Toxicity aluminum

L. V. Kochian, Cellular mechanisms of aluminum toxicity and resistance in plants. Aiwu Rev. Plan Physiol. Plant Mol. Biol. 46 231 (1995). 

The most dramatic consequence of sHPT is alterations in bone turnover and the development of ROD. Other complications of CKD can also promote ROD. Metabolic acidosis decreases bone formation and aluminum toxicity causes aluminum uptake into bone in place of calcium, weakening the bone structure. The pathogenesis of sHPT and ROD are depicted in Fig. 23-5. 

Solutions that contain sodium citrate/citric acid (Shohl s solution and Bicitra) provide 1 mEq/L (1 mmol/L) each of sodium and bicarbonate. Polycitra is a sodium/potassium citrate solution that provides 2 mEq/L (2 mmol/L) of bicarbonate, but contains 1 mEq/L (1 mmol/L) each of sodium and potassium, which can promote hyperkalemia in patients with severe CKD. The citrate portion of these preparations is metabolized in the liver to bicarbonate, while the citric acid portion is metabolized to C02 and water, increasing tolerability compared to sodium bicarbonate. Sodium retention is also decreased with these preparations. However, these products are liquid preparations, which may not be palatable to some patients. Citrate can also promote aluminum toxicity by augmenting aluminum absorption in the GI tract. 

During lactation, sucralfate maybe the best choice for treatment of heartburn because it is not absorbed systemically.25 If symptoms are not controlled, the H2 blockers are acceptable alternatives.14,25 Avoid aluminum-containing antacids during lactation owing to reports of aluminum toxicity in otherwise healthy infants.22... 

Factors that can predispose patients to developing metabolic bone disease include deficiencies of phosphorus, calcium, and vitamin D vitamin D and/or aluminum toxicity amino acids and hypertonic dextrose infusions chronic metabolic acidosis corticosteroid therapy and lack of mobility.35,39 Calcium deficiency (due to decreased intake or increased urinary excretion) is one of the major causes of metabolic bone disease in patients receiving PN. Provide adequate calcium and phosphate with PN to improve bone mineralization and help to prevent metabolic bone disease. Administration of amino acids and chronic metabolic acidosis also appear to play an important role. Provide adequate amounts of acetate in PN admixtures to maintain acid-base balance. 

In contrast to transition metals iron and copper, which are well-known initiators of in vitro and in vivo lipid peroxidation (numerous examples of their prooxidant activities are cited throughout this book), the ability of nontransition metals to catalyze free radical-mediated processes seems to be impossible. Nonetheless, such a possibility is suggested by some authors. For example, it has been suggested that aluminum toxicity in human skin fibroblasts is a consequence of the enhancement of lipid peroxidation [74], In that work MDA formation was inhibited by SOD, catalase, and vitamins E and C. It is possible that in this case aluminum is an indirect prooxidant affecting some stages of free radical formation. 

Wilkinson, K. J., Campbell, P. G. C. and Couture, P. (1990). Effect of fluoride complexation on aluminum toxicity towards juvenile atlantic salmon (Salmo salar), Can. J. Fish. Aquat. Sci., 47, 1446-1452. 

Neville, C. M. and Campbell, P. G. C. (1988). Possible mechanisms of aluminum toxicity in a dilute, acidic environment to fingerlings and older life stages of salmonids, Water, Air, Soil Poll., 42, 311-327. 

Aluminum toxicity Some products may contain aluminum. See individual product labeling for ingredients. 

Given projected levels of population growth, world food production must more than triple in the next 50 years to adequately feed 9.6 billion people. A long-term solution may turn on increasing crop productivity on the arable land affected by aluminum toxicity, and citric acid may play an important role in achieving this goal. 

Deferoxamine is isolated from Streptomycespilosus. It binds iron avidly but essential trace metals poorly. Furthermore, while competing for loosely bound iron in iron-carrying proteins (hemosiderin and ferritin), it fails to compete for biologically chelated iron, as in microsomal and mitochondrial cytochromes and hemoproteins. Consequently, it is the chelator of choice for iron poisoning (Chapters 33 and 59). Deferoxamine plus hemodialysis may also be useful in the treatment of aluminum toxicity in renal failure. Deferoxamine is poorly absorbed when administered orally and may increase iron absorption when given by this route. It should therefore be administered intramuscularly or, preferably, intravenously. It is believed to be metabolized, but the pathways are unknown. The iron-chelator complex is excreted in the urine, often turning the urine an orange-red color. 

The mechanism of action for aluminum toxicity is not known, but the element is known to compete in biological systems with cations, especially magnesium (MacDonald and Martin 1988) despite an oxidation state difference, and to bind to transferrin and citrate in the blood stream (Gannot 1986). It may also affect second messenger systems and calcium availability (Birchall and Chappell 1988), and irreversibly bind to cell nucleus components (Crapper-McLachlan 1989 Dryssen et al. 1987). Aluminum has also been shown to inhibit neuronal microtubule formation. However, much more work is needed before a mechanism can be proposed. 

In the cases in which human aluminum toxicity has occurred, the target organs appear to be the lung, bone, and the central nervous system. No specific molecular mechanisms have been elucidated for human toxicity to aluminum. In animal models, aluminum can also produce lung, bone, and neurotoxicity, as well as developmental effects in offspring. 

The mechanism of action for aluminum toxicity is not known thus there are no known ways of interfering with its mechanism of action. 

Effect The mechanisms of action for aluminum toxicity is not known. Aluminum has a number of subcellular effects, such as affecting cation protein interactions or microtubule structure and effects on cellular signaling mechanisms, which can be observed in vitro. Further information would be useful in indicating whether these subcellular effects lead to disease processes. Studies on the mechanism of action of aluminum may lead to biochemical tests that can be used in the early identification of aluminum toxicity. 

There are a large number of ongoing studies covering many aspects of aluminum toxicity. Studies supported by the federal government are listed in Table 2-5 (FEDRIP 1998). 

Golub MS Mouse model for chronic oral aluminum toxicity University of California Davis National Institute of Environmental Health Sciences... 

Table 2-5. Ongoing Studies for Aluminum Toxicity (continued)...

North Carolina State University, Crop Sciences Department Raleigh, NC Research on the mechanism of aluminum toxicity in plants. This study will determine the extent of aluminum accumulation inside cells at the root apex using microanalytical techniques and will define associated effects on cell division, cell expansion, and cellular accumulation of calcium and magnesium. U.S. Department of Agriculture... 

Abreo K, Glass J. 1993. Cellular, biochemical, and molecular mechanisms of aluminum toxicity. Nephrol Dial Transplant Suppl 1 5-11. 

Aitken RL, Moody PW, Compton BL. 1990. A simple bioassay for the diagnosis of aluminum toxicity in soils. Commun Soil Sci Plant Anal 21 511-529. 

Alfrey AC. 1993b. Aluminum toxicity in patients with chronic renal failure. Ther Drug Monit 15 593-597. 

Altmann P. 1993. Aluminum toxicity in dialysis patients No evidence for a threshold serum aluminum concentration. Nephrol Dial Transplant Suppl 1 25-34. 

Andia J, Cannata B. 1996. Aluminum toxicity Its relationship with bone and iron metabolism. Nephrol Dial Transplant ll(Suppl. 3) 69-73. 

Brenner SR, Yoon K-W. 1994. Aluminum toxicity in rat hippocampal neurons. Neurosci Lett 178 260-262. 

Burgess E. 1991. Aluminum toxicity from oral sucralfate therapy. Nephron 59 523-524. 

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