Abstract
Aluminum can facilitate Fe-mediated oxidative injury, which may contribute to Al neurotoxicity. It has been reported that Al potentiates Fe-induced oxidative stress in cultured granule cells, suggesting a mechanism for Al facilitation of Fe-mediated oxidative injury. However, the relationship of intracellular Al concentration to Fe-induced oxidative stress has not been reported. In the present study, neuronal oxidative stress and survival were investigated. Embryo rat hippocampal neuron cultures were treated with Al2(SO4)3 and/or FESO4. An ionophore, A23187, was utilized to facilitate cellular Al uptake. Intraneuronal Al concentration was ascertained by laser microprobe mass spectrometry (LMMS). Neuronal oxidative stress was measured by confocal laser scanning microscopy, using 2,7-dichlorofluorescin diacetate (DCFH-DA) as a probe. The study showed that neuronal Al uptake was facilitated by the ionophore and that an increase of intraneuronal Al concentration potentiated Fe-induced oxidative stress and neuronal death. The results indicate that Al potentiation of Fe-induced oxidative stress might contribute to Al facilitation of oxidative injury, and thus to Al neurotoxicity.
Original language | English (US) |
---|---|
Pages (from-to) | 271-277 |
Number of pages | 7 |
Journal | Brain Research |
Volume | 743 |
Issue number | 1-2 |
DOIs | |
State | Published - 1996 |
Externally published | Yes |
Keywords
- 2,7-dichlorofluorescin diacetate
- aluminum
- confocal laser scanning microscopy
- hippocampal neuron
- iron
- laser microprobe mass spectrometry
- oxidative stress
- reactive oxygen species
ASJC Scopus subject areas
- Neuroscience(all)