Autism Studies and Related Medical Conditions, January 2009 - TACA

into ferritin or heme. It is not yet known which steps in iron metabolism are
disrupted by Al, if they involve a single mechanism of action, or even if this
disruption in iron metabolism accounts for the anemia seen in Al toxicosis. In
kidney, research is needed to evaluate Al nephrotoxicity; there are almost no
studies in this area. Furthermore, research is needed to evaluate mechanisms of
renal Al excretion, presently shown by one study to occur at the distal tubule.
Such studies might well throw light on whether Al plays a role in aggravating
renal insufficiency, or whether the role of the kidney in Al toxicosis is limited
to the causative effect of renal compromise on Al accumulation. In summary, while
a number of mechanisms have been proposed for the toxic action of Al, no single
mechanism emerges to explain these diverse effects of systemic Al.
Recommendations for future research are presented and summarized in Table 1.
Publication Types:
Review
PMID: 8772804 [PubMed - indexed for MEDLINE]
18: J Toxicol Environ Health. 1996 Aug 30;48(6):585-97.
What we know and what we need to know about developmental aluminum toxicity.
Golub MS, Domingo JL.
Department of Internal Medicine, University of California, Davis 95616, USA.
Information concerning developmental aluminum (Al) toxicity is available from
clinical studies and from animal testing. An Al toxicity syndrome including
encephalopathy, osteomalacia, and anemia has been reported in uremic children
receiving dialysis. In addition, some components of the syndrome, particularly
osteomalacia, have been reported in non-dialyzed uremic children receiving
Al-based phosphate binders, nonuremic infants receiving parenteral nutrition with
Al-containing fluids, and nonuremic infants given high doses of Al antacids. The
number of children in clinical populations that are at risk of Al toxicity is not
known and needs to be determined. Work in animal models (rats, mice, and rabbits)
demonstrates that Al is distributed transplacentally and is present in milk. Oral
Al administration during pregnancy produces a syndrome including growth
retardation, delayed ossification, and malformations at doses that also lead to
reduced maternal weight gain. The severity of the effects is highly dependent on
the form of Al administered. In the postnatal period, reduced pup weight gain and
effects on neuromotor development have been described as a result of
developmental exposures. The significance of these findings for human health
requires better understanding of the amount and bioavailability of Al in food,
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