The role of intracellular oxidation in death induction (apoptosis and necrosis) in human promonocytic cells treated with stress inducers (cadmium, heat, X-rays)
| Autor: | Nuria Vilaboa, Alba Galán, Carlos Fernández, Elena de Blas, Patricio Aller, L. Garcia-Bermejo, Alfonso Troyano |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Histology
Necrosis Hot Temperature Antimetabolites chemistry.chemical_element Apoptosis Cadmium chloride medicine.disease_cause Antioxidants necrosis Pathology and Forensic Medicine chemistry.chemical_compound Adenosine Triphosphate Cadmium Chloride Oxidation medicine stress inducers Humans Buthionine Sulfoximine chemistry.chemical_classification Reactive oxygen species Cadmium Superoxide X-Rays Cell Biology General Medicine U937 Cells Fluoresceins Molecular biology Oxidative Stress chemistry Biochemistry Caspases U-937 cells medicine.symptom Reactive Oxygen Species Oxidative stress Intracellular |
| Zdroj: | Digital.CSIC. Repositorio Institucional del CSIC instname |
| ISSN: | 0171-9335 |
| Popis: | 9 p.- 8 fig. Treatment of U-937 human promonocytic cells with the stress inducers cadmium chloride (2 h at 200 μM), heat (2 h at 42.5 °C) or X-rays (20 Gy), followed by recovery, caused death by apoptosis and stimulated caspase-3 activity. In addition, all stress agents caused intracellular oxidation, as measured by peroxide and/or anion superoxide accumulation. However, while pre-incubation with antioxidants (N-acetyl-L-cysteine or butylated hydroxyanisole) inhibited the induction of apoptosis by cadmium and X-rays, it did not affect the induction by heat-shock. Pre-incubation for 24 h with the GSH-depleting agent L-buthionine-[S,R]-sulfoximine (BSO) switched the mode of death from apoptosis to necrosis in cadmium-treated cells. By contrast, BSO only caused minor modifacions in the rate of apoptosis without affecting the mode of death in heat- and X-rays-treated cells. BSO potentiated peroxide accumulation in cells treated with both cadmium and X-rays. However, while the accumulation of peroxides was stable in the case of cadmium, it was transient in the case of X-rays. Moreover, the administration of antioxidants during the recovery period sufficed to prevent necrosis and restore apoptosis in BSO plus cadmium-treated cells. Cadmium and X-rays caused a decrease in intracellular ATP levels, but the decrease was similar in both apoptotic and necrotic cells. Taken together, these results demonstrate that (i) stress inducers cause intracellular oxidation, but oxidation is not a general requirement for apoptosis; and (ii) the duration of the oxidant state seems to be critical in determining the mode of death This work was supported by Grant PB97 ± 0144 from the Dirección General de Enseñanza Superior e Investigación Científica (Spain) and Grant 08.1/0027/1997 from the Comunidad Autonóma de Madrid (Spain). A. Galán and A. Troyano are recipients of fellowships from the Ministerio de Educación y Cultura, Spain |
| Databáze: | OpenAIRE |
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