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PubMed2000

Aluminum speciation studies in biological fluids. Part 6. Quantitative investigation of aluminum(III)-tartrate complex equilibria and their potential implications for aluminum metabolism and toxicity.

Recent epidemiological studies have confirmed the existence of a correlation between aluminum level in low-silica drinking water and prevalence of Alzheimer's disease. Also, oral aluminum-based phosphate binders and antacids may induce acute aluminum toxicity. Whatever the source of the metal ingested, its bioavailability is a function of the chemical forms under which it occurs in the gastrointestinal tract, i.e. of the ligands with which the Al3+ ion may associate. Dietary acids in particular can favor the bioavailability of aluminum in different ways: by increasing its solubility, by complexing it into neutral species, and/or by acting indirectly on its absorption process. Among these, tartaric acid is commonly found in fruits and in industrial foods and drinks, and may therefore be ingested together with environmental or/and therapeutic aluminum. The present work examines its potential influence on aluminum bioavailability. Firstly, Al(III)-tartrate complex formation constants have been determined under physiological conditions (37 degrees C, 0.15 M NaCl). Then these constants have been used to simulate the influence of tartrate on aluminum speciation in different gastrointestinal situations in which phosphate was also taken into account. Under normal conditions of aluminum contamination, tartrate is expected to keep the metal soluble throughout the whole pH range of the small intestine, which is likely to enhance its bioavailability. Even at low concentrations, tartrate also gives rise to two neutral complexes that span over the 1.5-7.5 pH interval, a phenomenon that is aggravated by increased aluminum levels as may result from aluminum hydroxide therapy. The co-occurrence of dietary phosphate reduces the fraction of aluminum neutralized by tartrate under normal conditions, but this effect quickly decreases with increasing aluminum doses. Even the therapeutic use of aluminum phosphate is not expected to be totally safe in the presence of tartaric acid. As plasma simulations show that no aluminum mobilization can be expected from tartrate that could enhance aluminum excretion, avoiding ingestion of tartaric acid during any form of aluminum-based therapy appears advisable.

Aluminum↗
PubMed2001

Aluminum speciation studies in biological fluids. Part 7. A quantitative investigation of aluminum(III)-malate complex equilibria and their potential implications for aluminum metabolism and toxicity.

As a nonessential element, aluminum may be toxic at both environmental and therapeutic levels, depending on ligand interactions. Dietary acids that normally occur in fruits and vegetables and commonly serve as taste enhancers are good ligands of the Al(3+) ion. Malic acid is one of these and also one of the most predominant in food and beverages. The present paper reports an examination of its potential influence on aluminum bioavailability through speciation calculations based on Al(III)-malate complex formation constants especially determined for physiological conditions. According to the results obtained, malate appears to be extremely effective in maintaining Al(OH)(3) soluble over the whole pH range of the small intestine under normal dietary conditions. In addition, two neutral Al(III)--malate complexes are formed whose percentages are maximum from very low malate levels. When aluminum is administered therapeutically as its trihydroxide, the amount of metal neutralized by malate peaks as its solubility pH range regresses to its original limits in the absence of malate. The enhancing effect of malate towards aluminum absorption is therefore virtually independent of the aluminum level in the gastrointestinal tract. The presence of phosphate in the gastrointestinal juice is expected to limit the potential influence of malate on aluminum absorption. Under normal dietary conditions, phosphate effectively reduces the fraction of aluminum neutralized by malate but without nullifying it. Aluminum phosphate is predicted to precipitate when aluminum levels are raised as with the administration of aluminum hydroxide, but a significant amount of neutral aluminum malate still remains in solution. Even therapeutic aluminum phosphate is not totally safe in the presence of malate, even at low malate concentrations. As plasma simulations predict that no compensatory effect in favor of aluminum excretion may be expected from malate, simultaneous ingestion of malic acid with any therapeutic aluminum salt should preferably be avoided.

Aluminum↗
PubMed2003

Aluminum speciation studies in biological fluids. Part 9. A quantitative investigation of aluminum(III)-glutamate complex equilibria and their potential implications for aluminum metabolism and toxicity.

As a nonessential element, aluminum is likely to be toxic both at low usual dietary levels in the long run (chronic toxicity) and at high therapeutic levels in shorter periods of time (acute toxicity). In both situations, aluminum toxicity is a direct function of aluminum bioavailability, which is itself dependent on Al(3+) solubility and charge neutralization. Dietary acids, by their intrinsic acidity and coordinating capacity, can extend the pH range, thus the section of the gastrointestinal tract, within which the Al(3+) ion remains soluble, and also help Al(3+) diffusion across the intestinal epithelium through the formation of neutral complex species. The present work examines the impact of glutamic acid, an essential amino acid also widely used in industrial food and drinks, on aluminum speciation in the gastrointestinal tract and blood plasma. Complex formation between the Al(3+) ion and glutamate has first been investigated through potentiometric titrations, complex stoichiometries being then checked by ESI mass spectrometry and NMR measurements. A series of mono- and polynuclear species has been characterized, whose influence on aluminum distribution in vivo has been assessed by computer simulation. The capacity of glutamate to maintain Al(3+) ions in solution under normal dietary conditions is predicted to be intermediate between glycine-like amino acids and succinate on the one hand, and tartrate and malate on the other hand, its Al(3+) neutralization effect being similar to that of succinate, tartrate and malate. These results, which point to a potential aggravating role of glutamate on aluminum gastrointestinal absorption, substantiate recent observations made on rats. In spite of the moderate effect expected from glutamate on aluminum bioavailability under most aluminum-based therapies investigated, attention is therefore called to the risk of glutamic acid ingestion simultaneously to any aluminum therapeutic form. Incidentally, the former implication of 'the' aluminum glutamate complex in the transfer of aluminum through the blood-brain barrier of aluminum loaded rats may effectively be attributed to one of the species characterized here, but is of no significance at all to aluminum contamination in humans, even at most extreme levels.

Aluminum Compounds↗
PubMed1998

Aluminum speciation studies in biological fluids. Part 4. A new investigation of aluminum-succinate complex formation under physiological conditions, and possible implications for aluminum metabolism and toxicity.

Previous in vivo studies devoted to the capacity of succinate to influence aluminum metabolism have led to apparent contradictory results. Understanding the mechanisms that lie behind such discrepancies requires a knowledge of aluminum-succinate interactions at the molecular level. In the absence of possible direct analysis of the ultrafiltrable fraction of aluminum in vivo, computer simulations can help quantify the mobilizing power of succinate towards aluminum in the main biofluids. Based on this technique, a first attempt to elucidate the above issue was made using especially determined aluminum-succinate formation constants. However, further investigations have led to reconsider the stoichiometry of the aluminum-succinate complexes characterized on that occasion. The present work deals with these new investigations. The results obtained confirm the great complexity of the aluminum-succinate system. No less than seven species, among which five polynuclear complexes, have been characterized in two series of independent experiments. New simulations indicate that succinate is expected to facilitate aluminum gastrointestinal absorption to a greater extent than initially predicted when the metal is administered as its trihydroxide, especially at high concentrations of the metal. In contrast, succinate is not able to significantly increase aluminum absorption when ingested concomitantly with aluminum phosphate. It is also confirmed that succinate cannot influence the fate of aluminum in blood plasma, which supports the view that the protective effect of succinate against aluminum toxicity in mice is not due to aluminum complexation.

Aluminum↗
PubMed1993

Serum aluminum transport and aluminum uptake in chronic renal failure: role of iron and aluminum metabolism.

Several factors have been blamed for increasing gastrointestinal absorption of aluminum. The likely role of iron metabolism was suggested some years ago. As iron and aluminum share many chemical properties, it is reasonable to think they also share biological pathways. The aim of this study was: (a) to evaluate serum aluminum transport and its relationship with iron-binding capacity, and (b) to investigate aluminum hydroxide absorption as a function of iron and aluminum. We investigated 127 patients with chronic renal failure undergoing hemodialysis in a study divided into two phases: phase 1, a basal study to investigate serum iron and aluminum status, and phase 2 in which an aluminum absorption test was performed. In phase 1, we found that the lower basal serum iron and iron transferrin saturation the greater serum aluminum (p < 0.001). In phase 2, we found a negative relationship between serum aluminum increments after the test and basal levels of serum aluminum and iron (r = -0.70; p < 0.001). These results suggest that the amount of either aluminum or iron carried by transferrin may influence the transferrin capacity to bind the other element and also may modulate, together with other factors, the gastrointestinal absorption of iron and aluminum.

Aluminum↗
PubMed1992

Sequential serum aluminum and urine aluminum: creatinine ratio and tissue aluminum loading in infants with fractures/rickets.

Aluminum toxicity is associated with the development of bone disorders, including fractures, osteopenia, and osteomalacia. Fifty-one infants with a mean (+/- SEM) birth weight of 1007 +/- 34 g, gestational age of 28.5 +/- 0.3 weeks, and serial radiographic documentation at 3, 6, 9, and 12 months for the presence (n = 16) or absence (n = 35) of fractures and/or rickets were studied at the same intervals to determine the serial changes in serum aluminum concentrations and urine aluminum-creatinine ratios. Autopsy bone samples were used to determine the presence of tissue aluminum. Serum aluminum concentrations from 46 infants were stable and similar between groups, with mean values between 15 and 22 micrograms/L. Urine aluminum-creatinine (micrograms per milligram) ratios from 14 infants were higher in infants with fractures and/or rickets (0.26 +/- 0.06 vs 0.12 +/- 0.04) at onset, and rate of decrease in aluminum-creatinine ratio was faster in infants without fractures and/or rickets. All but three infants were tolerating complete enteral feeding at all sampling points. One infant who received aluminum-containing antacid had marked increase in serum aluminum to 83 micrograms/L while urine aluminum-creatinine ratio increased from 0.09 to a peak of 8.53. Vertebrae from three infants at autopsy (full enteral feeding was tolerated for 37 and 41 days in two infants, respectively) showed aluminum deposition in the zone of provisional calcification and along the newly formed trabecula.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗
PubMed2001

Aluminum activates a citrate-permeable anion channel in the aluminum-sensitive zone of the maize root apex. A comparison between an aluminum- sensitive and an aluminum-resistant cultivar.

In search for the cellular and molecular basis for differences in aluminum (Al) resistance between maize (Zea mays) cultivars we applied the patch-clamp technique to protoplasts isolated from the apical root cortex of two maize cultivars differing in Al resistance. Measurements were performed on protoplasts from two apical root zones: The 1- to 2-mm zone (DTZ), described as most Al-sensitive, and the main elongation zone (3-5 mm), the site of Al-induced inhibition of cell elongation. Al stimulated citrate and malate efflux from intact root apices, revealing cultivar differences. In the elongation zone, anion channels were not observed in the absence and presence of Al. Preincubation of intact roots with 90 microM Al for 1 h induced a citrate- and malate-permeable, large conductance anion channel in 80% of the DTZ protoplasts from the resistant cultivar, but only 30% from the sensitive cultivar. When Al was applied to the protoplasts in the whole-cell configuration, anion currents were elicited within 10 min in the resistant cultivar only. La3+ was not able to replace or counteract with Al3+ in the activation of this channel. In the presence of the anion-channel blockers, niflumic acid and 4, 4'-dinitrostilbene-2, 2'disulfonic acid, anion currents as well as exudation rates were strongly inhibited. Application of cycloheximide did not affect the Al response, suggesting that the channel is activated through post-translational modifications. We propose that the Al-activated large anion channel described here contributes to enhanced genotypical Al resistance by facilitating the exudation of organic acid anions from the DTZ of the maize root apex.

Aluminum↗
PubMed1991

Evaluation of potential aluminum chelators in vitro by aluminum solubilization ability, aluminum mobilization from transferrin and the octanol/aqueous distribution of the chelators and their complexes with aluminum.

Representative amino acids, carboxylic acids, a ketone, hydroxamic acids, 3-hydroxypyridinones and a linear catecholcarboxyamide were tested in vitro to estimate their aluminum (Al) chelation potential. Their ability to solubilize Al from insoluble Al borate in a previously described octanol/aqueous (o/a) system was tested. Salicylhydroxamic acid, rhodotorulic acid, the 3-hydroxypyridin-4-ones and a sulfonated linear polycatecholcarboxamide significantly increased solubilized Al, suggesting Al chelation potential. Some of the above compounds and some compounds previously shown to solubilize Al in the o/a system were tested for their ability to mobilize Al from the Al plasma binding protein transferrin. Chelators solubilizing Al in the o/a system were comparably effective in mobilizing Al from transferrin, supporting the utility of the o/a system as a screening method. The o/a distribution coefficient of each chelator was determined, when possible, to assess its hydrophilicity. When compared with the suggested desirable hydrophilicity of effective chelators, the o/a distribution coefficient of many of the 3-hydroxypyridin-4-ones and a sulfonated linear polycatecholcarboxamide suggest that they might be able to chelate intracellular Al. The o/a distribution coefficient of each Al-chelator complex was determined, when possible, to predict the likelihood of redistribution within or excretion from the intact animal of this complex. Complexation of chelators with Al usually increased chelator hydrophilicity. The results suggest several compounds that warrant further investigation as potential alternatives to desferrioxamine in the treatment of Al accumulation and toxicity.

1-Octanol↗
PubMed1990

Kinetics of Aluminum Uptake in Triticum aestivum L: Identity of the Linear Phase of Aluminum Uptake by Excised Roots of Aluminum-Tolerant and Aluminum-Sensitive Cultivars.

The identity of a linear phase of aluminum (Al) uptake in Triticum aestivum was investigated by analysis of the kinetics of Al uptake by excised roots and purified cell wall fractions. Classical interpretation of kinetic data suggests that a linear phase of uptake with time reflects uptake across the plasma membrane; however, in studies with Al the possibility that the linear phase of uptake includes accumulation of Al in both the symplasm and the apoplasm has not been discounted. In our experiments, we observed a linear phase of Al uptake at both ambient and low temperatures, although the rate of uptake at 0 degrees C was 53 to 72% less than at 23 degrees C, depending on cultivars. This nonsaturable phase of uptake at low temperature suggests that a portion of the linear phase of Al uptake is nonmetabolic. Furthermore, analysis of Al in cell wall fractions isolated from excised roots pretreated with Al suggests that the linear phase of uptake includes a cell wall component. When excised roots were pretreated with Al, accumulation of Al in purified cell wall material included a linear phase that could not be desorbed with a 30 minute wash in citrate. The rates of linear-phase accumulation of Al by cell wall material and cell contents were similar. In contrast, the linear phase of in vitro uptake of Al by purified cell wall material was completely desorbed by a 30 minute wash with citrate. These results suggest that the linear phase of Al uptake observed in excised roots of T. aestivum included metabolism-dependent binding of Al in apoplasm.

Journal Article↗
PubMed1988

Decrease of serum triglyceride in normal rat fed with 2000 ppm aluminum diet for 67 days. II. Feeding young and adult rats a sucrose diet with addition of aluminum hydroxide and aluminum potassium sulfate.

To confirm the hypotriglyceridemic effect of aluminum (Al), male weanling and adult Wistar rats were fed sucrose diets with the addition of aluminum hydroxide (Al(OH)3) or aluminum potassium sulfate (AlK(SO4)2) for 67 days. As in the foregoing report (C. Sugawara, N. Sugawara, H. Kiyosawa, and H. Miyake, Fundam. Appl. Toxicol. 10, 607-615), no Al-induced anemia or hypophosphatemia was observed and serum Al did not exceed 20 ng/ml. Serum triglyceride (TG) was decreased by aluminum. Serum TG was significantly correlated with the serum nonesterified fatty acid (NEFA) concentration in both the Young groups (R = 0.757, n = 22, p less than 0.01) and the Adult groups (R = 0.727, n = 19, p less than 0.01). Neither serum cholesterol nor phospholipids was affected by Al ingestion. Aluminum caused a decrease in hepatic glycogen in all groups, but the decrease was significant only in Adult groups. Glycerol tri[9,10(n)-3H]oleate was administered by gastric tube into rats fed for 81 days with experimental diets. In all the Al-treated groups serum 3H was significantly greater than in control groups at 3 hr after intubation. At 24 hr after intubation, serum 3H did not differ between Control and Al-treated groups. Total 3H at 24 hr found in serum, liver, and epididymal adipose tissue was not changed significantly by Al feeding. These effects were observed without measurable increase of Al in the serum.(ABSTRACT TRUNCATED AT 250 WORDS)

Alum Compounds↗
PubMed1998

Effect of oral aluminum and aluminum citrate on blood level and short-term tissue distribution of aluminum in the rat.

Aluminum (Al) absorption seems to be very low, but many factors can enhance it in animals and humans. In the present study, we investigated the acute effect of Na citrate on Al absorption by monitoring Al levels in blood and several tissues. For this purpose, 18 Wistar male rats were divided into 3 groups: control, Al, and Al + Na citrate. After a 14-h fasting period, animals were dosed orally with deionized water, or 2 mmol Al chloride, or 2 mmol Al chloride plus 2 mmol Na citrate. Blood samples were taken before and 1, 2, 4, and 6 h after the gavage. Al concentrations in blood, liver, tibia, kidney, and intestinal wall were determined by ICP-OES. In the Al and Al + citrate groups, Al blood concentrations peaked at 1 h and 2 h with higher levels in the Al + citrate group. Al gavage resulted in an increase in Al level in intestinal wall, but not in the other investigated tissues. Simultaneous gavage of citrate with Al significantly increased its tissue levels in tibia, kidney, and in intestinal wall. Our data show clearly that Al as chloride can be absorbed, but not well retained by the organism tissues. Furthermore, the model used in the present study is appropriate for acute studies to investigate the effect of various compounds on Al absorption in the rat.

Administration, Oral↗
PubMed2002

Aluminum deposition in the bone of patients with chronic renal failure--detection of aluminum accumulation without signs of aluminum toxicity in bone using acid solochrome azurine.

In this study, the sensitivity of the aurine tricarboxylic acid (ATA) and acid solochrome azurine (ASA) stain for aluminum were compared under special consideration of the relationship to bone histology in renal osteodystrophy. Al deposition in iliac crest bone biopsies taken from 78 patients with chronic renal failure (CRF) was assessed histochemically using the ATA and ASA stain; the Al accumulation was correlated with bone histology and histomorphometry. Significantly more Al was detectable with the ASA method on trabecular bone surfaces and cement lines (18 +/- 20% vs 4 +/- 12% on surfaces; 13 +/- 18% vs 0.4 +/- 1.3% on cement lines). In 31 cases in which ATA yielded negative results, ASA in contrast indicated Al deposits on up to 20% of the trabecular bone surface. The specimens with more Al on the trabecular bone surface had a significantly higher osteoid volume and osteoid surface. With ATA, these differences were observed at a staining of > or = 10% of the trabecular surface, with ASA at a staining of > or = 40% of the trabecular surface. Therefore, it seems to be possible to detect a very low Al deposition, without any Al-induced changes in bone morphology or signs of Al toxicity in the bone using the ASA method. By contrast, a positive ATA stain is mainly found in biopsies with typical signs of Al-induced changes of histomorphometric bone parameters. We, therefore, recommend the routine use of the ASA stain to detect Al deposition in bone.

Adult↗
PubMed1998

Low serum aluminum values in dialysis patients with increased bone aluminum levels.

BACKGROUND: Using an HPLC/ETAAS hybrid speciation technique we previously demonstrated iron to have a multifold effect on the binding of aluminum to transferrin by limiting the number of available binding sites and decreasing the affinity of transferrin for aluminum. Theoretically, at a 60% iron-transferrin saturation the aluminum-transferrin fraction in serum should not exceed 30 microg/l. In the present study previous experimental data were confronted with recent clinical observations in patients with either normal iron status or iron overload. PATIENTS AND RESULTS: Serum aluminum levels and iron overload: In 38 dialysis patients with a normal iron status and of whom 63% received Al(OH)3 for phosphate binding 26 (68%) had a serum aluminum level >30 microg/l. On the other hand out of 28 transfusional iron overloaded patients; 68% of them taking Al(OH)3, only 1 subject (4%) had a serum aluminum value in excess of 30 microg/l. Taking patients of both groups receiving Al(OH)3 together a significant (p = 0.001) negative correlation (r = -0.5017) was found between the iron-transferrin saturation and the serum aluminum levels. Iron status and parenteral aluminum loading: Also could a significant (p = 0.001) negative correlation (r = -0.6383) between these parameters be found in an independent group of 44 patients which were acutely intoxicated by the use of aluminum-contaminated dialysis fluids. Since in this population aluminum loading occurred parenterally and not via the gastrointestinal tract, a direct effect of iron on the transferrin binding of aluminum rather than on the element's gastrointestinal absorption must have been responsible for the inverse relationship. Bone aluminum and iron overload: Out of 22 patients with a normal iron status (mean + SD serum ferritin: 216 +/- 245 microg/l; iron-transferrin saturation 20.4 +/- 9.6%), all of them having aluminum overload (bone aluminum level >15 microg/g and/or positive Aluminon staining) none of them presented with a serum aluminum <30 microg/l (mean +/- SD: 82.2 +/- 51.6 microg/l). On the other hand out of 13 iron overloaded patients (serum ferritin >800 microg/l; iron-transferrin saturation 61.4 +/- 17.6%) 10 (77%) presented the proposed criteria of aluminum overload in the presence of a serum aluminum level <30 microg/l. CONCLUSIONS: Our data indicate that in dialysis patients with iron overload (iron-transferrin saturation >60%; serum ferritin >800 microg/l) serum aluminum levels are low (<30 microg/l) despite exposure to aluminum by the intake of Al(OH)3 or the use of aluminum-contaminated dialysis fluids. Low serum aluminum nevertheless may be associated with aluminum overload and even aluminum-related bone disease. An effect of iron on the serum aluminum speciation may at least in part explain our observations. Our findings allow a more accurate interpretation of baseline serum aluminum values.

Aluminum↗
PubMed1989

Effect of solubility on the gastrointestinal absorption of aluminum from various aluminum compounds in the rat.

The present study was carried out to determine whether the insoluble property of most aluminum compounds was the reason for the limited absorption of this element from the gastrointestinal tract. Aluminum compounds of varying degrees of solubility were studied. At pH 3, more than 25% of the aluminum from all of the compounds studied (with the exception of sucralfate [13%]) was in solution. At pH 6, the solubility of aluminum in Al(OH)3 and sucralfate was less than 1%; it was 15% in AlCl3 and 33% in aluminum lactate. Aluminum solubility did not change with a change in pH for the citrate compounds, which varied between 38%, with sucralfate plus citric acid, and 91%, with aluminum citrate. The fraction of the administered dose of aluminum absorbed as estimated by urinary excretion after gastric gavage was 0.015% for sucralfate and Al(OH)3, 0.037% for AlCl3 and aluminum lactate, and greater than 0.80% for all aluminum compounds administered with citrate. A similar relationship was found between the solubility of the aluminum compounds and absorption, as determined by calculated absorption from the changes in plasma aluminum levels. Solubility alone, however, could not totally explain the effect of citrate on aluminum absorption. The solubility of aluminum in aluminum lactate and sucralfate plus citric acid were the same at pH 6. Absorption of aluminum from aluminum lactate, however, was only 1.6% as much as that found for sucralfate plus citric acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1991

Calcium citrate markedly enhances aluminum absorption from aluminum hydroxide.

The effect of calcium citrate on intestinal aluminum absorption, assessed by the increment in urinary aluminum excretion, was evaluated in eight normal men. Baseline urinary aluminum excretion was determined for 2 days; thereafter, subjects ingested aluminum hydroxide for 3 days. In a cross-over study, subjects were given either calcium citrate, 950 mg four times a day, or placebo during the 3 days of aluminum hydroxide ingestion (2.4 g/d). Plasma aluminum levels were measured on the second control day and the third day of aluminum hydroxide ingestion. Baseline urinary aluminum excretion was 0.02 +/- 0.004 (6.5 +/- 1.1 micrograms/g creatinine) and 0.03 +/- 0.005 mumol/mmol creatinine (7.4 +/- 1.3 micrograms/g creatinine). These values increased during aluminum hydroxide therapy, but values were much greater when calcium citrate was ingested with aluminum hydroxide. On 3 consecutive days, urinary aluminum excretion levels were 11.1 +/- 3.23, 8.8 +/- 2.9, and 5.3 +/- 0.7 times greater during the administration of calcium citrate with aluminum hydroxide than with aluminum hydroxide alone. Plasma aluminum levels did not differ in the two treatment groups. Thus, calcium citrate markedly enhances the absorption of aluminum from aluminum hydroxide and the two must not be prescribed together in patients with renal failure.

Adult↗
PubMed2004

[Studies on effects of aluminum compounds on aluminum contents in serum and brain of mice with high performance capillary electrophoresis].

OBJECTIVE: To study the effects of alum, aluminum chloride and aluminum hydroxide on aluminum contents in serum and brain of mice with high performance capillary. METHOD: 60 days after the mice were given daily alum, aluminum chloride and aluminum hydroxide with the same aluminum content of 14.25, 57 mg x kg(-1) x d(-1), respectively, the aluminum content in serum and brain of mice were determined with high performance capillary chromatography. RESULT: The average recoveries of serum aluminum determination was 96.5%-103%. The average recoveries of brain aluminum assay was 92.2%-105.3%. Except control group, serum aluminum increased obviously. Brain aluminum increased in all the large doses groups. 2 weeks after the mice were stopped being given these drugs, serum and brain aluminum recovered to normal level, except aluminum chloride large doses group. CONCLUSION: The metabolism and excretion mechanism of aluminum in mice depends on the chemical states of the aluminum compound.

Administration, Oral↗
PubMed1997

Aluminum utensils contribute to aluminum accumulation in patients with renal disease.

Presently, aluminum utensils are widely used in the world, especially in the developing countries. However, whether aluminum leaching from such utensils contributes to aluminum accumulation or causes any damage in patients with renal disease remains unknown. We designed a prospective study to evaluate this problem. After excluding patients who were not examined at follow-up or who poorly complied during the study period, the opened randomized study consisted of 42 patients with chronic renal insufficiency (creatinine clearance <60 mL/min and >10 mL/min). All patients had not taken any aluminum-containing agents for 3 months, but used aluminum kitchen utensils for more than 1 year. Twelve patients comprised the control group; the other 30 patients comprised the study group. The aluminum kitchen utensils used by the study group patients were replaced with stainless steel utensils for 3 months, but those used by the control group were not. After 3 months, the decrements of serum aluminum (5.5 +/- 4.6 microg/L v 2.1 +/- 3.5 microg/L; P = 0.012) and daily urine aluminum excretion (14.3 +/- 15.2 microg/d v 2.1 +/- 5.6 microg/d; P = 0.005) in the study group patients were greater than those in the control group patients. The increments of transferrin saturation of the study group patients (1.8% +/- 9.5% v -3.7% +/- 9.5%; P = 0.052) were greater than those of the control group patients. In addition, the increments of iron (r = 0.368, P = 0.035) and transferrin saturation (r = 0.345, P = 0.049) positively correlated with the decrements of daily aluminum excretion in all patients. The study group patients with greater decrements of serum aluminum (>5.5 microg/L) had greater serum iron levels (90.2 +/- 27.7 microg/dL v 71.9 +/- 27.8 microg/dL; P = 0.047) and transferrin saturation (30.5% +/- 11.0% v 23.0% +/- 9.5%; P = 0.046) than those with less decrements of serum aluminum (<5.5 microg/L) after the study. Our study demonstrates that aluminum kitchen utensils may be the important aluminum exposure source for patients with chronic renal insufficiency who are not taking aluminum-containing agents, and hints that the long-term exposure of aluminum leaching from aluminum utensils probably affects iron levels in patients with chronic renal insufficiency. Further studies are clearly needed to confirm this observation.

Adult↗