A long-term intravenous model of aluminum maltol toxicity in rabbits: Tissue distribution, hepatic, renal, and neuronal cytoskeletal changes associated with systemic exposure

Bertholf, Roger L.; Herman, Mary M.; Savory, John; Carpenter, R. M.; Sturgill, Benjamin C.; Katsetos, Christos D.; VandenBerg, Scott R.; Wills, M. R.

doi:10.1016/0041-008x(89)90134-8

Cited by 99 publications

(38 citation statements)

References 29 publications

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“…This issue had been addressed in early attempts to develop a chronic model of aluminum neurotoxicity in which chronic intracisternal "reservoirs" of aluminum were utilized. Although the neuropathological changes were ultimately nonselective, a temporal analysis suggested a hierarchy to the neuronal sensitivity to aluminum [57][58][59][60]. The use of subcutaneous aluminum tartrate further supported this conclusion and also demonstrated that the neuropathology of such a model might be reversible [61,62].…”

Section: Chronic Aluminum Neurotoxicitysupporting

confidence: 50%

Motor neuron disease and trace element toxicity

Strong

2000

J. Trace Elem. Exp. Med.

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Section: Chronic Aluminum Neurotoxicitysupporting

confidence: 50%

Motor neuron disease and trace element toxicity

Strong

2000

J. Trace Elem. Exp. Med.

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“…Moreover, the rats presented (Yokel and McNamara. 1985;Domingo et al 1987;Bertholf et al 1989;Cherroret et al 1996). Nevertheless, there are data inferring that 3-month aluminum lactate administration in adult rats did not produce modifications in the corporal weight using the same total dose per week in adult animals (6.87 mg Al per week; Ballanti et al 1989).…”

Section: Discussionmentioning

confidence: 92%

Effects of aluminum on phosphate metabolism in rats: a possible interaction with vitamin D3 renal production

et al. 2004

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The effect of chronic aluminum (Al) administration on the phosphorous (Pi) metabolism of different target tissues was studied. Male Wistar rats received aluminum lactate for 3 months (5.75 mg/kg bodyweight of Al, i.p., three times per week). The animals were studied at the end of the 1st, 2nd and 3rd month of treatment. They were housed individually in metabolic cages for 4 days to study Pi and calcium (Ca) balance. Daily food and water intakes were recorded for all animals and urine and feces were collected for Pi and calcium assays. After 3 months the Pi intestinal absorption and the Pi deposition in bone were studied using 32Pi. Another group of rats was treated daily for 7 days with calcitriol (0.08 microg/kg body weight in sesame oil, i.p.) and the Pi balance was studied for the last 4 days. The results indicated that chronic administration of Al affected simultaneously the Pi and calcium balance, with a significant diminution of calcium and increased Pi accretion in bones, together with a diminution in the intestinal absorption of Pi. The treatment of the rats with calcitriol promoted a normalized Pi balance in Al treated rats. These findings suggest that Al could modify the Pi metabolism acting directly on intestine, kidney and bone, or indirectly through possible changes in the levels of vitamin D3.

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“…For Al treatment, Al maltolate was prepared as a stock solution of 25 mM in sterile water (Berthol et al, 1989) and then passed through 0.2 mm filter. Al was added to growth medium just before use.…”

Section: Cell Culturementioning

confidence: 99%

Aluminum Maltolate-Induced Toxicity in NT2 Cells Occurs Through Apoptosis and Includes Cytochrome c Release

et al. 2004

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Aluminum (Al) compounds are neurotoxic and have been shown to induce experimental neurodegeneration although the mechanism of this effect is unclear. In order to study this neurotoxic effect of Al, we have developed an in vitro model system using Al maltolate and human NT2 cells. Al maltolate at 500 mM caused significant cell death with a 24-h incubation and this toxicity was even more evident after 48 h. Lower doses of Al maltolate were also effective, but required a longer incubation for cell death. Nuclear fragmentation suggestive of apoptosis was observed as early as three hours and increased substantially through 24 h. Chromatin condensation and nuclear fragmentation were confirmed by electron microscopy. In addition, TUNEL positive nuclei were also observed. The release of cytochrome c was demonstrated with Western blot analysis. This in vitro model using human cells adds to our understanding of Al neurotoxicity and could provide insight into the neurodegenerative processes in human disease. #

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A long-term intravenous model of aluminum maltol toxicity in rabbits: Tissue distribution, hepatic, renal, and neuronal cytoskeletal changes associated with systemic exposure

Cited by 99 publications

References 29 publications

Motor neuron disease and trace element toxicity

Motor neuron disease and trace element toxicity

Effects of aluminum on phosphate metabolism in rats: a possible interaction with vitamin D3 renal production

Aluminum Maltolate-Induced Toxicity in NT2 Cells Occurs Through Apoptosis and Includes Cytochrome c Release

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