ArticleNeurotoxicity research2006
Cerebellar granule cell death induced by aluminum.
Article in Neurotoxicity research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 27 citations in OpenAlex.
- A systematic review for the development of Alzheimer's disease inFrontiers in aging neuroscience · 2023Article
- Review
- Docosahexaenoic acid ameliorates aluminum induced biochemical and morphological alteration in rat cerebellum.Annals of neurosciences · 2014Article
- Does melatonin ameliorate neurological changes associated with Alzheimer's disease in ovariectomized rat model?Indian journal of clinical biochemistry : IJCB · 2013Article
- Zinc, a neuroprotective agent against aluminum-induced oxidative DNA injury.Molecular neurobiology · 2013Article
- Aluminium sulphate exposure increases oxidative stress and suppresses brain development in Ross broiler chicks.Medical science monitor : international medical journal of experimental and clinical research · 2012Article
- Aluminum alters NMDA receptor 1A and 2A/B expression on neonatal hippocampal neurons in rats.Journal of biomedical science · 2011Article
- Cytotoxicity of environmentally relevant concentrations of aluminum in murine thymocytes and lymphocytes.Journal of toxicology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Using flow cytometry of acutely isolated cerebellar granule cell neurons, we have determined the effects of Al (III) on viability, membrane potential, intracellular calcium concentration and generation of reactive oxygen species (ROS). Al (III) killed granule cells in a time- and concentration-dependent fashion when monitored by use of the DNA-binding dye, propidium iodide. The threshold concentration was about 50 micromolar, and cell death at 100 micromolar was apparent after 30 min exposure and increased over time. Cell death was accompanied by cell swelling and a decrease in membrane potential, and was not dependent on external calcium concentration. While exposure to Al (III) was accompanied by an increase in ROS and an elevation of intracellular calcium concentration, calcium chelators and ROS scavengers did not reduce cell death. The action of Al (III) was not accompanied by activation of caspase-3 or an increase in annexin-V binding, both indicators of apoptosis. In the presence of intracellular O,O'-bis(2-aminophenyl)ethyleneglycol-N,N,N',N'-tetraacetic acid (BAPTA) and absence of extracellular calcium there was still a fluo-3 signal, which likely reflects an accumulation of intracellular Al (III). These observations suggest that the cell death is subsequent to intracellular accumulation of Al (III) and subsequent perturbation of cellular metabolism.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.