Toxic Effects Of Aluminum Research Articles

Toxic effects of aluminium, chromium and cadmium in intact and regenerating freshwater planarians

The effects of exposure to heavy metals were analyzed in the intact and regenerating planarian Dugesia etrusca. Al 3+ and Cr 3+ were lethal at 1.5 mM concentration. Intact specimens, treated with A1 at lower concentrations, exhibited a variety of sublethal responses; Al was significantly more toxic than Cr. Alterations in the cephalic regeneration of decapitated planarians were observed with both metals. Cd 2+ was tested at concentrations ranging from 0.18 μM to 18 μM. Until 1.8 μM, this metal did not produce any detectable sublethal responses in intact planarians, whereas higher concentrations were lethal. Sublethal Cd concentrations did not show any visible effect on cephalic regeneration.

Kinetics of uptake and elimination of silicic acid by a human subject: A novel application of 32Si and accelerator mass spectrometry

Silicon is possibly important in human physiology in protecting against the toxic effects of aluminium, but the kinetics of uptake and excretion of silicic acid, the bioavailable form, are not well characterised. We have used 32Si as a tracer in a human uptake experiment to determine a gastrointestinal uptake factor for silicic acid, and to elucidate the kinetics of renal elimination. Urine collections were made for extending intervals from 2 to 12 h over 2 days following ingestion by a single human subject of a neutral silicic acid solution containing tracer levels of 32Si (t 1/2 ≈ 150 y). Silicon was isolated as SiO 2 and the 32Si content determined by accelerator mass spectrometry (AMS), using a gas-filled magnet technique to eliminate a prolific isobaric interference from 32S. Silicon uptake appears to have been essentially complete within 2 h of ingestion. Elimination occurred by two simultaneous first-order processes with half-lives of 2.7 and 11.3 h, representing around 90% and 10%, respectively, of the total output. The rapidly eliminated 32Si was probably retained in the extracellular fluid volume, whilst the slower component may represent intracellular uptake and release. Elimination of absorbed 32Si was essentially complete after 48 h and was equivalent to 36% of the ingested dose. This establishes only a lower limit for gastrointestinal absorption as, although there was no evidence for longer term retention of additional 32Si, the possibility could not be excluded by these results.

1-45-06 Toxic effects of aluminum on neuromuscular system

1-45-06 Toxic effects of aluminum on neuromuscular system

Regional alterations in calcium homeostasis in the primate brain following chronic aluminium exposure.

The present study investigates the possible effects of chronic aluminium exposure on the various aspects of calcium homeostasis in the primate central nervous system. Aluminium administration caused a marked decline in the activity of Ca2+ ATPase in the monkey brain. The total calcium content was also significantly raised following aluminium exposure. Concomittant to the increase in the calcium content, the levels of lipid peroxidation were also augmented in the aluminium treated animals, thereby further accentuating the aluminium induced neuronal damage. In addition, aluminium had an inhibitory effect on the depolarization induced 45Ca2+ uptake via the voltage operated channels. The results presented herein, indicate that the toxic effects of aluminium could be mediated through modifications in the intracellular calcium homeostasis with resultant altered neuronal function.

Acid‐induced acute toxicity of aluminium to three species of filter feeding caddis larvae (Trichoptera, Arctopsychidae and Hydropsychidae)

1. Arctopsyche ladogensis, Hydropsyche angustipennis and Hydropsyche siltalai larvae were exposed to nominal aluminium concentrations of 0, 625, 1250, 2500 and 5000 μg Al l–1 at pH 5.0 for 96 h. Larvae reared at pH 6.4 and without any aluminium treatment were used as controls. Morphological abnormalities in the anal papillae of the larvae were used as the response variable in estimating the median effective concentrations (EC50) of aluminium.2. No morphological abnormalities were observed in the control larvae. Only a few individuals of A. ladogensis had darkened anal papillae at pH 5.0 without additional aluminium treatment, whereas increasing aluminium concentrations significantly increased the number of individuals in all species displaying darkening and reduction of the papillae.3. A. ladogensis appeared to be the most sensitive species to increasing aluminium concentrations, as reflected by the significantly lower mean EC50 value for this species compared with those of H. siltalai and H. angustipennis. H. angustipennis larvae were the most tolerant to aluminium.4. The results indicate that interspecific differences in sensitivity to aluminium may be a key factor influencing the guild structure of filter feeding caddis flies in acidified streams. The results also imply that toxic effects of aluminium on filter feeding caddis larvae occur due to the impairment of normal osmoregulation processes via damage to the ion‐regulatory organs.

Lignin deposition induced by aluminum in wheat (Triticum aestivum) roots

We investigated the relation between the toxic effect of aluminum (Al) on root growth and the lignin deposition in wheat (Triticum aestivum L. cvs Atlas 66 and Scout 66). In the Al‐tolerant cultivar Atlas 66, control treatment without AlCl3 at pH 4.75, cell length increased dramatically in the portion of the root that was 0.6 to 3.2 mm from the root cap junction (approximately 1.0 to 3.6 mm from the root tip). However, treatment with 20 μM AlCl3 for 24 and 48 h completely inhibited root elongation and markedly decreased the length and increased the diameter of the cells in the same portion of the root. Moreover, marked deposition of lignin was observed in the cells that corresponded to the portion 1.5 to 4.5 mm from the root tip in Atlas 66 roots treated with 20 μM AlCl3, while no deposition of lignin was detected in control roots. Treatment with 5 μM AlCl3 slightly inhibited root growth and there was no deposition of lignin in the root. On the other hand, in roots of the Al‐sensitive cultivar Scout 66, treatment with 5 μM AlCl3 completely inhibited root growth and markedly induced deposition of lignin. These results suggest that lignification in the elongating region coincided with the extent of inhibition of root growth by Al in two wheat cultivars that differed in their sensitivity to Al.

Adequacy of dialysis: trace elements in dialysis fluids.

A number of considerations suggest that trace element disturbances might occur in dialysed patients. These must at least in part be ascribed to the dialysis treatment itself during which these constituents may either be transferred to or removed from the patient. Tap water must be considered as the main source of dialysate trace metal contamination. These can adequately be removed during water treatment provided that, in addition to softening and deionization, reverse osmosis is available. However, even in the presence of the latter devices the possibility of serious contamination of the dialysis fluids leading to either chronic or acute intoxications still exists. The addition of chemical concentrates may also contribute to the increased concentrations of a number of trace metals. The toxic effects of aluminium in dialysis patients are well known and at the present time the element is still responsible for the greater part of trace metal-related problems in dialysis patients. Hence, the need for regular monitoring of aluminium cannot be ruled out at present. Strategies for diagnosis and treatment of aluminium overload have been updated. Recent studies demonstrated the efficacy of low desferrioxamine doses in diagnosis and treatment of aluminium overload, and optimal schedules for administration of the chelator and duration of treatment have been presented. Recently, in an epidemiological survey serum silicon concentrations in dialysis patients were found to be increased up to 100-fold compared to subjects with normal renal function. Moreover, it was noted that silicon concentrations in the dialysis population differ from one centre to another and that increased levels are due to either the use of silicon-contaminated dialysis fluids or an increased oral intake of the element originating from a high silicon content in the drinking water. Besides aluminium and silicon, a transfer towards the patients during dialysis has also been reported for a number of other elements including copper, zinc, nickel, strontium and chromium. The possible consequences of dialysate contamination with these elements will briefly be dealt with in the present paper. In contrast to trace metal accumulation, removal of trace metals during dialysis may at least in part contribute to the relative deficiency of particular essential elements. Selenium deficiency has repeatedly been observed. In view of the element's well-known essential role in glutathion peroxidase activity and the association of its deficiency with the development of some malignant diseases, further studies on the clinical impact of decreased serum selenium in dialysis patients are worthwhile. In conclusion, trace metal dialysate contamination/ depletion may contribute to the disturbed trace element concentration in dialysis patients. Aluminium accumulation is still an important problem in clinical nephrology. The clinical importance of the accumulation/ deficiency of trace elements other than aluminium is not yet fully understood and deserves further investigation.

Aluminium‐induced increase of zeatin riboside and dihydrozeatin riboside inPhaseolus vulgarisL. cultivars

Abstract Toxic effects of aluminium (Al) on root tips are considered to decrease export of cytokinins to shoots, and deficiency of cytokinins has been made responsible for Al‐induced inhibition of shoot growth. But no experimental data on the influence of Al on endogenous cytokinin levels in higher plants have been reported. In this study, the endogenous levels of zeatin riboside (ZR) and dihydrozeatin riboside (DHZR) of roots, stems, and leaves of two bean cultivars (Phaseolus vulgaris L. cv Contender and cv Strike) exposed to Al in continuously flowing nutrient solution (pH 4.5) was analysed. The supply of a high Al concentration (sum of monomeric Al species, 127 μM) caused severe inhibition of root elongation in both cultivars. The cv Strike was more affected by both Al‐induced mineral nutrient disorders and Al‐induced alteration of leaf water relationships. In both cultivars Al‐supply significantly increased ZR and DHZR. Leaves of Al‐treated plants exhibited a more than three times higher concentratio...

Biological evaluation of an ionomeric bone cement by osteoblast cell culture methods

Periosteal derived bovine osteoblast-like cells migrated in culture onto an ionomeric cement. Cell cultures were maintained for 4 weeks and used to study the in vitro behaviour of cells on the ionomeric bone cement (lC). The cells produced bone matrix proteins (osteocalcin, bone sialoprotein II) and were osteoblast-like. The osteoblast-like cells colonized the substrate in monolayers and produced an extracellular matrix as seen by light and scanning electron microscopy. Morphological comparison between cells growing on the ionomeric bone cement and cortical bone revealed no significant difference in phenotypic expression. Staining for aluminium in osteoblasts growing on the 1C showed an uptake and storage of aluminium in the cells. Energy dispersive X-ray microanalysis revealed high concentrations of aluminium and silicon in the periosteal tissue. Despite the known toxic effect of aluminium in vivo and in vitro on osteoblasts, no signs of toxicity were apparent on light and scanning electron microscopy analysis.

Effect of aluminium on the development of hyperparathyroidism and bone disease in the azotaemic rat

Aluminium toxicity in dialysis patients is associated with a relative parathyroid hormone (PTH) deficiency as well as osteomalacia. In-vitro studies of parathyroid cells have shown that aluminium inhibits PTH secretion. However, only limited data are available on how aluminium affects the development of hyperparathyroidism in the azotaemic animal. Four groups of azotaemic rats were studied; in each group, renal failure was induced by a two-stage 5/6 nephrectomy, after which rats were studied for 40 days. In three groups hyperparathyroidism was stimulated by the use of a high phosphorus (1.2%) diet (HPD). The four groups were (1) HPD; (2) HPD + high-dose aluminium (HDAL)--1.5 mg of aluminium was administered intraperitoneally (IP) 5 days per week; (3) HPD + low-dose aluminium (LDAL)--0.5 mg of aluminium was administered IP 5 days per week; and (4) moderate phosphorus (0.6%) diet (MPD); the MPD group was used to control hyperparathyroidism and thus provide a comparison of PTH levels and azotaemic bone disease. After 40 days, the serum PTH level was higher (P < 0.05) in the HPD + HDAL group (37 +/- 2 pmol/l) than the HPD, HPD + LDAL, and MPD groups (24 +/- 3, 28 +/- 4, and 6 +/- 1 pmol/l respectively). The correlation between serum PTH and calcium, serum PTH and phosphorus, and serum calcium and phosphorus was significant for the four groups (P < 0.02); however, the relationship between serum PTH and calcium, and between serum calcium and phosphorus was altered in the HPD + HDAL group (serum aluminium 30.8 +/- 2 mumol/l). Aluminium administration induced a decrease (P < 0.05) in the bone formation rate and the adjusted apposition rate, and an increase (P < 0.05) in osteoid volume and the mineralization lag time. Despite aluminium administration, diet-induced hyperparathyroidism resulted in an increase (P < 0.05) in the osteoblast surface. In conclusion, in the azotaemic rat (1) aluminium did not slow the development nor decrease the magnitude of hyperparathyroidism; (2) aluminium appeared to alter the relationship between serum PTH and calcium, and between serum calcium and phosphorus; (3) hyperparathyroidism changed the expression of aluminium-induced bone disease and may afford the bone some protection against the toxic effects of aluminium.

The effect of aluminum on the stromal cells (in vitro) on bone marrow in rats.

The aim of this study was to describe the effects of aluminum on the stromal cells of rat bone marrow using a combination of in vivo exposure and in vitro culture of bone marrow. The toxic effects of aluminum are manifested by a decrease in the erythrocyte count and hemoglobin level in the peripheral blood. Aluminum stimulated an increase in the number of fibroblasts while the macrophage count dropped. The number of adipocytes remained unaffected. An increase in mean corpuscular hemoglobin (MCH) was also found in the peripheral blood of experimental animals.

Elemental composition of polyphosphate bodies in aluminum-treated Pisolithus tinctorius: Comparison of chemical and freeze-substitution methods

The toxic effects of aluminum (Al) ions on plants growing in acidic soils may be ameliorated by mycorrhizal (M) fungi, which form symbiotic associations with roots of many forest trees. Pisolithus tinctorius, a M fungus found in many acid soils, is tolerant of high levels of Al. It is not known, however, if Al is excluded from the hyphae or compartmentalized within specific organelles or areas of the hyphae. Many M fungi have been shown to accumulate divalent cations, especially Ca, with P in polyphosphate (polyP) bodies. Whether Al ions might also be localized in polyP bodies is unclear. Previously, most ion localization studies in M fungi have been performed using conventional chemical fixation (CF) methods. However, ion movement due to aqueous fixation has been demonstrated. The inhibition of ion movement during fixation is a superior feature of specimen preparation by rapid freezing followed by freeze substitution (FS). The purpose of this study was to determine by energy dispersive X-ray microanalysis (EDS) of ultrathin sections the elemental composition of polyP bodies and other hyphal areas in P. tinctorius grown at different Al levels and prepared by CF or FS methods.

Some Effects of Dietary Aluminum and Silicon on Broiler Chickens

Experiments were conducted to determine whether dietary silicon will reduce the toxic effects of dietary aluminum on broiler chickens. The parameters measured were weight gain, feed efficiency, percentage bone ash, tibial dyschondroplasia, and the retention of calcium, phosphorus, and phytin phosphorus. Experiments 1 and 2 were conducted with casein and gelatin-based purified diets and Experiments 3 and 4 with corn and soybean meal-based practical diets. All experiments used day-old broiler cockerels and lasted 16 days. Aluminum significantly reduced weight gain, feed efficiency, and percentage bone ash in all four experiments. Aluminum supplementation reduced the incidence and severity of tibial dyschondroplasia, but this effect was associated with a reduction in weight gain. Increasing dietary aluminum reduced the retention of phosphorus and phytin phosphorus. Silicon did not alleviate the effects of aluminum toxicity on any of the parameters measured but did independently increase growth rate in Experiments 1 and 2. Supplementary dietary silicon does not appear to reduce aluminum toxicity in broiler chickens. Aluminum appears to exert its toxic effect on chickens by reducing the retention of phosphorus and phytin phosphorus.

Effect of aluminum and pH on the growth ofAnacystis nidulans

Anacystis nidulans is a typically rod-shaped unicellular cyanobacterium. It is an obligate photoautograph whose photosynthetic apparatus is very is very similar to eukaryotic chloroplasts in functional and molecular aspects. Of the toxic materials discharged, trace and heavy metals are of major concern. Metals are introduced into the environment by industrial agricultural and municipal wastes as well as by natural runoff. Metals emitted into the environment from combustion can also find their way into waterways. Aluminum is one of the most abundant metals in the earth's crust. It is reported that water draining from rock strata associated with coal seams may contain acid salts of aluminum, iron and manganese. The toxic effects of aluminum on plant growth have long been known. Several concentrations of aluminum, as well as various pH values were studied, to determine the extent to which some pollutants will effect the growth of Anacystis nidulans. Since reports have indicated that EDTA influences the effect of many metals, studies were performed with and without EDTA.

Modelling the phytotoxicity of aluminum, cadmium, copper, manganese, nickel, and zinc using the Weibull frequency distribution

The toxic effects of aluminum, cadmium, copper, manganese, nickel, and zinc stress on root growth of Triticum aestivum were modelled using a modified version of the Weibull frequency distribution. The modified Weibull function is a continuous, nonlinear mathematical function that provides direct estimates of several important biological parameters, including maximum growth, minimum growth, growth response, toxicity threshold, and maximum unit toxicity. The function was fit to experimental data using standard nonlinear regression techniques. Despite variation among metals in the characteristics of observed dose responses, the Weibull function provided a close fit for each of the metals tested (0.96 ≤ R2 ≤ 0.99). Estimates of maximum unit toxicities indicated that cadmium was most toxic to T. aestivum (152% growth reduction (GR)/(μmol∙L)), followed by copper (19.0% GR/(μmol∙L)), nickel (3.9% GR/(μmol∙L)), aluminum (1.3% GR/(μmol∙L)), zinc (0.5% GR/(μmol∙L)), and manganese (0.2% GR/((μmol∙L)). Estimated toxicity thresholds also indicated that cadmium was most toxic. Cadmium showed the lowest threshold for metal injury (0.02 μM), followed by copper (3.4 μM), nickel (11 μM), aluminum (18 μM), manganese (37 μM), and zinc (45 μM). The shift in the relative position of Mn and Zn suggests that unit toxicity and the toxicity threshold may be independent measures of the response of plants to metal stress. These experiments clearly demonstrate the utility of the Weibull function in modelling the response of plants to metal stress. Furthermore, the ability of the function to model primary growth data directly provides a suitable technique for investigation of potential interactions between phytotoxic metals. Key words: dose response, modelling, metal stress, toxicity threshold, unit toxicity.

Neurologic Complications of Renal Disease

Renal failure and its treatment are associated with a number of neurologic complications that must be differentiated from the nervous system complications of the disease leading to renal failure. Uremic encephalopathy is characterized by clinical signs of depressed brain function coexisting with excitation, often in the form of generalized epileptic seizures. Peripheral neuropathy, due to axonal involvement, is common and is characterized by ascending sensory and motor dysfunction. The treatment of renal failure also may lead to the development of neurologic abnormalities in the form of dialysis disequilibrium characterized by headache, nausea, irritability that may progress to seizures, coma, and death, which is caused by the entry of free water into the brain and swelling. Dialysis dementia, caused by the toxic effects of aluminum, is now rare. Renal transplant recipients may develop cerebrovascular disease, infections by opportunistic organisms, or malignant neoplasms, particularly primary lymphoma of the brain. As transplant recipients live longer and more operations are performed, additional complications may be seen in the future.

ALUMINIUM CHELATION THERAPY IN DIALYSIS PATIENTS: EVIDENCE FOR INHIBITION OF HAEMOGLOBIN SYNTHESIS BY LOW LEVELS OF ALUMINIUM

To investigate the possibility that aluminium may exacerbate anaemia in dialysis patients with only modest aluminium accumulation, 15 patients whose exposure to aluminium had been low were treated for three months with the aluminium chelating agent desferrioxamine, 30 mg/kg intravenously at the end of each dialysis session. Serum aluminium concentrations before treatment were 5-125 μg/ml. After one month of desferrioxamine, serum aluminium (including the chelate) had risen from 54·6 (SEM 11·2) to 167·0 (27·5) μg/l; and after three months haemoglobin had risen from 8·46 (0·70) to 10·43 (0·80) g/l. Mean cell volume and mean cell haemoglobin concentration also increased significantly. The maximum rise in haemoglobin correlated with the patients' aluminium burden as estimated by the mean serum aluminium concentration after one month of desferrioxamine therapy (r = 0·85). The greatest response to desferrioxamine occurred in patients with a baseline serum aluminium of 15-75 μg/l (mean increase in haemoglobin 38%). The results indicate that even the modest aluminium accumulation found in most dialysis patients has a pronounced inhibitory effect on haemoglobin synthesis. The possible toxic effect of aluminium should be considered in all anaemic dialysis patients.

The toxic effect of aluminium in vines

The split-root technique was used to study the effect of varying the growth media on the elemental content of nutrient elements in the roots of grape vines. The varieties 2-1 (R99 x Jacquez) and Sauvignon blanc (Vitis vinifera) were grown in Hoagland water culture with and without added aluminium. The elemental concentrations of Mg, Al, Si, P. S, Cl, K and Ca in the dried roots were determined by PIXE. Roots grown in Al-rich media were deficient in Mg and Ca, but enriched in Al. There was a correlation between Al and Si but the uptake differed in the two varieties.

Aluminum and Alzheimer??s disease

CRAPPER McLACHLAN, D. R. Aluminum and Alzheimer's disease. NEUROBIOL AGING 7(6) 525-532, 1986.--There is now substantial evidence indicating that an accumulation of aluminum occurs in grey matter in diseases associated with A Izheimer neurofibrillary degeneration. Four principle sites of aluminum accumulation have been identified in Alzheimer's disease: DNA containing structures of the nucleus, the protein moieties of neurofibrillary tangles, the amyloid cores of senile plaques and cerebral ferritin. Consideration of the extensive intormation now available on the toxic effects of aluminum in these four loci strengthens the hypothesis that aluminum could be important in the pathogenesis of this neurodegenerative process. The evidence, however, does not support an etiological role for aluminum in Alzheimer's disease. The primary pathogenic events responsible for Alzheimer's disease are presumed to have affected the genetically determined barriers to aluminum resulting in increased amounts of this toxic element to vulnerable target sites.

Long-Term Ecosystem Stress: The Effects of Years of Experimental Acidification on a Small Lake

Experimental acidification of a small lake from an original pH value of 6.8 to 5.0 over an 8-year period caused a number of dramatic changes in the lake's food web. Changes in phytoplankton species, cessation of fish reproduction, disappearance of the benthic crustaceans, and appearance of filamentous algae in the littoral zone were consistent with deductions from synoptic surveys of lakes in regions of high acid deposition. Contrary to what had been expected from synoptic surveys, acidification of Lake 223 did not cause decreases in primary production, rates of decomposition, or nutrient concentrations. Key organisms in the food web leading to lake trout, including Mysis relicta and Pimephales promelas, were eliminated from the lake at pH values as high as 5.8, an indication that irreversible stresses on aquatic ecosystems occur earlier in the acidification process than was heretofore believed. These changes are caused by hydrogen ion alone, and not by the secondary effect of aluminum toxicity. Since no species of fish reproduced at pH values below 5.4, the lake would become fishless within about a decade on the basis of the natural mortalities of the most long-lived species.