Nutritional Aspects of Aluminium Toxicity

Klein, Gordon L.

doi:10.1079/nrr19900009

Cited by 20 publications

(8 citation statements)

References 119 publications

(157 reference statements)

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“…A study of drinking water by Martyn et al (1989) concluded that the occurrence of Alzheimer's disease was 1.5 times higher in areas where the mean aluminium concentrations exceeded 0.11 mg L -1 compared with areas where the mean concentrations were less than 0.01 mg L -1 . An epidemiological survey by Neri and Hewitt (1991) appears to confirm the findings of Martyn et al .. A recent paper by Klein (1990) reviews the nutritional aspects of aluminium toxicity, and concludes that the method by which aluminium reaches the brain, whether it can do so under conditions that produce neurodegenerative diseases, and the action of aluminium in the brain under these conditions all require further study. Deloncle et al ( 1990) have shown that an Al-glutamate complex was able to cross the erythrocyte membrane and the blood-brain barrier to be deposited in the brain.…”

Section: Introductionsupporting

confidence: 52%

Aluminium in tea: SEC-ICP-MS speciation studies of infusions and simulated gastrointestinal digests

Owen

Crews

Massey

1992

Chemical Speciation & Bioavailability

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The speciation of aluminium in tea infusions and in vitro gastrointestinal digests of tea infusions has been investigated using size exclusion chromatography coupled to inductively coupled plasma mass spectrometry (SEC-ICP-MS). At pH 2.5, following simulated gastric treatment, AI from tea eluted at a similar retention volume to that obtained for an aqueous AI standard. At pH 5.5, an aqueous AI standard was eluted from an SEC column in Tris buffer (AI recovery "" 1 00%) only in the presence of a complexing agent (NaF), and at a retention volume corresponding to a molecular mass greater than that expected for an ionic species. Aluminium associated with a tea infusion eluted in two fractions: a higher molecular weight fraction corresponding to AI strongly bound to ligands in the tea, and a lower molecular weight fraction probably comprised of labile AI eluting as AI-F complexes. Simulated gastrointestinal digestion produced three Al-bearing fractions, of which the two at higher molecular mass represented ligand-bound AI. The molarity of the Tris buffer strongly influenced the retention volume of the AI fractions, particularly for the ligand-bound AI. After simulated gastrointestinal digestion, the soluble labile fraction (15% of the AI from the tea infusion) was considered to be potentially available for absorption. The actual proportion of the fraction that might be absorbed would depend upon a number of physiological and nutritional factors.

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Section: Introductionsupporting

confidence: 52%

Aluminium in tea: SEC-ICP-MS speciation studies of infusions and simulated gastrointestinal digests

Owen

Crews

Massey

1992

Chemical Speciation & Bioavailability

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“…Detailed analysis of the TPN solution components and intravenously administered medications revealed Al contamination of many of the components. A full list, when last determined by our group, is given in Table 1 below [ 15 , 31 ], but the main sources were calcium and phosphate salts, albumin and heparin. On careful examination of the contaminated solutions shown in Table 1 the wide variability of Al content is evidence supporting the lack of quality control during the manufacturing process.…”

Section: Sources Of Al Contaminationmentioning

confidence: 99%

Aluminum toxicity to bone: A multisystem effect?

Klein

2019

Osteoporosis and Sarcopenia

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Aluminum (Al) is the third most abundant element in the earth's crust and is omnipresent in our environment, including our food. However, with normal renal function, oral and enteral ingestion of substances contaminated with Al, such as antacids and infant formulae, do not cause problems. The intestine, skin, and respiratory tract are barriers to Al entry into the blood. However, contamination of fluids given parenterally, such as parenteral nutrition solutions, or hemodialysis, peritoneal dialysis or even oral Al-containing substances to patients with impaired renal function could result in accumulation in bone, parathyroids, liver, spleen, and kidney. The toxic effects of Al to the skeleton include fractures accompanying a painful osteomalacia, hypoparathyroidism, microcytic anemia, cholestatic hepatotoxicity, and suppression of the renal enzyme 25-hydroxyvitamin D-1 alpha hydroxylase. The sources of Al include contamination of calcium and phosphate salts, albumin and heparin. Contamination occurs either from inability to remove the naturally accumulating Al or from leeching from glass columns used in compound purification processes. Awareness of this long-standing problem should allow physicians to choose pharmaceutical products with lower quantities of Al listed on the label as long as this practice is mandated by specific national drug regulatory agencies.

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“…A1 is found as a contaminant in dialysis and total parenteral nutrition (TPN) solutions and is therefore a hazard for long term TPN and dialysis patients (Monteagudo et al 1989). Absorption from dietary sources is generally regarded to be low (< 3 YO) and is < 1 O h for Al-containing antacids (Malluche & Faugere, 1988;Klein, 1990).…”

Section: A L U M I N I U Mmentioning

confidence: 99%