Bioavailability and Intestinal Absorption of Aluminum in Rats : Effects of Aluminum Compounds and Some Dietary Constituents

Abstract

In the present investigation, the deposition of aluminum in intestinal fragment and the appearance in blood were studied in a perfused rat intestine in situ for 1 h with several aluminum forms (16 mM). We observed that aluminum absorption was positively correlated with the theoretic affinity of aluminum and the functional groups of the chelating agent. The absorption of aluminum after ingestion of organic compounds is more important than after ingestion of mineral compounds, with the following order: Al citrate > Al tartrate, Al gluconate, Al lactate > Al glutamate, Al chloride, Al sulfate, Al nitrate. Absorption depends on the nature of the ligands associated with the Al3+ ion in the gastrointestinal fluid. The higher the aluminum retention in intestinal fragment, the lower the absorption and appearance in blood. However, the higher aluminum concentration is always in the jejunal fragment because of the influence of pH variation on this fragment. Another objective of the present study was to determine the influence of several parameters on aluminum citrate absorption: with or without 0.1 mmol dinitrophenol/L, with aluminum concentration from 3.2, 16, 32, and 48, to 64 mmol/L, media containing 0, 3, or 6 mmol Ca/L, with or without phosphorus or glucose. It is concluded that aluminum is absorbed from the gastrointestinal tract by (1) a paracellular energy independent and nonsaturable route, mainly used for high aluminum concentration, which is modified by extracellular calcium, and (2) a transcellular and saturable route, the aluminum level was not modified with enhancement of aluminum quantity in intestinal lumen. This pathway can be similar with calcium transfer through the intestine and is energy dependent because of a decrease of aluminum absorption that follows the removal of glucose and phosphorus.

Potential of Lactobacillus plantarum CCFM639 in Protecting against Aluminum Toxicity Mediated by Intestinal Barrier Function and Oxidative Stress

“…The intestinal tract is the first barrier against Al exposure. Previous studies reported that the intestinal tract was the main storage organ for Al: forty percent of the ingested Al was found to accumulate in the intestinal mucosa [6,7]. The intestinal barrier consists of a single layer of epithelial cells and tight junction (TJ) proteins, acting as the body’s first line of defense against harmful substances, including heavy metals [8].…”

Aluminium content of selected foods and food products

“…Increased aluminium concentrations were found in the brains of deceased Alzheimer's patients. Other studies, however, have been unable to find definite indications supporting the hypothesis that aluminium plays a causative role in Alzheimer's disease or causes pathological alterations in vivo in the species studied [14][15][16][17][18][19][20].…”

Neuroprotective Activity of Garcinia pedunculata Roxb ex Buch Ham Fruit Extract Against Aluminium Chloride Induced Neurotoxicity in Mice

“…Aluminium acts as a pro oxidant and on continuous exposure starts accumulation in cortex, hypothalamus and different parts of brain, where it induces the formation of reactive oxygen species (ROS) and result in oxidative damage. 4 Aluminium also promotes amyloidosis β peptide formation and amyloidosis which leads to Alzheimer's disease. Increased accumulation of AlCl 3 in brain will affect the slow and fast axonal transports and cause neuro-inflammation and synoptic structural abnormality resulting in neurodegeneration.…”