AhFRDL1-mediated citrate secretion contributes to adaptation to iron deficiency and aluminum stress in peanuts.

Although citrate transporters are involved in iron (Fe) translocation and aluminum (Al) tolerance in plants, to date none of them have been shown to confer both biological functions in plant species that utilize Fe-absorption Strategy I. In this study, we demonstrated that AhFRDL1, a citrate transporter gene from peanut (Arachis hypogaea) that is induced by both Fe-deficiency and Al-stress, participates in both root-to-shoot Fe translocation and Al tolerance. Expression of AhFRDL1 induced by Fe deficiency was located in the root stele, but under Al-stress expression was observed across the entire root-tip cross-section. Overexpression of AhFRDL1 restored efficient Fe translocation in Atfrd3 mutants and Al resistance in AtMATE-knockout mutants. Knocking down AhFRDL1 in the roots resulted in reduced xylem citrate and reduced concentrations of active Fe in young leaves. Furthermore, AhFRDL1-knockdown lines had reduced root citrate exudation and were more sensitive to Al toxicity. Compared to an Al-sensitive variety, enhanced AhFRDL1 expression in an Fe-efficient variety contributed to higher levels of Al tolerance and Fe translocation by promoting citrate secretion. These results indicate that AhFRDL1 plays a significant role in Fe translocation and Al tolerance in Fe-efficient peanut varieties under different soil-stress conditions. Given its dual biological functions, AhFRDL1 may serve as a useful genetic marker for breeding for high Fe efficiency and Al tolerance.

Evidence for participation of aluminum in neurofibrillary tangle formation and growth in Alzheimer's disease.

This study examines hippocampal CA1 cells from brains of aged humans, with and without Alzheimer's disease, for hyperphosphorylated tau and aluminum during early neurofibrillary tangle (NFT) formation and growth. A very small proportion of hippocampal pyramidal cells contain cytoplasmic pools within their soma that either appear homogeneous or contain short filaments (i.e., early NFTs). The cytoplasmic pools are aggregates of an aluminum/hyperphosphorylated tau complex similar to that found in mature NFTs. The photographic evidence presented combines with existing evidence to support a role for aluminum in the formation and growth of NFTs in neurons of humans with Alzheimer's disease.

Thermodynamics of the interaction of aluminum ions with DNA: implications for the biological function of aluminum.

Aluminum is a known neurotoxic agent and its neurotoxic effects may be due to its binding to DNA. However, the mechanism for the interaction of aluminum ions with DNA is not well understood. Here, we report the application of isothermal titration calorimetry (ITC), fluorescence spectroscopy, and UV spectroscopy to investigate the thermodynamics of the binding of aluminum ions to calf thymus DNA (CT DNA) under various pH and temperature conditions. The binding reaction is driven entirely by a large favorable entropy increase but with an unfavorable enthalpy increase in the pH range of 3.5-5.5 and at all temperatures examined. Aluminum ions show a strong and pH-dependent binding affinity to CT DNA, and a large positive molar heat capacity change for the binding, 1.57 kcal mol(-1) K(-1), demonstrates the burial of the polar surface of CT DNA upon groove binding. The fluorescence of ethidium bromide bound to CT DNA is quenched by aluminum ions in a dynamic way. Both Stern-Volmer quenching constant and the binding constant increase with the increase of the pH values, reaching a maximum at pH 4.5, and decline with further increasing the pH to 5.5. At pH 6.0 and 7.0, aluminum ions precipitate CT DNA completely and no binding of aluminum ions to CT DNA is observed by ITC. Combining the results from these three methods, we conclude that aluminum ions bind to CT DNA with high affinity through groove binding under aluminum toxicity pH conditions and precipitate CT DNA under physiological conditions.

Accretion, partitioning and sequestration of calcium and aluminum in red spruce foliage: implications for tree health.

Calcium (Ca) is an essential macronutrient in plants and is an important component of many cellular structures and physiological processes as well as overall forest function. Aluminum (Al) in soil solution can inhibit Ca uptake by plants and disrupt many Ca-dependent metabolic and physiological processes of plants. The ratio of Ca to Al in soil solution can be an important indicator of forest health, especially on acid soils. We used sequential chemical extractions (water, acetic acid and hydrochloric acid) to assess the chemical availability of Ca and Al in foliage from mature red spruce (Picea rubens Sarg.) trees growing under ambient environmental conditions. In plants deficient in Ca and with intermediate total foliar Ca concentration ([Ca]), Ca preferentially accrued in labile and physiologically available forms (water- and acetic acid-extractable). In plants with total foliar [Ca] above a "sufficiency" threshold, Ca also accrued in a chemically sequestered form with low solubility (HCl-extractable), suggesting that Ca sequestration is an inducible process in response to excess foliar Ca. Because it has low solubility, it is likely that sequestered Ca is unavailable for Ca-dependent physiological processes. Immobilization of Al in foliage was related to Ca sequestration, suggesting that Ca sequestration may provide a passive mechanism for Al tolerance in the foliage of these trees. Aluminum immobilization was evident based on the ratio of HCl-extractable Al to the more labile (water- and acetic acid-extractable) forms of Al. Sufficient labile Ca combined with Al sequestration was associated with plant health, including enhanced foliar accretion of Mg and Mn, greater tree growth, enhanced foliar cold hardiness and reduced winter injury. These findings demonstrate that not all chemical forms of foliar Ca and Al are of equal physiological significance and underscore the importance of assessing the biologically significant element forms in biogeochemical research.

Aluminum induced oxidative events and its relation to inflammation: a role for the metal in Alzheimer's disease.

Aluminum (Al) is a simple trivalent cation incapable of redox changes. The toxicity of the metal has been the subject of much controversy in the past few decades. Although it has been generally believed that the metal is innocuous to human health, a causal role for Al has been established in dialysis dementia (Alfrey et al., 1976), osteomalacia (Bushinsky et al., 1995) and microcytic anemia without iron deficiency (Touam et al., 1983). Aluminum has also been implicated in Alzheimer's disease (AD) although a direct causal role has not been determined. The exact mechanism of Al toxicity is not known. However, there are several lines of evidence that show the metal's capacity to exacerbate oxidative events. The present review is intended to propose a coherent pathway linking Al-induced oxidative events to Alzheimer's disease. The preliminary segment is an introduction to reactive oxygen species and their potential involvement in the pathogenesis of AD and the generation of an inflammatory response. Evidence on the relation between AD and inflammatory processes is also presented. The epidemiological and clinical evidence of Al neurotoxicity is summarized in the second section of the review. Finally, a hypothesis indicating that aluminum can exacerbate AD by activating ROS generation and initiation of an inflammatory cascade is presented.

Aluminum decreases the magnesium concentration of spinal cord and trabecular bone in rats fed a low calcium, high aluminum diet.

Current epidemiological surveys in the Western Pacific (Guam, and Kii Peninsula and West New Guinea) have suggested that low calcium (Ca), magnesium (Mg) and high aluminum (Al) and manganese (Mn) in river, soil and drinking water may be implicated in the pathogenetic process of foci of amyotrophic lateral sclerosis (ALS) and parkinsonism-dementia (PD). The condition of unbalanced minerals was experimentally mimicked in this study using rats. Male Wistar rats, weighing 200 g, were maintained for 60 days on the following diets: (A) standard diet, (B) low Ca diet, (C) low Ca diet plus high Al. Magnesium concentrations were determined in spinal cord and trabecular bone using inductively coupled plasma emission spectrometry (ICP). In the experimental group maintained on a low Ca, high Al diet, magnesium concentration of the spinal cord was lower than the group fed a standard diet. Also, magnesium concentration of lumbar vertebra showed lower values in the experimental group fed a low Ca, high Al diet than did those on a standard diet or low Ca diet without supplemental aluminum. Our data indicate that low Ca, high Al diet influences Mg concentration in bone and central nervous system (CNS) tissues and that a low Ca, high Al diet diminishes Mg in bone and CNS tissues, thereby inducing loss of calcification in bone and degeneration of CNS tissue due to alteration of the normal biological effects of Mg.

[Aluminum and the human body]. / Hliník a lidský organismus.

Aluminium is one of the trace elements in the human organism the presence of which is described as contamination. The authors describe the toxic action in subjects working in an environment contaminated with powdered aluminium or its compounds. Non-professional exposure is observed in subjects with renal failure as aluminium is retained, in particular in case of concurrent antacid therapy on the basis of aluminium salts. Dialyzation encephalopathy may develop, aluminium osteopathy and microcytic anaemia. The most effective prevention is dialysis using a dialyzation solution with a low aluminium content and elimination of aluminium binding phosphates. The results of hitherto accomplished studies call for further research into the action of this element on the human organism.

Sodium fluoride stimulates exocytosis at a late site of calcium interaction in stimulus-secretion coupling: studies with the RINm5F beta cell line.

In the insulin-secreting beta cell line RINm5F, sodium fluoride stimulated exocytosis in a concentration (5-15 mM)- and temperature-dependent manner. Depletion of aluminum with the chelator deferoxamine or addition of aluminum to the buffer failed to affect the NaF-stimulated insulin release. This suggests that stimulation of heterotrimeric G proteins or inhibition of phosphatases or other enzymes by fluoroaluminate, an analog of the phosphate moiety, is not involved in the insulinotropic action of NaF. Removal of extracellular Ca2+ suppressed the NaF-stimulated insulin release. However, nitrendipine, a blocker of L-type voltage-dependent Ca2+ channels, did not inhibit the NaF-stimulated insulin release and NaF did not cause any changes in the cytosolic free calcium concentration ([Ca2+]i). Decreasing [Ca2+]i with thapsigargin or increasing [Ca2+]i with ionomycin or a depolarizing concentration of KCl resulted in suppression or enhancement of NaF-stimulated insulin release, respectively. Furthermore, NaF enhanced Ca(2+)-induced insulin release in electrically permeabilized RINm5F cells. These findings indicate that the effect of NaF on exocytosis is dependent on [Ca2+]i, although NaF itself does not change [Ca2+]i. Inhibitors of protein kinase C, such as staurosporine and bisindolylmaleimide, in concentrations sufficient to block the effects of phorbol esters, did not attenuate the NaF-stimulated insulin release. Neither cellular cAMP content nor [3H]arachidonic acid release was increased by NaF. NaF-stimulated insulin release was synergistically enhanced by the activation of protein kinases A and C. Finally, trifluoperazine, an inhibitor of calmodulin and other Ca(2+)-binding proteins, inhibited the insulinotropic action of NaF in a concentration-dependent manner. Trifluoperazine (50 microM) and W-7 (100 microM) nullified the 10 mM NaF-stimulated insulin release. It is concluded that NaF evokes exocytosis by a novel mechanism of sensitization to Ca2+, possibly on a Ca(2+)-responsive protein that is sensitive to trifluoperazine and W-7, leading to exocytosis. Protein kinases A and C also act at this site or at a more distal point.

In vivo effect of beta 2-microglobulin on bone resorption.

beta 2-Microglobulin (beta 2-M) deposits have been found in the destructive bone lesions associated with dialysis-related amyloidosis. To examine whether beta 2-M can cause bone resorption in vivo, doses of beta 2-M alone were compared with parathyroid hormone (PTH), aluminum, and vehicle alone. Eleven injections of 10 micrograms each were made over a period of 56 hours into the subcutaneous tissue overlying the occipital region of mice. Using a computerized image analysis system we measured (1) periosteal and inner bone length, (2) bone marrow interface length, and (3) the extent of resorption along these surfaces expressed as percentage of total length. Injections of either beta 2-M or PTH were associated with 22% +/- 4% and 25% +/- 4% resorption of periosteal surface, respectively, and 15.9% +/- 2% and 19.9% +/- 5% resorption of marrow bone surfaces, respectively, compared with control. In contrast, aluminum did not increase bone resorption over controls. The simultaneous injection of calcitonin, an osteoclast inhibitor, with beta 2-M or PTH did not increase periosteal resorption over controls. The resorption of inner bone surface was similar in all groups. These studies show that beta 2-M and PTH cause bone resorption in the bone surfaces proximate to the site of injection. This suggests that beta 2-M may contribute to the development of the bone cysts in dialysis-related amyloidosis.

Dietary aluminum and Alzheimer's disease--a review.

Current evidence suggests that dietary aluminum is neither an essential nutrient nor a toxic element causing neurological damage. The phosphate and fluoride salts of aluminum are very insoluble. When fed in excess, aluminum increases the dietary needs for these anions. Aluminum hydroxide is used as an antacid that can prevent the phosphatemia seen in severe kidney damage. In Alzheimer's disease there is progressive decrease in brain mass with the accumulation of phospholipid-rich cell debris. These membrane tangles tend to accumulate aluminum and are easily stainable with silver.