
- Toxicology
- Cell Biology
- Environmental Health
Background:
- Inorganic arsenic (As) exists in trivalent (As(III)) and pentavalent (As(V)) forms.
- Arsenic toxicity is a significant environmental and health concern.
- Understanding the differential cytotoxicity and cellular response to As(III) and As(V) is crucial.
Purpose of the Study:
- To investigate the cytotoxicity of As(III) and As(V) in cultured mouse fibroblasts.
- To compare the cellular uptake and biotransformation of As(III) and As(V).
- To determine the effect of arsenic pretreatment on cellular sensitivity to arsenic toxicity.
Main Methods:
- Cultured mouse fibroblasts were exposed to varying concentrations of As(III) and As(V).
- Cellular proliferation, viability, lactate dehydrogenase (LDH) release, and lactate production were assessed.
- Intracellular arsenic uptake and biotransformation to monomethylarsonic (MMA) and dimethylarsinic (DMA) acids were analyzed.
- Cells were pretreated with low arsenic concentrations before exposure to toxic doses.
Main Results:
- As(III) and As(V) reduced cellular proliferation and viability, with As(III) being more potent.
- LDH release and lactate production increased with arsenic exposure.
- As(III) showed greater cellular uptake compared to As(V).
- Intracellular biotransformation of inorganic arsenic to MMA and DMA occurred, with subsequent release into the medium.
- Pretreatment with low As(III) concentrations conferred resistance to subsequent toxic doses of both As(III) and As(V).
- Enhanced biotransformation of inorganic arsenic to MMA and DMA was observed in pretreated, more resistant cells.
Conclusions:
- Both As(III) and As(V) are cytotoxic to mouse fibroblasts, affecting cellular proliferation and viability.
- Cellular resistance to arsenic toxicity can be induced by prior exposure to low arsenic concentrations.
- Increased intracellular biotransformation of inorganic arsenic to methylated forms plays a role in developing arsenic resistance.
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