Most metals are deposited to a much greater extent than average in a few organs: liver, kidneys, and skeleton. However, the proportion of the total body burden deposited in these is variable and depends on many factors, including the chemical properties of the ion and the age, sex, and metabolic status of the individual. The major site of deposition of aluminum is the skeleton. Skeletal deposits of aluminum have been demonstrated in normal bone using chemical analysis and are easily detected in bone from renal failure patients using histochemical staining techniques.
The levels of aluminum deposited in the liver are uncertain. Published measurements of total liver aluminum suggest values of 6-9 mg for normal adults, indicating that a significant fraction of the aluminum body burden is present in this organ. However, external counting of 26Al did not indicate large liver deposits. Moreover, a comparative failure of aluminum to deposit in the normal liver would be consistent with the low levels of fecal excretion seen and with the low concentrations of aluminum found in the livers of some dialyed renal patients. Also, at least in rats, the relative depositions of trivalent metals in the skeleton and liver have been shown to be a function of ion size, with appreciable liver deposition occurring only where the ion size is large. The ion size of aluminum is very small. However, the observation that with time aluminum levels build up in red blood cells may indicate the presence of a delayed pathway of aluminum accumulation by the liver since this organ is involved in the breakdown of hemoglobin.
Within the skeleton, aluminum, in common with most other polyvalent metal ions, initially deposits as a very thin layer on bone surfaces. The mechanisms of deposition have not been investigated, but one report suggests that three may be involved: entrapment of aluminum ions within the hydration shell of existing bone mineral; incorporation of aluminum into new bone mineral at sites of bone apposition; and binding of the metal to acidic organic components of the bone matrix, such as phosphoproteins.
Subsequently, aluminum remains on bone surfaces until it back-exchanges into tissue fluids, the bone surface is removed by osteoclasts, or the bone surface is buried by the apposition of new bone. These processes will result in the gradual loss of bone aluminum and in a transfer of aluminum from bone surfaces to the volume of the bone matrix. Such volume deposits are clearly seen in stained biopsy sections from dialysis patients.
The back-exchange of deposited aluminum, from bone surfaces to blood, may occur relatively quickly and its rate will be an important determinant of the rate of early loss of aluminum from the body. At longer times after deposition, more aluminum will be removed by bone turnover. Given that in adult man the rate of bone turnover is very low (3-20% per year), most firmly deposited metal may be expected to be retained in the body for tens of years. This accounts for the reported body retention of 2% of the injected 26Al at 5 years postinjection and its low rate of loss at this time (equivalent retention half-time greater than 5 years). In children, who exhibit high rates of bone growth and turnover, aluminum is lost more rapidly.
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