Differential toxicity of novel aluminium compounds in hippocampal culture

Bettina Platt, Alison Jayne Drysdale, Christiane Nday, Eva Von Roloff, Benjamin David Drever, Athanasios Salifoglou

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

The dependence of aluminium (Al) toxicity on its chemical form has been implicated in previous studies, but the complex chemistry of Al in solutions of biological preparations has hampered a reliable assessment. Here, we assessed the toxicity of select and pure Al(III) citrate compounds, well-characterized at physiological pH, and compared it with Al from standard solution (in HCl). Cell death rates of neurones and glia were established in hippocampal cultures following 3h incubations in a HEPES-buffered solution and 24h incubations in full culture medium. Overall, Al toxicity was found to vary considerably between compounds, with duration of exposure, medium type, and cell type as factors. While Al (from atomic absorption standard solution) induced the highest levels of cell death, AlCit1, ((NH(4))(5)[Al(C(6)H(4)O(7))(2)].2H(2)O) was the most toxic citrate compound, and affected viability of neurones more than glia (viability at 500 microM/3h-neurones: 40%; glia: 60%). AlCit2 (K(4)[Al(C(6)H(4)O(7))(C(6)H(5)O(7))].4H(2)O) did not show any toxicity after 3h, but severe toxicity after 24h in both cell types (viability at 500 microM/24h-neurones: 50%, glia: 30%). AlCit3 ((NH(4))(5)[Al(3)(C(6)H(4)O(7))(3)(OH)(H(2)O)].(NO(3)).6H(2)O), exhibited a cell type specific toxicity profile, and only affected neuronal viability at both time points (neuronal viability at 500 microM/3h: 20%). The medium type and presence of serum (FBS) was also found to contribute to the toxicity pattern, with serum providing partial protection. Since the Al(III) compounds introduced here are assumed to form in vivo, our data raise further awareness for the toxicity of Al(III) in general, and for the importance of Al speciation and cell type specific actions in its toxicity.
Original languageEnglish
Pages (from-to)576-586
Number of pages11
JournalNeurotoxicology
Volume28
Issue number3
Early online date4 Jan 2007
DOIs
Publication statusPublished - May 2007

Keywords

  • aluminum compounds
  • animals
  • cell death
  • cell survival
  • cultured cells
  • culture media
  • serum free culture media
  • hippocampus
  • computer assisted image processing
  • neuroglia
  • neurons
  • organometallic compounds
  • rats
  • atomic spectrophotometry,
  • structure activity relationship
  • X-Ray diffraction
  • glia
  • Alzheimer
  • toxicity
  • citrate

Cite this

Platt, B., Drysdale, A. J., Nday, C., Roloff, E. V., Drever, B. D., & Salifoglou, A. (2007). Differential toxicity of novel aluminium compounds in hippocampal culture. Neurotoxicology, 28(3), 576-586. https://doi.org/10.1016/j.neuro.2006.12.008

Differential toxicity of novel aluminium compounds in hippocampal culture. / Platt, Bettina; Drysdale, Alison Jayne; Nday, Christiane; Roloff, Eva Von; Drever, Benjamin David; Salifoglou, Athanasios.

In: Neurotoxicology, Vol. 28, No. 3, 05.2007, p. 576-586.

Research output: Contribution to journalArticle

Platt, B, Drysdale, AJ, Nday, C, Roloff, EV, Drever, BD & Salifoglou, A 2007, 'Differential toxicity of novel aluminium compounds in hippocampal culture' Neurotoxicology, vol. 28, no. 3, pp. 576-586. https://doi.org/10.1016/j.neuro.2006.12.008
Platt, Bettina ; Drysdale, Alison Jayne ; Nday, Christiane ; Roloff, Eva Von ; Drever, Benjamin David ; Salifoglou, Athanasios. / Differential toxicity of novel aluminium compounds in hippocampal culture. In: Neurotoxicology. 2007 ; Vol. 28, No. 3. pp. 576-586.
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AU - Salifoglou, Athanasios

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N2 - The dependence of aluminium (Al) toxicity on its chemical form has been implicated in previous studies, but the complex chemistry of Al in solutions of biological preparations has hampered a reliable assessment. Here, we assessed the toxicity of select and pure Al(III) citrate compounds, well-characterized at physiological pH, and compared it with Al from standard solution (in HCl). Cell death rates of neurones and glia were established in hippocampal cultures following 3h incubations in a HEPES-buffered solution and 24h incubations in full culture medium. Overall, Al toxicity was found to vary considerably between compounds, with duration of exposure, medium type, and cell type as factors. While Al (from atomic absorption standard solution) induced the highest levels of cell death, AlCit1, ((NH(4))(5)[Al(C(6)H(4)O(7))(2)].2H(2)O) was the most toxic citrate compound, and affected viability of neurones more than glia (viability at 500 microM/3h-neurones: 40%; glia: 60%). AlCit2 (K(4)[Al(C(6)H(4)O(7))(C(6)H(5)O(7))].4H(2)O) did not show any toxicity after 3h, but severe toxicity after 24h in both cell types (viability at 500 microM/24h-neurones: 50%, glia: 30%). AlCit3 ((NH(4))(5)[Al(3)(C(6)H(4)O(7))(3)(OH)(H(2)O)].(NO(3)).6H(2)O), exhibited a cell type specific toxicity profile, and only affected neuronal viability at both time points (neuronal viability at 500 microM/3h: 20%). The medium type and presence of serum (FBS) was also found to contribute to the toxicity pattern, with serum providing partial protection. Since the Al(III) compounds introduced here are assumed to form in vivo, our data raise further awareness for the toxicity of Al(III) in general, and for the importance of Al speciation and cell type specific actions in its toxicity.

AB - The dependence of aluminium (Al) toxicity on its chemical form has been implicated in previous studies, but the complex chemistry of Al in solutions of biological preparations has hampered a reliable assessment. Here, we assessed the toxicity of select and pure Al(III) citrate compounds, well-characterized at physiological pH, and compared it with Al from standard solution (in HCl). Cell death rates of neurones and glia were established in hippocampal cultures following 3h incubations in a HEPES-buffered solution and 24h incubations in full culture medium. Overall, Al toxicity was found to vary considerably between compounds, with duration of exposure, medium type, and cell type as factors. While Al (from atomic absorption standard solution) induced the highest levels of cell death, AlCit1, ((NH(4))(5)[Al(C(6)H(4)O(7))(2)].2H(2)O) was the most toxic citrate compound, and affected viability of neurones more than glia (viability at 500 microM/3h-neurones: 40%; glia: 60%). AlCit2 (K(4)[Al(C(6)H(4)O(7))(C(6)H(5)O(7))].4H(2)O) did not show any toxicity after 3h, but severe toxicity after 24h in both cell types (viability at 500 microM/24h-neurones: 50%, glia: 30%). AlCit3 ((NH(4))(5)[Al(3)(C(6)H(4)O(7))(3)(OH)(H(2)O)].(NO(3)).6H(2)O), exhibited a cell type specific toxicity profile, and only affected neuronal viability at both time points (neuronal viability at 500 microM/3h: 20%). The medium type and presence of serum (FBS) was also found to contribute to the toxicity pattern, with serum providing partial protection. Since the Al(III) compounds introduced here are assumed to form in vivo, our data raise further awareness for the toxicity of Al(III) in general, and for the importance of Al speciation and cell type specific actions in its toxicity.

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KW - cell death

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KW - hippocampus

KW - computer assisted image processing

KW - neuroglia

KW - neurons

KW - organometallic compounds

KW - rats

KW - atomic spectrophotometry,

KW - structure activity relationship

KW - X-Ray diffraction

KW - glia

KW - Alzheimer

KW - toxicity

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EP - 586

JO - Neurotoxicology

JF - Neurotoxicology

SN - 0161-813X

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