Mechanism Of Aluminium Toxicity Research Articles

Determination of aluminum concentrations in biological specimens: application in the clinical laboratory.

Aluminum enters the body primarily through diet or occupational exposure, and is cleared through urine. However, this trace element may accumulate and cause toxicity in subjects with renal insufficiency, and even in dialysis patients. The mechanism of aluminum toxicity is related to increased oxidative and inflammatory stress, iron and calcium dyshomeostasis, or cholinergic dysregulation, among other. A review was conducted on the specimens and analytical methods used to determine aluminum in biological specimens and dialysis water. This paper describes the most relevant aspects related to quality assurance. This is a practical guideline for the development and implementation of a reliable method for determination of aluminum in the clinical laboratory. Serum aluminum is the main biomarker of toxicity. For cases of chronic exposure, urine testing is recommended. At present, inductively coupled plasma mass spectrometry (ICP-MS) is the gold-standard determination method, since it has been proven to have the best quantification limits, selectivity and robustness. Clear recommendations are provided in relation to the specimens used for aluminum determination. Relevant pre-analytical, analytical, and post-analytical considerations are also presented.

Aluminum induces oxidative damage in Saccharomyces cerevisiae

The mechanism of aluminum toxicity was studied in the model cells of Saccharomyces cerevisiae. Cell growth of yeast was inhibited by aluminum. The spot assay showed that the mechanism of aluminum detoxification in yeast cells was different from that of heavy metal cadmium. After treatment with aluminum, intracellular levels of reactive oxygen species, protein carbonyl, and thiobarbituric acid reactive substances were dramatically increased. Meanwhile, the percentage of aluminum-treated cells permeable to propidium iodide was augmented significantly. These data demonstrated that aluminum toxicity was attributed to oxidative stress in yeast, and it induced oxidative damage by causing lipid peroxidation, injuring cell membrane integrity. Moreover, aluminum triggered the antioxidant defense system in the cells. Glutathione levels were found to be decreased, while activities of superoxide dismutase and catalase were increased after treatment with aluminum. Additionally, an oxidative-stress-related mutation sensitivity assay showed that aluminum-induced yeast oxidative stress was closely related to glutathione. These data demonstrated that the oxidative damage caused by aluminum was different from that of hydrogen peroxide, in yeast. Aluminum could cause DNA damage, and aluminum toxicity was associated with sulfhydryl groups, such as glutathione, while it was independent of YAP1.

Aluminium Induced DNA-damage and Oxidative Stress in Cultures of the Marine Sponge Hymeniacidon perlevis

Aluminium is the most abundant element in the earth crust, and has no known biological function. However, it is an established neurotoxicant in its trivalent oxidation state, with exposure resulting in neurodegenerative diseases like Parkinson’s disease and presenile dementia. Although, the potential genotoxic and carcinogenic effects of aluminium are established in mammalian and other model system, there is however very limited information on aluminium genotoxicity in aquatic invertebrates. Mechanism of aluminium toxicity is also largely unclear. With a concentration range between 0.001– 0.05mg/L in near neutral pH water, and up to 0.5-1mg/L in an acidic water , aluminium poses a potential threat to the marine ecosystem, however it is poorly studied. This study, therefore presents for the first time, aluminium-induced DNA damage using the comet assay and reactive oxygen Species (ROS) formation using 2’, 7’-dichlorodihydrofluorescein diacetate (H2DCF-DA) assay as biomarkers of genotoxicity and oxidative stress in the inter-tidal marine sponge Hymeniacidon perlevis, respectively. H. perlevis is widely distributed in the British Isles, Mediterranean and the Arctic sea and has been reported as a model for environmental biomonitoring in aquatic ecosystem and as a suitable alternative to bivalves. In this study, cryopreserved single sponge cells of H. perlevis were cultured as viable aggregates and were thereafter treated with 0.1, 0.2, 0.3 and 0.4mg/L aluminium chloride (AlCl3) for 12 hours. Cell viability was determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Our results showed that non-cytotoxic concentrations of AlCl3 caused a statistically significant concentration-dependent increase in the level of DNA-strand break and reactive oxygen species formation single sponge cells of H. perlevis. There was also a statistically significant positive linear correlation between aluminium-induced DNA strand break and ROS formation suggesting the involvement of ROS in the causative mechanism of the aluminium induced DNA-strand breaks observed.

Molecular Physiology of Aluminum Toxicity and Tolerance in Plants

ABSTRACT Aluminum being the third most abundant metal in the earth's crust poses a serious threat to crop productivity in acid soils, which comprise almost half of the arable land. This review travels across time and updates research done on aluminum stress in plants. In its phytotoxic forms, aluminum affects root growth by acting in the root apical zone, resulting in growth inhibition in a very short time at micromolar concentrations. The mechanisms of aluminum toxicity in plants may proceed by growth inhibition, callose accumulation, cytoskeletal distortion, disturbance of plasma membrane surface charge, and H+-ATPase activity, lipid peroxidation of membranes, production of reactive oxygen species in cytosol and mitochondria, respiratory dysfunction, opening of mitochondrial permeability transition pores, collapsing of inner mitochondrial membrane potential, activation of mitochondrial protease, and induction of nuclear apoptosis, resulting ultimately in programmed cell death. In contrast, the mechanism...

Aluminum-induced 1-->3-beta-D-glucan inhibits cell-to-cell trafficking of molecules through plasmodesmata. A new mechanism of aluminum toxicity in plants.

Symplastic intercellular transport in plants is achieved by plasmodesmata (PD). These cytoplasmic channels are well known to interconnect plant cells to facilitate intercellular movement of water, nutrients, and signaling molecules including hormones. However, it is not known whether Al may affect this cell-to-cell transport process, which is a critical feature for roots as organs of nutrient/water uptake. We have microinjected the dye lucifer yellow carbohydrazide into peripheral root cells of an Al-sensitive wheat (Triticum aestivum cv Scout 66) either before or after Al treatment and followed the cell-to-cell dye-coupling through PD. Here we show that the Al-induced root growth inhibition is closely associated with the Al-induced blockage of cell-to-cell dye coupling. Immunofluorescence combined with immuno-electron microscopic techniques using monoclonal antibodies against 1-->3-beta-D-glucan (callose) revealed circumstantial evidence that Al-induced callose deposition at PD may responsible for this blockage of symplastic transport. Use of 2-deoxy-D-glucose, a callose synthesis inhibitor, allowed us to demonstrate that a reduction in callose particles correlated well with the improved dye-coupling and reduced root growth inhibition. While assessing the tissue specificity of this Al effect, comparable responses were obtained from the dye-coupling pattern in tobacco (Nicotiana tabacum) mesophyll cells. Analyses of the Al-induced expression of PD-associated proteins, such as calreticulin and unconventional myosin VIII, showed enhanced fluorescence and co-localizations with callose deposits. These results suggest that Al-signal mediated localized alterations to calcium homeostasis may drive callose formation and PD closure. Our data demonstrate that extracellular Al-induced callose deposition at PD could effectively block symplastic transport and communication in higher plants.

Cellular Mechanisms of Aluminum Toxicity and Resistance in Plants

Cellular Mechanisms of Aluminum Toxicity and Resistance in Plants

Silicon, aluminium and the biological availability of phosphorus in algae

Silicon is an essential element for growth in diatoms. It is, for example, used to build the silicieous frustule surrounding the diatom cell wall. Silicon starvation studies have also inferred that silicon is essential in the vital metabolic processes of DNA and chlorophyll synthesis. The mechanism of essentiality is, however, uncertain. In laboratory cultures at circumneutral pH and using a non-growth-limiting, but environmentally realistic, concentration of the essential nutrient phosphorus, we have demonstrated aluminium toxicity in the freshwater diatom Navicula pelliculosa and the amelioration of this toxicity with silicon, present in aqueous solution as silicic acid. The mechanism of aluminium toxicity was an aluminium-induced reduction in the biologically available phosphorus fraction and silicic acid protected against this effect by preferentially binding aluminium in competition with phosphorus. Silicon-stimulated growth in the presence of aluminium was also demonstrated in the non-silicon-dependent green alga, Chlorella vulgaris, in which, once again, the increase in growth rate upon the addition of silicon could be directly correlated with an increase in the biologically available phosphorus fraction. We contend that a possible hitherto unrecognized mechanism of silicon essentiality in biology is to increase the biological availability of phosphorus in the presence of aluminium.

Possible mechanisms of aluminum toxicity in a dilute, acidic environment to fingerlings and older life stages of salmonids

The respiratory, acid-base, and ionoregulatory responses of juvenile rainbow trout (Salmo gairdneri) were monitored during exposure of the fish in the laboratory to inorganic Al (2.8 μM) over the pH range 4.0 to 6.5. Responses to Al were most severe at pH 6.1 and 4.5, mortality being primarily due to asphyxia at pH 6.1 and to electrolyte loss at pH 4.5. Competition between the H+-ion and Al for binding at the gill surface is offered as an explanation for the decreased toxicity of Al at pH 4.0, one which is compatible with the free-ion toxicity model that has been developed for other metals. The physiologically distinct response of S. gairdneri to Al at pH 6.1 is less amenable to unambiguous interpretation. If a mixed ligand hydroxo-Al complex is incorporated in the free-ion model, and if it is assumed that the two Al species, [Al-L-gill] and [HO-Al-L-gill], provoke distinct toxicological responses, then a bimodal toxicological response to Al is indeed predicted. An alternative explanation of the apparent toxic action of Al at pH 6.1, i.e., at pH values close to that of minimum Al solubility, is the precipitation of solid Al(OH)3 at the gill surface, i.e., a ‘physical’ effect rather than a biochemical one.