Melatonin prevents oxidative stress in ovariectomized rats treated with aluminium.

This study is designed to determine the simultaneous effect of aluminium (Al) and melatonin (Mel) treatment in intact and ovariectomized (Ovx) female rats on oxidative stress and their inter-organ relationship in the kidney and liver. Al-treated rats received an intra-peritoneal injection of solution of aluminium lactate (0.575 mg Al/100 g of body weight, three times a week), during 12 weeks. Mel groups received intra-peritoneal injections of melatonin at a dose of 10 mg/kg/day, 5 days/week, during 12 weeks. The results of this study showed that Al treatment in female rats modifies homeostasis of glutathione and the antioxidant capacity of the rat liver and kidney. The alteration of glutathione homeostasis and oxidative status was not associated with an increased lipid peroxidation in both organs with the exception of the increase observed in the liver of Ovx rats. Al also induced modifications in the activity of some enzymes related to the glutathione cycle: GSH-Px in the liver and kidney and glutathione reductase only in the kidney. Al exposure decreased CAT activity in both the kidney and liver of intact and Ovx groups. The administration of Mel in the intact and castrated females treated with Al seems to reduce oxidative changes in the liver and kidney of intact and Ovx rats.

Protective role of Cynodon dactylon in ameliorating the aluminium-induced neurotoxicity in rat brain regions.

Cynodon dactylon (Poaceae) is a creeping grass used as a traditional ayurvedic medicine in India. Aluminium-induced neurotoxicity is well known and different salts of aluminium have been reported to accelerate damage to biomolecules like lipids, proteins and nucleic acids. The objective of the present study was to investigate whether the aqueous extract of C. dactylon (AECD) could potentially prevent aluminium-induced neurotoxicity in the cerebral cortex, hippocampus and cerebellum of the rat brain. Male albino rats were administered with AlCl(3) at a dose of 4.2 mg/kg/day i.p. for 4 weeks. Experimental rats were given C. dactylon extract in two different doses of 300 mg and 750 mg/keg/day orally 1 h prior to the AlCl(3) administration for 4 weeks. At the end of the experiments, antioxidant status and activities of ATPases in cerebral cortex, hippocampus and cerebellum of rat brain were measured. Aluminium administration significantly decreased the level of GSH and the activities of SOD, GPx, GST, Na(+)/K(+) ATPase, and Mg(2+) ATPase and increased the level of lipid peroxidation (LPO) in all the brain regions when compared with control rats. Pre-treatment with AECD at a dose of 750 mg/kg b.w increased the antioxidant status and activities of membrane-bound enzymes (Na(+)/K(+) ATPase and Mg(2+) ATPase) and also decreased the level of LPO significantly, when compared with aluminium-induced rats. The results of this study indicated that AECD has potential to protect the various brain regions from aluminium-induced neurotoxicity.

Exogenous gamma-aminobutyric acid alleviates oxidative damage caused by aluminium and proton stresses on barley seedlings.

BACKGROUND: Proton (H(+)) and aluminium (Al(3+)) toxicities are major factors limiting crop production on acid soils, while gamma-aminobutyric acid (GABA) is a non-protein amino acid involved in various stress tolerances in plants. In this study, to determine whether exogenous GABA is functional in alleviating oxidative stress induced by H(+) and Al(3+) toxicities, the antioxidant defence response regulated by GABA was investigated in barley (Hordeum vulgare L.). RESULTS: After 24 h treatments of seedlings under H(+), Al(3+) and combined stresses with and without GABA, morphological and biochemical assays were conducted. It was observed that the inhibition of seedling root elongation caused by Al(3+) and H(+) toxicities was significantly mitigated by GABA. The amount of carbonylated proteins with molecular masses of 14.4-97 kDa was decreased. The activities of antioxidant enzymes were enhanced, the content of malondialdehyde was reduced and the accumulation of reactive oxygen species (ROS), as shown by staining roots with nitroblue tetrazolium, declined in GABA-treated seedlings. CONCLUSION: GABA can alleviate oxidative damage caused by H(+) and Al(3+) toxicities in barley seedlings by activating antioxidant defence responses and reducing the elevated levels of carbonylated proteins caused by ROS.

Neuroprotective role of Convolvulus pluricaulis on aluminium induced neurotoxicity in rat brain.

AIM OF THE STUDY: Convolvulus pluricaulis (Convolvulaceae) has long been used as traditional herbal medicine in India as nerve tonic. We investigated neuroprotective effects of aqueous extract from Convolvulus pluricaulis (CP) against aluminium chloride induced neurotoxicity in rat cerebral cortex. MATERIAL, METHOD AND RESULT: Daily administration of CP (150 mg/kg) for 3 months along with aluminium chloride (50 mg/kg) decreased the elevated enzymatic activity of acetylcholine esterase and also inhibited the decline in Na(+)/K(+)ATPase activity which resulted from aluminium intake. Beside, preventing accumulation of lipid and protein damage, changes in the levels of endogenous antioxidant enzymes associated with aluminium administration were also rectified. Oral administration of CP preserved the mRNA levels of muscarinic receptor 1 (M1 receptor), choline acetyl transferase (ChAT) and Nerve Growth Factor-Tyrosine kinase A receptor (NGF-TrkA). It also ameliorated the upregulated protein expression of cyclin dependent kinase5 (Cdk5) induced by aluminium. The potential of CPE to inhibit aluminium induced toxicity was compared with rivastigmine tartrate (1mg/kg), which was taken as standard. The potential of the extract to prevent aluminium-induced neurotoxicity was also reflected at the microscopic level, indicative of its neuroprotective effects. CONCLUSION: Convolvulus pluricaulis possesses neuroprotective potential, thus validating its use in alleviating toxic effects of aluminium.

Curcumin attenuates aluminium-induced functional neurotoxicity in rats.

Curcumin is a polyphenol extracted from the rhizome of Curcuma longa and well known as a multi-functional drug with antioxidative, anti-cancerous and anti-inflammatory activities. Curcumin's antiaging and neuroprotective potential is widely reported. In the present study, effect of curcumin treatment dose 30 mg kg(-1) day(-1) was investigated against aluminium neurotoxicity in young and old animals. Direct and indirect intakes of aluminium have been reported to be involved in the etiology of several neurodegenerative disorders like Alzheimer's and Parkinson's diseases. Long term Al was administered through drinking water at a dose of 50 mg/kg/day for 6 months in both young (4 months) and old (18 months) male Wistar rats. Result obtained demonstrates that curcumin treatment attenuates the Al-induced alterations at biochemical, behavioral and ultrastructural levels which was well reflected in the electrophysiological recordings. Our results indicate that curcumin's ability to bind redox active metals and cross the blood-brain barrier could be playing crucial role in preventing against Al-induced neurotoxicity.

The homeostasis of iron and suppression of HO-1 involved in the protective effects of nimodipine on neurodegeneration induced by aluminum overloading in mice.

Aluminum intoxication can cause damage to the cognitive function and neurodegenerative diseases. In the present study, we investigated the role of iron homeostasis and heme oxygenase-1 (HO-1) expression in the protective effects of nimodipine on the neurodegeneration induced by aluminum overloading in mice. 2 microl of 0.25% aluminum chloride solution was intracerebroventricularly injected once a day for five days to induce the neurodegeneration of mice. Nimodipine was administered by intragastric gavage (80 mg/kg per day) for 30 days. We observed that nimodipine could improve the performance of behavior test related to the learning and memory function and ameliorate pathological changes of hippocampi caused by aluminum. Results of western blot, immunohistochemistry study, biochemical test and inductively coupled plasma-atomic emission spectrometry showed that nimodipine could suppress the increased expression of HO-1 protein, and decrease the elevation of both HO activity and iron level in hippocampi, induced by aluminum overloading. These results indicate that nimodipine can suppress the neurodegenerative development induced by aluminum overloading and the mechanism of its action is at least partly related to keeping the homeostasis of iron through blunting the expression of HO-1 in hippocampus.

Aluminium-induced phospholipid signal transduction pathway in Coffea arabica suspension cells and its amelioration by silicic acid.

Coffee (Coffea arabica L.) is of economic importance worldwide. Its growth in organic-rich acidic soils is influenced by aluminium such that coffee yield may be impaired. Herein we have used the Al-sensitive C. arabica suspension cell line L2 to analyse the effect of two different Al species on the phosphoinositide signal transduction pathway. Our results have shown that the association of Al with coffee cells was affected by the pH and the form of Al in media. More Al was associated with cells at pH 4.3 than 5.8, whereas when Al was present as hydroxyaluminosilicates (HAS) the association was halved at pH 4.3 and unchanged at pH 5.8. Two signal transduction elements were also evaluated; phospholipase C (PLC) activity and phosphatidic acid (PA) formation. PLC was inhibited ( approximately 50%) when cells were incubated for 2 h in the presence of either AlCl(3) or Al in the form of HAS. PA formation was tested as a short-term response to Al. By way of contrast to what was found for PLC, incubation of cells for 15 min in the presence of AlCl(3) decreased the formation of PA whereas the same concentration of Al as HAS produced no effect upon its formation. These results suggest that Al is capable to exert its effects upon signal transduction as Al((aq))(3+) acting upon a mechanism linked to the phosphoinositide signal transduction pathway.

Short-term alleviation of aluminum phytotoxicity by urea application in acid soils from south China.

A laboratory experiment was conducted to study effects of urea fertilizer on the chemical composition of soil solutions over time, and to determine Al toxicity as a function of rates of urea application. The experiment revealed that addition of urea fertilizer to soils caused drastic changes in soil pH during the hydrolysis and nitrification stages of urea transformation in the experiment. These pH changes, depending on the N rate of urea application and time courses, had variable effects on soil exchangeable Al, extracted with artificial solutions containing 1 mol l(-1) KCl. The Al mobilization rate could be resolved into two phases: A declining phase for Al was attributed to the urea-induced hydrolysis while a second rising phase was dependent with the nitrification of added N fertilizer. The decreases in exchangeable Al reached the greatest in 4-7 days after fertilization, consistent with soil pH increase. Decreased Al availability had been observed as a consequence of increasing urea addition and soil pH when using Root elongation of maize seedlings as the estimators. Results from the present study demonstrate that urea fertilizer to the surface of soils may lead to a temporary immobilization of Al and, therefore, alleviated Al toxicity to plant seedlings.

Aluminum-induced neurotoxicity and oxidative damage in rabbits: protective effect of melatonin.

OBJECTIVE: The present study was aimed to investigate: (1) the neurotoxic oxidative damage of orally administered aluminum chloride (AlCl3) in rabbits (Biochemical and morphopathological studies). (2) The effect of melatonin as an antioxidant and free radical scavenger on oxidative neuropathic changes. METHODS: Thirty-five male rabbits were divided into 4 groups (A, B, C [10 animals each] and D [5 animals]). Group A received AlCl3 (20 mg/l via drinking water for 3 months). Group B received AlCl3 for 3 months then administered with melatonin (10 mg/kg b.w. sc daily for 15 days). Group C received AlCl3 plus melatonin for 3 months. Group D received the solvent and served as control. Malondialdehyde (MDA) and 4-hydroxyalkenals (4-HDA) as lipid peroxides as well as superoxide dismutase (SOD) as an antioxidant enzyme were measured. Aluminum residue in the brain tissue was measured spectrophotometerically. The morphopathological changes were also examined by light and electron microscopes. RESULTS: MDA and 4-HAD were significantly increased in group A versus those of controls while significantly decreased in groups B and C compared with those of A group. SOD run in an opposite manner. Aluminum concentration was significantly increased in groups A, B and C when compared with group D while it significantly decreased in groups B and C when compared with that of group A. The neuropathlogical examination in the animals of group A revealed atrophy and apoptosis of the neurons in cerebral cortex and hippocampus. This was associated with neurofibrillary degeneration as well as argyrophilic inclusion. Schwan cell degeneration and nerve fiber demylination were also encountered. The elaboration of lipid peroxidation products, inhibition of antioxidant enzymes and the morphopathological changes were minimized in the Al/Mel treated groups and markedly improved in Al+Mel treated group CONCLUSION: Chronic aluminum exposure in rabbits had dramatic encephalopathic morphopathological lesions. It enhances the lipid peroxidation production and inhibits the SOD enzyme. Melatonin had a good prophylactic effect as an antioxidant in aluminum encephalopathy.

Apoplastic binding of aluminum is involved in silicon-induced amelioration of aluminum toxicity in maize.

The alleviating effect of silicon (Si) supply on aluminum (Al) toxicity was suggested to be based on ex or in planta mechanisms. In our experiments with the Al-sensitive maize (Zea mays) cultivar Lixis, Si treatment but not Si pretreatment ameliorated Al-induced root injury as revealed by less root-growth inhibition and callose formation. Si treatment did not affect monomeric Al concentrations in the nutrient solution, suggesting an in planta effect of Si on Al resistance. A fractionated analysis of Si and Al in the 1-cm root apices revealed that more than 85% of the root-tip Al was bound in the cell wall. Al contents in the apoplastic sap, the symplastic sap, and the cell wall did not differ between -Si and +Si plants. Si did not affect the Al-induced exudation of organic acid anions and phenols from the root apices. However, Al treatment greatly enhanced Si accumulation in the cell wall fraction, reducing the mobility of apoplastic Al. From our data we conclude that Si treatment leads to the formation of hydroxyaluminumsilicates in the apoplast of the root apex, thus detoxifying Al.

Developmental aluminum toxicity in mice can be modulated by low concentrations of minerals (Fe, Zn, P, Ca, Mg) in the diet.

Female Swiss Webster mice were fed diets containing 7 (control) or 1000 microg Al/g diet from conception to weaning. Pregnancy weight gain, birth weight, litter size, postnatal mortality, and weaning weight were measured. In different groups, diets low in Fe, Zn, P, or Ca and Mg (CaMg) were used as basal diets, to which Al was added. Relative to controls, who received NRC recommended levels of these nutrients, all diets with marginal essential trace elements impacted development, as demonstrated by effects on birth weight (CaMg, Fe) or weaning weight (Fe, Zn, P). Compared to diets low in Al, the 1000-mg Al/g diet led to reduced weaning weight regardless of the essential element content of the diet. Other end points were influenced by Al only within the basal diet group; pregnancy weight gain with the low-P diet, litter size with the low-Fe diet, pregnancy completion with the low-Zn diet, and postnatal mortality with the low-CaMg or low-Zn diet. Thus, diets marginal in selected minerals can differentially alter the toxicological profile of developmental Al exposures. A basal diet was also used in which the NRC diet was supplemented with ascorbic acid, which promotes Al absorption. No modification of Al toxicity was seen with ascorbic acid supplementation.

Inhibition of cusp and aortic wall calcification in ethanol- and aluminum-treated bioprosthetic heart valves in sheep: background, mechanisms, and synergism.

BACKGROUND AND AIM OF THE STUDY: Calcification of bioprosthetic heart valves fabricated from glutaraldehyde (GA)-pretreated heterograft tissue is frequently responsible for the clinical failure of these devices. Stentless bioprostheses fabricated from GA-fixed porcine aortic valves pose an important challenge in this regard, as pathologic calcification can affect not only the bioprosthetic cusps, but also the aortic wall segment. METHODS: A synergistic approach was used to prevent bioprosthetic cusp and aortic wall calcification. Ethanol pretreatment of bioprosthetic heart valves was shown to inhibit cuspal calcification due to multiple mechanisms, including alterations of collagen structure and lipid extraction. AlCl3 pretreatment of bioprostheses to prevent calcification was also investigated; this alters elastin structure, inhibits alkaline phosphatase, and complexes with phosphoesters, thereby inhibiting aortic wall mineralization. RESULTS: Experimental data from rat subdermal implants and sheep mitral replacements showed successful synergism with co-pretreatment of porcine aortic valve bioprostheses with ethanol and AlCl3. Significant inhibition of both cusp and aortic wall calcification was achieved by differential pretreatments that restrict AlCl3 to only the aortic wall, and not the cusp, accompanied by ethanol cuspal exposure. Sequential exposure of bioprostheses, first to AlCl3 and then to ethanol, led to unexpectedly severe cuspal calcification. CONCLUSION: Differential pretreatment of stentless bioprostheses with ethanol and AlCl3 can effectively inhibit both cuspal and aortic wall calcification.

Silica reduces the toxicity of aluminium to a tropical freshwater fish (Mogurnda mogurnda).

The toxicity of aluminium (Al) to fish in acidic waters has been well documented. It was therefore expected that Al toxicity would be significant in fish communities in Gadjarrigamarndah (Gadji) Creek, a seasonally flowing stream in tropical northern Australia. This creek receives acidic groundwater containing elevated concentrations of Al from earlier land irrigation of treated mine tailings water from the former Nabarlek uranium mine. It was hypothesised that Al toxicity was reduced by high levels of silica (Si) in the water, and the subsequent formation of Al-silicate complexes. This prompted a laboratory assessment of the toxicity of Gadji Creek water to sac-fry of the native fish, Mogurnda mogurnda, followed by more detailed investigation of the toxicity of Al and the influence of Si in reducing Al toxicity. No mortality of M. mogurnda sac-fry was observed in two toxicity tests using Gadji Creek water collected in August 1997 and September 1998. The majority of Al (80-95%) was calculated to be complexed with humic substances and sulfate, with < 1% being complexed with silicate. Assessment of the influence of silica on the acute toxicity of Al in the absence of natural organic complexants (i.e. in reconstituted freshwater, pH 5) revealed that Si reduced Al toxicity. As the molar ratio of Si:Al was increased, the percent survival of M. mogurnda sac-fry increased until there was no significant (P > 0.05) difference from the controls. However, speciation modelling again predicted that little (< 3%) Al complexed with silicate, with the speciation and bioavailability of Al remaining constant as the molar ratio of Si:Al increased. Therefore, the original hypothesis that Al-silicate complexes in solution reduced the toxicity of Al to M. mogurnda could not be supported. This potential mechanism, and an alternative hypothesis, that Si competes with Al for binding sites at the fish gill surface, requires further investigation.

Aluminum accumulation and membrane fluidity alteration in synaptosomes isolated from rat brain cortex following aluminum ingestion: effect of cholesterol.

In the present work, we studied the effect of cholesterol/phospholipid (CH/PL) molar ratio on aluminum accumulation and aluminum-induced alteration of membrane fluidity in rat brain cortex synaptosomes. We observed that sub-acute (daily supply of 1.00 g of AlCl(3) during 10 days) and chronic (daily supply of 0.03 g of AlCl(3) during 4 months) exposure to dietary aluminum leads to a synaptosomal aluminum enrichment of 45 and 59%, respectively. During chronic exposure to AlCl(3), the enhancement of aluminum content was prevented by administration of colestipol (0.31 g/day), which decreased the synaptosomal membrane CH/PL molar ratio (nmol/nmol) from 1.2 to 0.4. Fluorescence anisotropy analysis, using 1,6-diphenyl-1,3,5-hexatriene (DPH) and 1-(4-(trimethylamino)phenyl)-6-phenylhexa-1,3,5-triene (TMA-DPH), showed that after treatment with colestipol a decrease in membrane order occurs at the level of hydrophilic lipid-water surface and deeper hydrophobic region of the synaptosomal membrane. When the rats were exposed to aluminum, it was observed a significant enhancement of membrane fluidity, which was more pronounced at the level of the membrane hydrophilic regions. Meanwhile, when chronic exposure to dietary AlCl(3) was accompanied by treatment with colestipol, the aluminum-induced decrease in membrane order was negligible when compared to TMA-DPH and DPH anisotropy values measured upon colestipol treatment. In contrast, in vitro incubation of synaptosomes (isolated from control rats) with AlCl(3) induced a concentration-dependent rigidification of this more hydrophilic membrane region. The opposite action of aluminum on synaptosomal membrane fluidity, during in vivo and in vitro experiments, appears to be explained by alteration of synaptosomal CH/PL molar ratio, since a significant reduction (approximately 80%) of this parameter occurs during in vivo exposure to aluminum. In conclusion, during in vivo exposure to aluminum, fluidification of hydrophilic regions and reduction of CH/PL molar ratio of presynaptic membranes accompany the accumulation of this cation, which appear to restrict aluminum retention in brain cortex nerve terminals.

Nerve growth factor protects against aluminum-mediated cell death.

In the present study, we examined the effect of two salts of aluminum (Al), aluminum maltolate (Almal) and aluminum chloride (AlCl(3)), on the cell viability of PC12 cells in the absence and presence of nerve growth factor (NGF). A 72-h exposure of PC12 cells to Almal (300 microM) resulted in a marked increase of lactic dehydrogenase (LDH) release from the cells and a decrease of 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) activity. These results indicate that Almal induces a decrease in the cell viability. Under the same conditions, Almal also caused DNA ladder formation and chromatin condensation. In contrast, AlCl(3) did not showed an increased LDH release and a decreased MTT activity in the concentration range of the salt tested (0.1-1 mM). The extent of LDH release and MTT activity decrease induced by Almal treatment closely depended on the amount of Almal incorporated into the cells. An increase in the fluorescence intensity of 6-carboxy-2',7'-dichlorodihydrofluorescein diacetate, di(acetoxymethyl ester) (C-DCDHF-DA) which was loaded into the cell by Almal treatment and its prevention by pyrrolodine dithiocarbamate, a potent antioxidant, suggested that Almal-induced cell death partly proceeds via reactive oxygen species (ROS) production. NGF effectively inhibited the increase of LDH release and the decrease of MTT activity, as well as DNA fragmentation and chromatin condensation. However, NGF did not inhibit the increase of C-DCDHF-DA fluorescence in the cells induced by Almal treatment. From these results, it is suggested that ROS production associated with accumulation of Al is one possible important factor in the onset of Al neurotoxicity via apoptotic cell death and that NGF protects against cell degeneration associated with Al accumulation, but independently of ROS production.

Aluminum modulates brain amyloidosis through oxidative stress in APP transgenic mice.

Epidemiological studies have implicated aluminum (Al) exposure in the pathogenesis of Alzheimer's disease (AD); however, other studies have failed to confirm these results. Oxidative stress is a feature of AD, and Al can exacerbate oxidative events. This biological property has been suggested as a possible mechanism by which this metal could influence the onset and/or evolution of the disease. To test this hypothesis, we fed transgenic mice that over express human amyloid precursor protein (Tg2576) with a diet enriched in Al and measured isoprostane levels, sensitive and specific markers of in vivo oxidative stress, as well as amyloid b peptide formation and deposition. Here, we show an increase in brain isoprostane levels that correlated with increased amyloid b levels and accelerated plaque deposition in Tg2576 mice but not in wild-type (WT) littermates fed with high dietary Al. Significantly, these in vivo effects of Al were reversed by vitamin E, as judged by a reduction of isoprostane production, amyloid b levels, and plaque deposition. These results indicate that dietary Al can modulate in vivo AD-like amyloidosis in Tg2576 by increasing brain oxidative stress.

Metal ion inhibition of nonenzymatic pyridoxal phosphate catalyzed decarboxylation and transamination.

Nonenzymatic pyridoxal phosphate (PLP) catalyzed decarboxylations and transaminations have been revisited experimentally. Metal ions are known to catalyze a variety of PLP-dependent reactions in solution, including transamination. It is demonstrated here that the rate accelerations previously observed are due solely to enhancement of Schiff base formation under subsaturating conditions. A variety of metal ions were tested for their effects on the reactivity of the 2-methyl-2-aminomalonate Schiff bases. All were found to have either no effect or a small inhibitory one. The effects of Al(3+) were studied in detail with the Schiff bases of 2-methyl-2-aminomalonate, 2-aminoisobutyrate, alanine, and ethylamine. The decarboxylation of 2-methyl-2-aminomalonate is unaffected by metalation with Al(3+), while the decarboxylation of 2-aminoisobutyrate is inhibited 125-fold. The transamination reaction of ethylamine is 75-fold slower than that of alanine. Ethylamine transamination is inhibited 4-fold by Al(3+) metalation, while alanine transamination is inhibited only 1.3-fold. Metal ion inhibition of Schiff base reactivity suggests a simple explanation for the lack of known PLP dependent enzymes that make direct mechanistic use of metal ions. A comparison of enzyme catalyzed, PLP catalyzed, and uncatalyzed reactions shows that PLP dependent decarboxylases are among the best known biological rate enhancers: decarboxylation occurs 10(18)-fold faster on the enzyme surface than it does free in solution. PLP itself provides the lion's share of the catalytic efficiency of the holoenzyme: at pH 8, free PLP catalyzes 2-aminoisobutyrate decarboxylation by approximately 10(10)-fold, with the enzyme contributing an additional approximately 10(8)-fold.

Possible involvement of protein phosphorylation in aluminum-responsive malate efflux from wheat root apex.

In many plants, efflux of organic anions from roots has been proposed as one of the major Al resistance mechanisms. However it remains unknown how plants regulate efflux of organic anions in response to Al. In this study, the regulatory mechanisms of Al-responsive malate efflux in wheat (Triticum aestivum) were characterized focusing on the role of protein phosphorylation. Al-resistant wheat (cv Atlas) initiated malate efflux at 5 min after addition of Al, and this response was sensitive to temperature. K-252a, a broad range inhibitor of protein kinases, effectively blocked the Al-induced malate efflux accompanied with an increased accumulation of Al and intensified Al-induced root growth inhibition. A transient activation of a 48-kD protein kinase and an irreversible repression of a 42-kD protein kinase were observed preceding the initiation of malate efflux, and these changes were canceled by K-252a. Malate efflux was accompanied with a rapid decrease in the contents of organic anions in the root apex, such as citrate, succinate, and malate but with no change in the contents of inorganic anions such as chloride, nitrate, and phosphate. These results suggest that protein phosphorylation is involved in the Al-responsive malate efflux in the wheat root apex and that the organic anion-specific channel might be a terminal target that responds to Al signaling mediated by phosphorylation.

Effects of pig manure and wheat straw on growth of mung bean seedlings grown in aluminium toxicity soil.

Crop production in red soil areas may be limited by Al toxicity. A possible alternative to ameliorate Al toxicity is the application of such organic manure as crop straw and animal manure. A pot experiment was conducted to investigate the effects of organic materials on the alleviation of Al toxicity in acid red soil. Ground wheat straw, pig manure or CaCO3 were mixed with the soil and incubated, at 85% of water holding capacity and 25 degrees C, for 8 weeks. After the incubation, 14 seedlings of mung bean (Phaseolus aures Roxb) were allowed to grow for 12 days. Results showed that application of organic material or CaCO3 increased soil pH and decreased soil monomeric inorganic Al concentrations. Growth of mung bean seedling was improved sustantially by the application of organic material or CaCO3. Pig manure or wheat straw was more effective in ameliorating Al toxicity than was CaCO3. Mung bean plants receiving pig manure or wheat straw contained relatively high concentrations of P, Ca and K in their leaves. It is suggested that the beneficial effect of organic manure on mung bean is likely due to decreasing concentrations of monomeric inorganic Al concentrations in soil solution and improvement of mineral nutrition.