The effect of dealuminated jellyfish in mitigating toxicity on mice exposed to aluminum.

In the present study, the removal effect of dealuminated jellyfish on Aluminum (Al) in mice was evaluated. The results showed that the consumption of dealuminated jellyfish significantly decreased Al accumulation in the liver of mice, indicating an Al-removing effect of dealuminated jellyfish on Al-enriched mice. In addition, the effect of dealuminated jellyfish consumption on an Al-overload model was further evaluated. The result showed that the Al content in different tissues and organs of mice was significantly reduced, but it had no significant effect on the other metallic element content. These results indicated that the samples from oral administration have a certain Al-removing effect in Al-overloaded mice. Moreover, the cluster analysis of differentially expressed proteins in blood and liver showed that a high dose of dealuminated jellyfish improve the expression of amine oxidase B and enhance the effect of Al discharge.

Selenium-Rich Yeast protects against aluminum-induced peroxidation of lipide and inflammation in mice liver.

To investigate the effect of Selenium Rich Yeast (SeY) on hepatotoxicity of Aluminium (Al), SeY (0.1 mg/kg) was orally administrated to aluminium-exposed mice (10 mg/kg) for 28 days. The risk of oxidative stress was assessed by detecting the total antioxidant capacity (T-AOC), catalase activity, H2O2 content, and mRNA levels of the Keap1/Nrf-2/HO-1 pathway. Inflammatory reactions were assessed by detecting the mRNA levels of inflammatory biomarkers. Our results showed that SeY protected against the liver histological changes induce by Al. The body weight gain of mice treated with SeY + Al restore to normal compare with mice exposed to Al alone. Al treatment significantly decreased the activities of antioxidant enzymes, reduced T-AOC levels, and up-regulated the mRNA level of Nrf2 and HO-1, thereby ultimately leading to peroxidation. SeY shown a significant protective effect against oxidative stress caused by Al. In addition, Al exposure induced inflammatory responses in rat liver by promoting the release of inflammatory cytokines (TNF-a, NF-kB, TNF-R1, IL-1, IL-6, and COX-2). SeY protected against changes in liver by regulating the mRNA expression levels of inflammatory factors. These results suggested that Se protected the liver from the Al-induced hepatotoxicity by regulating the mRNA level of Keap1/Nrf2/HO-1, and inhibited inflammatory responses by down-regulating the expression level of inflammatory cytokine.

Combined vitamin C sonophoresis and neodymium-doped yttrium aluminum garnet (NdYAG) laser for facial hyperpigmentation: An outcome observation study in Asian patients.

BACKGROUND: The neodymium-doped yttrium aluminum garnet (NdYAG) laser therapy has been a popular technique for facial rejuvenation but certain adverse effects like post-inflammatory hyperpigmentation are issues of concern to Asian patients. AIMS: To assess the outcome following combined treatment with vitamin C sonophoresis and NdYAG laser, in selected cases of facial hyperpigmentation. METHODS: Twenty three women with dyschromia or melasma who had undergone five sessions of Q-switched NdYAG laser therapy followed by transdermal delivery of vitamin C via sonophoresis were selected after a retrospective review of case records. The objective and subjective clinical outcomes and the side effects, including erythema, scaling, pruritus, dryness and post-inflammatory hyperpigmentation were evaluated. RESULTS: In both objective or subjective outcomes, 91.3% (21/23) of the patients showed an excellent or better outcome, while 8.7% (2/23) showed no change. A majority of the patients (73.9%, 17/23) experienced no post-inflammatory hyperpigmentation or had slight post-inflammatory hyperpigmentation which quickly resolved within 1 week. Only one (4.3%) patient had extreme post-inflammatory hyperpigmentation which lasted for over a month. LIMITATIONS: This was a retrospective study without a control group; a comparative study with a control group (patients treated with the laser alone, without vitamin C sonopheresis) is needed to determine the difference in the outcome. CONCLUSION: The use of vitamin C sonophoresis along with NdYAG laser may reduce the incidence of adverse effects in Asian patients. Patients experienced obvious improvement in hyperpigmentation and had lower chances of experiencing extreme or severe post-inflammatory hyperpigmentation.

Aluminum adjuvant dose guidelines in vaccine formulation for preclinical evaluations.

Aluminum (Al) salt-based adjuvants are present in a large variety of licensed vaccines and their use is widely considered for formulations in clinical trials. Although the regulatory agencies have clearly stated the acceptable levels of Al salts in vaccines for human use, there are no general indications for preclinical research. This brief commentary reviews the current status of Al concentrations in licensed vaccines, the related potential toxicity in preclinical species, and proposes a general guideline for selection of suitable Al salt levels in preclinical models, focusing on the formulation development for recombinant protein antigens. A table with conversion factors is included in order to provide a tool for calculation of doses with different Al salts.

Aluminium and nutrients induce changes in the profiles of phenolic substances in tea plants (Camellia sinensis CV TTES, No. 12 (TTE)).

BACKGROUND: Tea plants are always cultivated in acid soils in hilly regions and their growth can be dependent on to soluble aluminium (Al). The mechanism of Al detoxification and the influence of Al on phenolic compounds (i.e. catechin) in the roots of tea plants has remained obscure. This study aimed to investigate the influence of Al changes on the concentrations of phenolic substances in tea plants through hydroponic experiments. RESULTS: Tea plants were cultivated in nutrient solution containing 1.5 and 2.5 mmol L(-1) Al, and these treatments enhanced the growth of new buds and roots. Aluminium stimulated the uptake of Ca, Mg, K and Mn, whereas the uptake of Fe, Cu and Zn was retarded. Moreover, total phenol concentrations in tea plant tissues increased with increasing Al concentrations. In general, catechin concentrations in leaves increased with increasing Al concentrations in the hydroponic experiments. High correlation coefficients were obtained between Al and (-)-ECG (r(2) = 0.85, P < 0.01) and between Al and total phenols (r(2) = 0.92, P < 0.01). CONCLUSIONS: The Al concentration in tea plants indeed increases catechin concentrations and plays an important role in the growth of tea plants.

Aluminium and strontium in calcium supplements and antacids: a concern to haemodialysis patients?

Trace elements, most notably aluminium and strontium, have been noted for their role in the development of secondary bone disorders in haemodialysis patients. Due to the large dosages of calcium required for the maintenance of dialysis patients, this study investigated whether the source of calcium chosen for supplementation, including the form of administration (i.e. chewable forms or capsules), has an influence on the total amount of strontium and aluminium ingested daily. A convenience sample of various calcium supplement tablets and antacids was acquired, and strontium and aluminium quantification was performed by wavelength-dispersive X-ray fluorescence spectrometry. The use of readily available oyster shell-based calcium was found potentially to increase the total amount of ingested strontium substantially with concentrations reaching (2.26 +/- 0.05) (mg Sr).(g Ca)(-1), while the use of antacids or chewable supplements was found to contain concentrations reaching as high as (1.2 +/- 0.3) (mg Al).(g Ca)(-1) in the supplements analysed within this work. It is recommended that the choice of calcium supplement prescribed to individuals undergoing haemodialysis be closely regulated and noted as a possible factor in the prevalence of bone disorders reported in these patients.

Dietary exposure to aluminium of the Hong Kong population.

A total of 256 individual food samples were collected in Hong Kong for aluminium testing. Most of food samples were analysed in ready-to-eat form. High aluminium levels were found in steamed bread/bun/cake (mean: 100-320 mg kg(-1)), some bakery products such as muffin, pancake/waffle, coconut tart and cake (mean: 250, 160, 120 and 91 mg kg(-1), respectively), and jellyfish (ready-to-eat form) (mean: 1200 mg kg(-1)). The results demonstrated that aluminium-containing food additives have been widely used in these food products. The average dietary exposure to aluminium for a 60 kg adult was estimated to be 0.60 mg kg(-1) bw week(-1), which amounted to 60% of the new PTWI established by JECFA. The main dietary source was "steamed bread/bun/cake", which contributed to 60% of the total exposure, followed by "bakery products" and "jellyfish", which contributed to 23 and 10% of the total exposure, respectively. However, the estimation did not include the intake of aluminium from natural food sources, food contact materials or other sources (e.g. drinking water). Although the results indicated that aluminium it is unlikely to cause adverse health effect for the general population, the risk to some populations who regularly consume foods with aluminium-containing food additives cannot be ruled out.

Aluminum content of parenteral nutrition in neonates: measured versus calculated levels.

BACKGROUND AND OBJECTIVE: Aluminum (Al) is associated with significant central nervous system toxicity and bone and liver damage. Because Al is a contaminant of parenteral nutrition (PN) components including calcium and phosphate additives, premature infants are at potentially high risk for toxicity. The US Food and Drug Administration (FDA) has mandated PN component product labeling and recommended maximum Al daily exposure limits. The objective of this article is to determine the actual Al content of neonatal PN solutions, compare these values to the calculated amounts from manufacturers' PN product labels, and ascertain whether the actual Al exposure exceeds the FDA recommended maximum of 5 microg . kg(-1) . day(-1). MATERIALS AND METHODS: Samples from 40 neonatal patient PN solutions were selected for sampling and Al content determination. Samples were also taken from 16 manufacturer's component products used in PN formulation. All of the samples were sent to Mayo Laboratories for Al content measurement. The calculated Al concentrations in PN samples were determined from the manufacturer's labeled content. RESULTS: Both measured and calculated Al concentrations exceeded the FDA recommended safe limit of <5 microg . kg(-1) . day(-1). The actual measured Al content was significantly lower than the calculated Al content in both the patient PN solutions and the component product samples. CONCLUSIONS: Al exposure exceeded the FDA recommended maximum limit for all patient samples; however, the actual measured Al content of all the samples was significantly less than the calculated Al content based on manufacturer's labels. These findings suggest that manufacturers label their products with actual Al content at the time of product release rather than at time of expiration. Periodic monitoring of Al levels should be considered with prolonged PN therapy. Changes in manufacturing processes, including the use of better raw materials, are essential to reduce Al contamination to meet FDA mandates.

Trace copper levels in the drinking water, but not zinc or aluminum influence CNS Alzheimer-like pathology.

Mounting evidence suggests copper may influence the progression of Alzheimer's disease by reducing clearance of the amyloid beta protein (Abeta) from the brain. Previous experiments show that addition of only 0.12 PPM copper (one-tenth the Environmental Protection Agency Human consumption limits) to distilled water was sufficient to precipitate the accumulation of Abeta in the brains of cholesterol-fed rabbits (1). Here we report that addition of copper to the drinking water of spontaneously hypercholesterolemic Watanabe rabbits, cholesterol-fed beagles and rabbits, PS1/APP transgenic mice produced significantly enhanced brain levels of Abeta. In contrast to the effects of copper, we found that aluminum- or zinc-ion-supplemented distilled water did not have a significant effect on brain Ab accumulation in cholesterol-fed rabbits. We also report that administration of distilled water produced a reduction in the expected accumulation of Ab in three separate animal models. Collectively, these data suggest that water quality may have a significant influence on disease progression and Ab neuropathology in AD.

Lake restoration by dosing aluminum relative to mobile phosphorus in the sediment.

In the sediment of the shallow, hypertrophic Lake Sønderby, Denmark, potentially mobile phosphorus (Pmobile) was determined by a sequential extraction technique as the sum of porewater P, iron-bound P, and nonreactive P (i.e., polyphosphates and organic P). A good agreement was observed between loss rates of Pmobile in the top 10 cm of the sediment from winter to summer, P release rates measured in undisturbed sediment cores, and rates of P accumulation in the lake water from winter to summer (22, 32, and 30 mg of P m(-2) day(-1), respectively). This suggests that the operationally defined Pmobile was the sediment P fraction responsible for the internal loading in the lake. In autumn 2001, 11 mg of aluminum (Al) L(-1), equivalent to 31 g of Al m(-2), was added to the lake water. This dosage represented a 4:1 molar ratio between Al and Pmobile. The Al treatment significantly decreased lake water P, and P precipitated from the lake water was recovered as Al-bound P in the sediment after the treatment. Internal P loading was reduced by 93% in the two posttreatment years, relative to 2001. Accordingly, average summer concentrations of total P in lake water declined from 1.28 (SE = 0.17) and 1.3 (SE = 0.14) mg L(-1) in the two pretreatment years to 0.09 (SE = 0.01) and 0.13 (SE = 0.01) mg L(-1) in the posttreatment years. pH levels remained unchanged relative to pretreatment levels, while the total alkalinity was reduced from 3.2 (SE = 0.04) to 2.7 (SE = 0.03) mequiv L(-1).

Cognitive impairment and composition of drinking water in women: findings of the EPIDOS Study.

BACKGROUND: The concentration of aluminum or silica in drinking water may be a potential environmental risk factor for Alzheimer disease (AD). OBJECTIVES: The objective was to investigate at baseline the potential association between the composition of drinking water and the level of cognitive function in women taking part in the Epidemiology of Osteoporosis (EPIDOS) Study and to determine during follow-up the effects of the composition of drinking water on the risk of AD. DESIGN: Women aged >/=75 y (n = 7598) were recruited between 1992 and 1994 in 5 geographic areas of France. The participants from one center (n = 1462) were followed for

Effect of folic acid supplementation on aluminum accumulation in rats.

OBJECTIVE: Exposure to many xenobiotics may cause depletion of folic acid (folate), which is an essential vitamin for humans. Replacement of folate can be effective in protection against some diseases and in partial or total prevention of adverse effects related to xenobiotics. Aluminum (Al) is the most widely distributed metal in the outer crust of the earth. Its toxicity in humans is well known. However, there is no evidence that folate can decrease accumulation of Al to which humans can be exposed in many ways. The aim of the present study was to quantify organ Al accumulation and to evaluate whether there is any protective (or reductive) effect of folic acid on Al accumulation. METHODS: Male Wistar rats were assigned oral Al chloride (200 mg x kg(-1) x d(-1), n = 10, group 1) alone or in combination with folic acid (20 mg x kg(-1) x d(-1), n = 10, group 2) for 8 wk. At the end of the period, bone, kidney, brain, and blood samples were collected, and Al concentrations were determined by electrothermal atomic absorption spectrophotometry. RESULTS: Mean values of Al in the tissue samples from group 1 were higher than those from group 2 (all P < 0.05). No difference was observed in serum Al levels between groups (P > 0.05). CONCLUSION: These results suggest that folate supplementation might be useful to decrease Al accumulation in its main target organs, i.e., bone, kidney, and brain.

Aluminium-induced changes in the rat brain serotonin system.

Aluminium exposure, apart from producing cholinotoxicity, can include changes in other neurotransmitter levels since neurotransmitter levels are closely interrelated. Reports of aluminium (Al) effects on brain neurotransmitters are limited. To investigate the effect of Al on the rat brain serotonergic system, the present study was conducted to explore brain region-specific changes and duration-specific changes. Male Wistar albino rats were exposed orally to Al chloride (AlCl(3).6H(2)O; 320 mg/kg body weight) daily for up to 60 days and changes in the 5-hydroxytrytamine (5-HT) and its metabolite 5-hydroxyindole acetic acid (5-HIAA) levels were observed after 4, 14 and 60 days of exposure in olfactory lobe (OLB), cerebellum (CBL), pons (PON), medulla oblongata (MOB), spinal cord (SPI), hypothalamus (HYP), hippocampus (HIP), striatum (STR), midbrain (MBR) and cortex (COR) brain regions. Significantly increased 5-HT levels observed in brain regions OLB (60 days), HIP (4,14 days), STR (14 days), HYP (14, 60 days), MBR (4 and 14 days), PON (4 days), MOB (4 days) and SPI (4, 14 and 60 days) following Al exposure may be due to Al deactivating 5-HT system by decreased release and subsequent breakdown of 5-HT. Decreased 5-HT levels observed in cerebral COR, HIP (60 days) and in CBL after 4 and 60 days of exposure suggest an inhibitory effect of Al on the 5-HT system due to withdrawal of cholinergic input in these brain regions. 5-HIAA level changes correlate with 5-HT level changes in many brain regions studied. The results reveal that the neurochemical changes due to Al were dependent on the duration of exposure and are brain-region-specific. The observed changes may be related to the cholinergic toxicity of Al.

Altered dopamine turnover in murine hypothalamus after low-dose continuous oral administration of aluminum.

Aluminum, a known neurotoxic substance, has been suggested as a possible contributing factor in the pathogenesis of Alzheimer's disease. Ground-water pollution by aluminum has been recently reported. In the current study groups of 5 male BALB/c mice were administered aluminum ammonium sulfate in drinking water ad libitum at 0, 5, 25, and 125 mg/L aluminum for 4 weeks. At the termination of aluminum exposure, their brains were removed and dissected into cerebrum, cerebellum, medulla oblongata, midbrain, corpus striatum, and hypothalamus. The concentration of norepinephrine (NE), dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), serotonin (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA), were determined in each brain area. DA, DOPAC, and HVA levels were lower in the hypothalamus of aluminum-treated mice, most notably in the low-dose group, as compared with control. No marked alterations in NE, 5-HT, and 5-HIAA levels were detected in any brain region. Changes in the concentration of DA and its metabolites measured in the hypothalamus suggest an inhibition of DA synthesis by aluminum.

Silicon reduces aluminum accumulation in rats: relevance to the aluminum hypothesis of Alzheimer disease.

In recent years, a possible relation between the aluminum and silicon levels in drinking water and the risk of Alzheimer disease (AD) has been established. It has been suggested that silicon may have a protective effect in limiting oral aluminum absorption. The present study was undertaken to examine the influence of supplementing silicon in the diet to prevent tissue aluminum retention in rats exposed to oral aluminum. Three groups of adult male rats were given by gavage 450 mg/kg/day of aluminum nitrate nonahydrate 5 days a week for 5 weeks. Concurrently, animals received silicon in the drinking water at 0 (positive control), 59, and 118 mg Si/L. A fourth group (-Al, - Si) was designated as a negative control group. At the end of the period of aluminum and silicon administration, urines were collected for 4 consecutive days, and the urinary aluminum levels were determined. The aluminum concentrations in the brain (various regions), liver, bone, spleen, and kidney were also measured. For all tissues, aluminum levels were significantly lower in the groups exposed to 59 and 118 mg Si/L than in the positive control group; significant reductions in the urinary aluminum levels of the same groups were also found. The current results corroborate that silicon effectively prevents gastrointestinal aluminum absorption, which may be of concern in protecting against the neurotoxic effects of aluminum.

Aluminum and acid effects on calcium and phosphorus metabolism in young growing chickens (Gallus gallus domesticus) and mallard ducks (Anas platyrhynchos).

Acidification is associated with increased mortality, reduced growth, and bone abnormalities in birds. Associated with acid deposition is an increase in aluminum availability due to solubilization from soil and other sources. (Conversely, experimental diets containing aluminum sulfate have much reduced pHs.) The present studies compare the effects of two levels of dietary acid (sulfuric acid) (0.122 and 0.56 mol H+ per kg feed; 0.056 and 0.277 mol sulfate per kg feed) and dietary aluminum (aluminum sulfate at 0.1 and 0.5%; sulfate at 0. 056 and 0.277 mol sulfate per kg feed) on bone growth, mineralization, and phosphorous/calcium homeostasis in growing birds (chickens and mallard ducks). Growth was reduced by the high acid (chicken) and aluminum (ducks and chickens) diets. A reduction in bone mineralization was observed in birds receiving aluminum-containing diets [low aluminum diet: decreased tibia ash, calcium, and phosphorus (chickens); high aluminum diet: decreased tibia dry weight, % of ash and mg; ash, calcium (chickens, ducks as % of ash), and phosphorus (chickens mg/duck, % of ash)]. Moreover, plasma concentrations of inorganic phosphate were reduced in chicks on the high aluminum diet. There were also marked decreases in bone growth and mineralization [tibia weight, ash (mg), calcium (mg), phosphorus (mg)] and plasma concentrations of 1,25-dihydroxy vitamin D3 in chicks on the high acid diet compared to those on a control diet. These changes were probably due to reduced feed intake; changes in bone indices being of a greater or similar magnitude in pairfed control. There was little change in bone indices, growth rate or feed consumption in ducklings receiving either the low or high acid diets. It is concluded that aluminum directly adversely affected bone mineralization whereas acid effects are mediated in part by changes in feed consumption.

Effects of dietary supplementation with aluminum and citrate on iron metabolism in the rat.

The metabolism of iron (Fe) has been shown to interact with that of aluminum (Al) in relation to intestinal absorption, transport in the blood plasma, and the induction of lipid peroxidation and cellular damage. Also, dietary supplementation with citrate has been shown to increase the absorption of both metals and, in the presence of high intakes of Fe and Al, leads to excessive accumulation of both metals in the body. In this study, the likely interaction between Al and internal Fe metabolism was investigated using rats fed diets that were either deficient, sufficient, or loaded with Fe, with or without the addition of Al and sodium citrate. These diets commenced when the rats were 4 wk old and were continued for 9-11 wk. At that time, Fe metabolism as assessed by measurement of organ uptake of 59Fe and 125I-transferrin, after iv injection of transferrin labeled with both isotopes, plus measurement of tissue concentrations of nonheme Fe and Al. The Fe-deficient diet and Fe-loaded diet led to states of Fe deficiency and Fe overload in the rats, and supplementation of the diet with Al increased Al levels in the kidneys, liver, and femurs, but, generally, only when the diet also contained citrate. Neither Al nor citrate supplementation of the diet had any effect on nonheme Fe concentrations in the liver, kidney, or brain, or on the uptake of 59Fe or 125I-transferrin by liver, kidney, brain, or spleen. Only with the femurs was a significant effect observed: increased 59Fe uptake in association with increased Al intake. Therefore, using this animal model, there was little evidence for interaction between Fe and Al metabolism, and no support was obtained for the hypothesis that dietary supplementation with Fe and citrate can lead to excessive Fe absorption and deposition in the tissues.

Metabolic responses of postmenopausal women to supplemental dietary boron and aluminum during usual and low magnesium intake: boron, calcium, and magnesium absorption and retention and blood mineral concentrations.

Findings from animal studies indicate that dietary boron affects several aspects of mineral metabolism, especially when animals are subjected to nutritional stressors. Eleven postmenopausal volunteers living on a metabolic ward for 167 d (one 23-d equilibration period and six 24-d treatment periods) were fed a conventional basal diet that supplied a daily average intake of 0.36 mg B, 109 mg Mg, and < 0.10 mg A1/8400 kJ. They were given supplements of 0 (BB) or 3 mg B (SB, last two periods only), 0 (BMg) or 200 mg Mg (SMg) (with magnesium supplements held constant during the last two periods), or 0 (BAl) or 1000 mg A1 (SAl)/d. The SB treatment, compared with the BB treatment, provided a 9.0-fold increase in dietary boron but yielded only a 1.5-fold increase in plasma boron concentrations. Regardless of boron dietary treatment, fecal plus urinary excretion of boron accounted for nearly 100% of dietary boron intake with no evidence of boron accumulation over time. Lack of boron accumulation and relatively small changes in blood boron values during a substantial increase in dietary boron support the concept of boron homeostasis. In subjects fed BMg, SB decreased the percentage of dietary calcium lost in the urine but increased that percentage in volunteers fed SMg, a relation that may be important in understanding metabolic mineral disorders that perturb calcium balance. Reduced calcium absorption during SAl suggests that aluminum supplementation should be limited or at least monitored in postmenopausal women prone to excessive calcium loss. Decreased total urinary oxalate during SB in BMg subjects indicates a possible role for boron in the control of urolithiasis during low-magnesium nutriture.

Effect of small variations of aluminum intake on calcium metabolism in young rats.

BACKGROUND: While in the adult Al intoxication requires high dosages, little is known on the threshold level of Al toxicity in the young. METHODS: Weaning rats were fed for 90 days ore of four diets differing by their content in Ca (7.5 vs < 0.5 g/< g diet)(Ca+/-) and Al (10.6 vs 8.4 mg/kg)(Al+/-); Al supplementation was 30% above the standard level of diet. Ca and Al levels were measured in liver, bone (femur), and brain. RESULTS: Ca- had a significant negative effect on growth which was further reduced by Al+; in Ca sufficient/Al+ animals, Al concentrations were significantly increased in bone and brain and tended to increase in liver; Ca decreases observed in these three organs were only significant in brain. Ca deficiency further enhanced the Al deposit in bone at both levels of Al intakes, and reduced Ca concentrations in these three organs in Al+ animals; in Ca-/Al- animals, the decrease in Ca displayed in the three tissues reached a significant level in brain. CONCLUSIONS: This study suggests that in the growing subject the side effects of small variations of Al intake can be enhanced when they are combined with other mineral imbalances.