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Aluminum uptake by neuroblastoma cells
Journal of Neurochemistry
|August 1, 1990
Summary
Cellular aluminum uptake is pH-dependent, increasing as acidity rises. Mediators like apotransferrin and fatty acids facilitate uptake at neutral pH, while chelators inhibit it.
Area of Science:
- Neuroscience
- Cell Biology
- Toxicology
Background:
- Aluminum is a metal with potential neurotoxic effects.
- Understanding aluminum transport into cells is crucial for assessing its biological impact.
Purpose of the Study:
- To investigate the mechanisms and conditions governing aluminum uptake in neuroblastoma cells.
- To identify factors influencing aluminum cellular accumulation.
Main Methods:
- Studies involved viable neuroblastoma cells exposed to varying pH and aluminum concentrations.
- Mediators like apotransferrin, fatty acids, and chelators were used to assess their influence.
- Energy metabolism blockers were employed to determine the nature of uptake mechanisms.
Main Results:
- Aluminum uptake significantly increased with decreasing pH, plateauing around pH 6.0.
- At pH 6.0, cells accumulated substantial aluminum (5 nmol/mg protein), primarily in the postmitochondrial fraction.
- Apotransferrin and fatty acids facilitated aluminum uptake at neutral pH, while citrate inhibited it.
- Uptake was largely unaffected by energy metabolism blockers, suggesting passive transport.
Conclusions:
- Aluminum uptake by neuroblastoma cells is a complex process influenced by medium pH and specific mediators.
- Different uptake pathways exist, operating under various physiological and experimental conditions.
- The findings highlight the importance of environmental factors in cellular aluminum exposure.