Abstract
The hypothesis was tested whether the lysis of erythrocytes by silica is related to lipid peroxidation induced by this cytotoxic dust. Ascertaining lipid peroxidation by measuring the formation of malondialdehyde, fluorescent product, and profile of fatty acids in control and silica treated erythrocytes, we found an enhancement of lipid peroxidation due to silica. EDTA inhibited this reaction, while α-tocopherol did not. Hemolysis by silica occurred at a much faster rate and was not affected by EDTA. Incubation of silica with purified erythrocyte ghosts did not induce changes in markers of lipid peroxidation, unless hemoglobin was added. Hemoglobin-catalyzed peroxidation of ghosts by silica was prevented by EDTA. It is concluded that hemolysis by silica is an independent process, not related to induction of lipid peroxidation by silica.
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