Excretion Of Aluminium Research Articles

ИЗУЧЕНИЕ ГЕПАТОТОКСИЧЕСКОГО ВОЗДЕЙСТВИЯ ГИДРОКСИДА АЛЮМИНИЯ, ВВОДИМОГО В ЖЕЛУДОЧНО-КИШЕЧНЫЙ ТРАКТ КРЫС, В ПОДОСТРОМ ЭКСПЕРИМЕНТЕ

Aluminum (Al) has various toxic effects on biosystems. Essential properties of aluminum have not been established, the mechanisms of impairment are insufficiently studied. The negative impact of aluminum on the human body leads to liver damage, increased oxidative stress and development of hepatotoxicity. Blood enzymes are characteristic markers of liver function and are used to assess the toxicity of environmental pollutants. The aim of the study was to investigate the activity of enzyme markers of hepatotoxicity, aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and alkaline phosphatase (ALP) in the blood of laboratory animals after subacute intoxication with aluminum hydroxide (Al(OH)3). The experiment was conducted on 80 white rats divided into 4 groups. Three groups of animals orally received Al(OH)3 solution of different concentrations for a month, the control group was administered distilled water. At the end of the experiment, enzyme activity in the blood serum was measured. The increase in the AST level in the first group is associated with changes in hepatocytes. The decrease in ALT activity in the experimental groups is associated with the peculiarities of aluminum excretion. By analogy with AST, an increase in the concentration of LDH was registered in the first group, while a decrease in the level of the indicator was shown in the second and third groups. A decrease in the activity of alkaline phosphatase indicates a violation of metabolic processes in cells. The effect of Al(OH)3 for a month caused certain changes in liver markers in the blood serum of experimental animals. For a more complete understanding of the hepatotoxic effects of aluminum, additional biochemical studies are needed to assess the activity of antioxidant defense enzymes.

Effect of an aluminum foil-processed diet on internal human aluminum burden

Background and purposeAluminum can be released into food by aluminum-containing food-contact materials (Al-FCM) during preparation or storage. There is considerable concern that extra aluminum intake may have negative effects on public health, especially with regard to its high background exposure and neurotoxic properties of aluminum in high exposures. Human in-vivo data on the additional aluminum load from Al-FCM, however, are lacking. As such, the objective of this study was to explore whether the consumption of a diet highly exposed to such products leads to an increased systemic Al load in real-world conditions. Materials and methodsAn exploratory, single-arm intervention study with a partially standardized diet was designed and carried out with 11participants. The same 10-day sequence of dishes was repeated three times. Participants were exposed to Al-FCM from Days 11 to 20, whereas control-phase meals were prepared without Al-FCM during the first and last 10–day periods. Spot urine samples were collected each morning and evening and analyzed for their aluminum concentration; appropriate contamination countermeasures were taken.Principal results: Urinary aluminum excretion showed a strong dependency on the creatinine concentration in urine and required adjustment in further analyses. The creatinine-adjusted aluminum excretion during the exposure phase (median 1.98 µg/g creatinine) was higher than in both control phases (1.78 µg/g creatinine each). Two different mixed-effects regression models showed a significant effect in the exposure phase. Considering a discrete time effect, the creatinine-adjusted mean increase in the exposure phase was estimated to be 0.19 µg/L (95% CI: 0.07–0.31; p = 0.0017).Major conclusions: This study demonstrated a measurable but fully reversible additional Al burden in humans from subacute Al-FCM exposure under real-world conditions. The estimated increase from Al-FCM corresponds to 8% of the baseline concentration. These data enable a more robust assessment of human health risks by Al-FCM.

Investigating toxic aluminium levels in haemodialysis patients after “Day Zero” drought in Cape Town, South Africa

Introduction: Aluminium is the most abundant metallic element in the earth’s crust and can be consumed through water, medications, and by using metallic cooking utensils. Aluminium levels become a concern when they are above biological exposure limits and can present with multiple clinical complications. When patients have chronic kidney disease and are on haemodialysis, impaired aluminium excretion can lead to its accumulation. Significantly elevated serum aluminium levels were noted in patients with chronic kidney disease (stage 5) on haemodialysis at Groote Schuur Hospital, Cape Town, South Africa. This coincided with one of the worst water crises ever experienced in this metropolitan area, with extreme water restrictions being imposed and alternative water sources being accessed.

Fecal Excretion and Whole-Body Retention of Macro and Micro Minerals in Atlantic Salmon Fed Torula Yeast Grown on Sugar Kelp Hydrolysate.

Simple SummaryCultivation of seaweed for various purposes has gained more focus in Europe during the last decades. Our study demonstrates the potential of seaweed as a substrate for yeast production, uptake of seaweed minerals into the yeast, and the bioavailability of minerals from this yeast in Atlantic salmon. We show that several minerals, especially the microminerals that are normally supplemented to commercial salmon diets, can be provided by yeast produced on seaweed hydrolysate.Yeast is a microbial feed ingredient that can be produced from non-food biomasses. Brown seaweed contains high levels of complex carbohydrates that are not digested to any extent by monogastric animals but can be used as carbon sources for yeast production. The objective of this study was to investigate how minerals originating from brown macroalgae (Saccharina latissima) are incorporated in Cyberlindnera jadinii yeast and to assess the bioavailability of these different minerals as well as their accumulation into different organs of Atlantic salmon. The yeast C. jadinii was produced on a seaweed hydrolysate mixed with a sugar-rich wood hydrolysate in a 9:1 volume ratio and fed to Atlantic salmon (Salmo salar) in two different experiments: a digestibility experiment with 30% dietary inclusion of yeast and a retention experiment with increasing inclusion of yeast (5, 10, and 20%). Seaweed minerals such as zinc (Zn), copper (Cu), iodine (I), manganese (Mn), and cobalt (Co) were incorporated to a high degree in the yeast. The apparent fecal excretion of minerals was similar in both experiments, in general, with low excretion of, I, bromine (Br), and arsenic (As) (ranging from 18.0% to 63.5%) and high excretion of iron (Fe), Cu, Mn, aluminum (Al), cadmium (Cd) and lead (Pb) (ranging from 56.9% to <100%), despite the different fish size and fecal sampling method. High levels of Cu, I, Br, and Co in the yeast resulted in a linear decrease (p < 0.05) in retention of these minerals in salmon fed increasing levels of yeast. Despite increasing amounts of these minerals in the feed, whole-body levels of Cu and Mn remained stable, whereas whole-body levels of Co, somewhat unexpectedly, decreased with increased dietary yeast inclusion. The Cd from the yeast had low bioavailability but was concentrated more in the kidney (0.038 mg kg−1) and liver (0.025 mg kg−1) than in muscle (0.0009 mg kg−1). The given Cd level in fish strengthens the indication that it is safe to feed salmon with up to 20% inclusion of seaweed yeast without exceeding the maximum limit for Cd of 0.05 mg kg−1 w.w. in fish meat. The level and retention (p < 0.05) of As were lower in the yeast compared to fishmeal. The high level of iodine in S. latissima (3900 mg kg−1) was partly transferred to the yeast, and salmon fed increasing levels of yeast displayed a linear increase in whole-body I content (p < 0.05). There is, however, a need for a growth experiment with larger fish to draw any firm conclusions regarding food safety. Overall, this study shows that yeast grown on hydrolyzed seaweed can be a suitable mineral source for Atlantic salmon, especially when diets are low in fishmeal.

Increased urinary excretion of aluminium after ingestion of the food additive sodium aluminium phosphate (SALP) – a study on healthy volunteers

ABSTRACTFood is an important source of human aluminium (Al) exposure and regular consumption of foods containing Al-based food additives may result in high Al intakes above health-based tolerable intakes. However, some additives are Al salts with low solubility, and little is known about bioavailability of Al in these additives. We investigated urine Al concentrations in healthy adult volunteers (N = 18, women/men) before (base-line) and after 7 days of ingestion of pancakes with a low Al content (median: <0.5 mg Al/kg) and high Al content (median: 860 mg/kg). The high-Al pancakes contained the common additive sodium aluminium phosphate (SALP). The participants did not know if the pancakes contained SALP or not during the experiment. After adjusting for creatinine content of the urine samples, median base-line Al concentrations before pancake ingestion were in the range 30–40 µmol Al/mol creatinine. Urine Al concentrations after ingestion of low-Al pancakes (average intake: <0.042 Al mg/day) did not differ significantly from the base-line levels. After ingestion of high-Al pancakes (72 mg Al/day) the median Al concentration in urine was more than 2-fold higher than at the base-line sampling before the high-Al pancake ingestion. At the end of the experiment the volunteers ingested an Al-containing antacid (Al-OH, 1800 mg Al/day) for 7 days as a positive control of Al absorption. This caused a 10-fold increase in median urine Al concentration compared to base-line. Our results strongly suggest that Al in the form of SALP in a pancake mix is bioavailable for absorption in humans, which should be taken into account in risk assessment of Al in food in countries with a high use of SALP as a food additive.

Dietary supplementation with probiotics regulates gut microbiota structure and function in Nile tilapia exposed to aluminum.

Backgrounds and aimsAluminum contamination of water is becoming increasingly serious and threatens the health status of fish. Lactobacillus plantarum CCFM639 was previously shown to be a potential probiotic for alleviation aluminum toxicity in Nile tilapia. Considering the significant role of the gut microbiota on fish health, it seems appropriate to explore the relationships among aluminum exposure, probiotic supplementation, and the gut microbiota in Nile tilapia and to determine whether regulation of the gut microbiota is related to alleviation of aluminum toxicity by a probiotic in Nile tilapia.Methods and resultsThe tilapia were assigned into four groups, control, CCFM639 only, aluminum only, and aluminum + CCFM639 groups for an experimental period of 4 weeks. The tilapia in the aluminum only group were grown in water with an aluminum ion concentration of 2.73 mg/L. The final concentration of CCFM639 in the diet was 108 CFU/g. The results show that environmental aluminum exposure reduced the numbers of L. plantarum in tilapia feces and altered the gut microbiota. As the predominant bacterial phyla in the gut, the abundances of Bacteroidetes and Proteobacteria in aluminum-exposed fish were significantly elevated and lowered, respectively. At the genus level, fish exposed to aluminum had a significantly lower abundance of Deefgea, Plesiomonas, and Pseudomonas and a greater abundance of Flavobacterium, Enterovibrio, Porphyromonadaceae uncultured, and Comamonadaceae. When tilapia were exposed to aluminum, the administration of a probiotic promoted aluminum excretion through the feces and led to a decrease in the abundance of Comamonadaceae, Enterovibrio and Porphyromonadaceae. Notably, supplementation with a probiotic only greatly decreased the abundance of Aeromonas and Pseudomonas.ConclusionAluminum exposure altered the diversity of the gut microbiota in Nile tilapia, and probiotic supplementation allowed the recovery of some of the diversity. Therefore, regulation of gut microbiota with a probiotic is a possible mechanism for the alleviation of aluminum toxicity in Nile tilapia.

Advances in dialysis encephalopathy research: a review.

Dialysis encephalopathy (DE) is a progressive, fatal disease with a high mortality rate. Understanding the causes of this disease and the efforts to prevent and treat it would help improve the prognosis and quality of life of affected patients. This paper reviews the etiology, clinical features, methods of examining accessory features, diagnosis, treatment, and prevention of DE. We found that DE is likely to be related to aluminum poisoning. The clinical manifestations of DE include language disorders, mental and behavioral disorders, cognitive decline, and movement disorders. Electroencephalogram (EEG) findings mainly consist of an abundance of low waves, intermittent bilateral synchronous high-amplitude spikes, and ridge waves. Assessing the clinical features and obtaining an EEG are of great value in diagnosis, and DE is treated by both reducing aluminum intake and increasing aluminum excretion. Deferoxamine (DFO) is an effective treatment for DE.

Protective effects of banana pectin against aluminum-induced cognitive impairment and aluminum accumulation in mice

To investigate the effect of pectin on absorption and bio-toxicity of aluminum, pectin extract (100 mg kg−1 d−1) from banana pulp was orally administrated to aluminum exposed mice (35 mg kg−1 d−1) for 6 weeks. Our result showed that body weight gain of the mice treated with aluminum plus banana pectin was 32.5% higher than that of mice exposed to aluminum alone after 6 weeks of the administration. In both the step-down inhibitory avoidance task and Morris water maze test, memory retention of aluminum-exposed mice was significantly improved by the pectin administration. Treatment with banana pectin effectively prevented absorption of aluminum from the gastrointestinal tract, total aluminum excretion of mice treated with banana pectin plus aluminum was 9.3% higher than that of mice exposed to aluminum alone on the 12th day. Aluminum level in serum, cerebrum, or cerebellum of mice treated with aluminum plus banana pectin was 30.8%, 17.5%, or 17.9% lower than that of mice exposed to aluminum alone on the 42nd day, respectively. In conclusion, banana pectin extract can effectively reduce aluminum toxicity in mice.

Anti‐neurotoxic evaluation of synthetic and characterized metal complexes of thiosemicarbazone derivatives

Quinoline‐2‐caboxyaldehyde thiosemicarbazone (HL1) and quinoline ‐2‐caboxyaldehyde N‐dimethyl thiosemicarbazone (HL2) metal complexes were prepared and characterized using analytical and spectroscopic techniques. The measurements showed that ligands behave as monovalent or neutral tridentate ligands bonding via azomethine, quinoline ring nitrogen atoms and sulfur atoms in thiol or thion forms. The anti‐neurotoxic effect of ligands and their complexes showed that, exposure to aluminum increase oxidative stress in the brain, an effect that could be offset by concomitant thiosemicarbazone complexes. Complexes could be having an effect on absorption or excretion of aluminum, due to their chelating activity. These findings may shed light on the potential clinical importance of thiosemicarbazone complexes in Alzheimer's disease.

Urinary Excretion of Aluminium and Silicon in Secondary Progressive Multiple Sclerosis

BackgroundProgressive multiple sclerosis is a chronic autoimmune condition of unknown aetiology and few therapeutic options. Human exposure to aluminium has been linked with multiple sclerosis and affected individuals are known to excrete unusually high amounts of aluminium in their urine. Silicon-rich mineral waters facilitate the removal of aluminium from the body in urine and herein we have tested their efficacy in affecting urinary excretion of aluminium in individuals diagnosed with secondary progressive multiple sclerosis (SPMS). MethodsUrinary excretion of aluminium and silicon, measured using transversely-heated graphite furnace atomic absorption spectrometry, was determined in 15 individuals diagnosed with SPMS over 24weeks, a 12week baseline period (control) followed by a 12week treatment period, during which individuals consumed up to 1.5L of a silicon-rich mineral water every day. FindingsIndividuals with SPMS excreted high amounts of aluminium during the baseline period (135.2nmol/mmol Crt (70.3–222.2, n=180) and females excreted significantly more aluminium than males. Regular drinking of a silicon-rich mineral water increased the urinary excretion of aluminium significantly (349.0nmol/mmol Crt (231.7–524.7, n=180; three-way ANOVA, F1,13=59.17, p-value=0.000003) relative to the baseline period. The majority of individuals, 14 out of 15, excreted more aluminium (μmol/24h) following drinking of a silicon-rich mineral water (independent-test, p<0.05). Silicon-rich mineral waters may be an effective and non-invasive therapy for the removal of aluminium from the body of individuals with SPMS.

A study of the association between urinary aluminum concentration and pre-clinical findings among aluminum-handling and non-handling workers.

BackgroundAluminum is considered to be a relatively safe metal for humans. However, there are some reports that aluminum can be toxic to humans and animals. In order to estimate the toxicity of aluminum with respect to humans, we measured the aluminum concentration in urine of aluminum-handling and non-handling workers and investigated the relationships between their urinary aluminum concentrations and pre-clinical findings.MethodsTwenty-three healthy aluminum-handling workers and 10 healthy non-aluminum-handling workers participated in this study. Their medical examinations, which were otherwise unremarkable, included the collection of urine and blood. Urinary aluminum levels were analyzed using ICP analysis. As pre-clinical tests, we measured KL-6, SP-D, TRCP-5b, IL-6, and IL-8 in blood and δ-ALA and β2-microglobulin in urine. These were considered to be lung, bone, kidney and inflammation markers. Moreover, we measured 8-OHdG in urine as an oxidative DNA damage marker.ResultsThe aluminum concentration in urine ranged from 6.9 to 55.1 μg/g cre (median: 20.1 μg/g cre) in the aluminum-handling workers and from 5.6 to 15.6 μg/g cre (median: 8.8 μg/g cre) in the non-aluminum-handling workers, with a significant difference between them. In the pre-clinical findings, there were no significant differences between these two groups except in the case of δ-ALA. However, there were no significant relationships between aluminum concentration and the pre-clinical findings, work years, age or 8-OHdG in the aluminum-handling workers.ConclusionsWhile the excretion of aluminum in urine was elevated in aluminum-handling workers, our findings suggest that low-dose aluminum is not directly harmful to humans, at least when workers’ urinary aluminum concentration is below 55 μg/g cre.

Serum Aluminum Level and Its Relation with Parathyroid Hormone and Anemia in Children on Maintenance Hemodialysis

Aim: Renal excretion of aluminum is impaired in patients with chronic kidney disease, thereby increasing the risk of toxicity. Our aims were to determine the serum aluminum level in children on regular haemodialysis and to assess the effect of aluminum on PTH and blood parameters. Methodology: This is a case control study was done on 120 children, a group of 60 cases on regular hemodialysis, their ages ranged from 3 to 16 year. They were 27 males (45%) and 33 females (55%) they were selected from the hemodialysis unit and outpatient clinic of Al-Zahraa hospital, AL-Azhar University during the period from January 2014 to September 2014. The studied cases were divided into two groups according to the serum aluminum level; group A 50 μg/L. Another group of 60 apparently healthy children with matched age and sex with the patient group served as a control. All subjects underwent thorough history taking, clinical examination and the following investigations: complete blood count, blood urea, serum creatinine, Original Research Article Hegazy et al.; BJMMR, 7(6): 494-502, 2015; Article no.BJMMR.2015.355 495 total serum calcium, serum phosphorus, serum aluminum, ferritin, PTH and aluminum level of drinking water and water for dialysis. Results: In this study serum aluminum level was significantly higher in cases compared with controls, it was (60±20 μg/L) and (20±10 μg/L) respectively (P=.000). Also we found serum PTH was significantly higher while serum calcium was significantly lower in cases compared to controls particularly in children whose aluminum >50 μg/L. We found a significant positive correlation between serum aluminum levels with PTH (r=.50, P=.001). Also our study reported that the aluminum level in both tap water (for drinking) and water from the dialysis unit their levels were 300 μg/L and 1 μg/L respectively. Conclusion: Drinking water is the main source of high aluminum level in our study and its overload is still a serious health problem in hemodialysis children. So aluminum should be diminished from drinking water to reach the permissible limit; routine monitoring of aluminum level and new modalities of hemodialysis is recommended.

Ferric citrate hydrate as a phosphate binder and risk of aluminum toxicity.

Ferric citrate hydrate was recently approved in Japan as an oral phosphate binder to be taken with food for the control of hyperphosphatemia in patients with chronic kidney disease (CKD). The daily therapeutic dose is about 3 to 6 g, which comprises about 2 to 4 g of citrate. Oral citrate solubilizes aluminum that is present in food and drinking water, and opens the tight junctions in the intestinal epithelium, thereby increasing aluminum absorption and urinary excretion. In healthy animals drinking tap water, oral citrate administration increased aluminum absorption and, over a 4-week period, increased aluminum deposition in brain and bone by about 2- and 20-fold, respectively. Renal excretion of aluminum is impaired in patients with chronic kidney disease, thereby increasing the risk of toxicity. Based on human and animal studies it can be surmised that patients with CKD who are treated with ferric citrate hydrate to control hyperphosphatemia are likely to experience enhanced absorption of aluminum from food and drinking water, thereby increasing the risk of aluminum overload and toxicity.

Efficacy of Supplemental Natural Zeolite in Broiler Chickens Subjected to Dietary Calcium Deficiency

Natural zeolite, or sodium aluminosilicate, influences calcium (Ca) and phosphorus (P) utilisation in chicks. A 2×2 factorial arrangement of treatments was used to investigate the effect of dietary Ca (recommended and below recommended levels) and zeolite (0 and 0.8%) on growth, plasma, tibia and faeces in chickens from 1 to 42 days of age. Zeolite supplementation did not affect overall body weight (BW) gain, feed intake (FI) or feed conversion ratio (FCR) of broiler chickens (P>0.05). Overall mortality of zeolite-fed chickens was lower than in untreated ones (P<0.01). Reduction of dietary Ca of approximately 10 to 18% decreased (P<0.05) BW at 14 and 42 days of age in association with reduced FI, but overall FCR was unchanged. Serum protein and sodium constituents were reduced in birds fed zeolite (P<0.05). Decreasing dietary Ca level increased (P<0.01) serum, total protein and glucose concentrations, but decreased Ca level. Zeolite decreased bone ash in birds fed a Ca-deficient diet while increased faecal excretion of ash, Ca, P and aluminum. However, zeolite increased tibia weight (P<0.05) and thickness (P<0.01). No significant response (P>0.05) in relative weight and gross lesion scores of liver or footpad lesion scores was found related to changes in dietary regimens.The results of the present study do not corroborate the hypothesis that the effectiveness of zeolite may be improved in Ca-deficient diets in association with its ion exchange capability.

Aluminium in human sweat

It is of burgeoning importance that the human body burden of aluminium is understood and is measured. There are surprisingly few data to describe human excretion of systemic aluminium and almost no reliable data which relate to aluminium in sweat. We have measured the aluminium content of sweat in 20 healthy volunteers following mild exercise. The concentration of aluminium ranged from 329 to 5329μg/L. These data equate to a daily excretion of between 234 and 7192μg aluminium and they strongly suggest that perspiration is the major route of excretion of systemic aluminium in humans.

Influence of Essential Trace Minerals and Micronutrient Insufficiencies on Harmful Metal Overload in a Mongolian Patient with Multiple Sclerosis

Parkinson's disease and other neurological disorders are prevalent in Mongolia. Our previous studies revealed a significant correlation of these diseases with high oxidative stress due to a high body burden of harmful metals, such as manganese, iron, lead, cadmium, and aluminum. This report describes a 37-year-old male Mongolian patient with multiple sclerosis and essential micronutrient deficiency. This patient demonstrated high oxidative stress, as shown by high urinary 8-hydroxy-2'-deoxyguanosine levels of 14.7 and 14.3 ng/mg creatinine (crea), although his hair levels of these toxic metals were markedly lower than other Mongolians. In addition, this patient was deficient not only in various essential minerals, including selenium, magnesium, copper, cobalt, vanadium, and nickel, but also in micronutrients such as vitamin B6, C, E, folic acid, niacin, and β-carotene. Furthermore, after taking 2,3-dimercaptosuccinic acid, a chelating agent, urinary excretion of lead, cadmium, manganese, aluminum, iron, copper, and lithium were increased 156-, 8.4-, 7.6-, 4.3-, 3.3-, 2.1-, and 2.1-fold, respectively. These results suggest that this patient suffered from a deficiency in micronutrients such as essential minerals and vitamins, which resulted in a disturbance in the ability to excrete harmful metals into the urine and hair. It is possible that a deficiency of micronutrients and a high burden of heavy metals play a role in the pathogenesis of multiple sclerosis. Nutritional treatment may be an effective approach to this disease.

Chelation of aluminum by combining deferasirox and deferiprone in rats

The hypothesis that two known chelators deferasirox and deferiprone (L1) might be more efficient as combined treatment than as single therapies in removing aluminum from the body was tested in a new acute rat model. Seven-week-old male Wistar rats received chelators: deferasirox (orally [p.o.]), L1 (p.o.) or deferasirox + L1 as 100 or 200 mg/kg dose half an hour after a single intraperitoneal administration of 6 mg Al/kg body weight in the form of chloride. Serum aluminum concentration, urinary aluminum and iron excretions were determined by graphite furnace atomic absorption spectrometry. Both chelators were effective only at the higher dose level. While deferasirox was more effective than L1 in enhancing urinary aluminum excretion, L1 was more effective than deferasirox in enhancing urinary iron excretion. In the combined treatment group, deferasirox did not increase the L1 effect on aluminum and L1 did not increase the effect of deferasirox on iron elimination. Our results support the usefulness of this animal model for preliminary in vivo testing of aluminum chelators. Urinary values were more useful due to the high variability of serum results.

Accumulation and toxicity of aluminium-contaminated food in the freshwater crayfish, Pacifastacus leniusculus

The accumulation and toxicity of aluminium in freshwater organisms have primarily been examined following aqueous exposure. This study investigated the uptake, excretion and toxicity of aluminium when presented as aluminium-contaminated food. Adult Pacifastacus leniusculus were fed control (3 μg aluminium/g) or aluminium-spiked pellets (420 μg aluminium/g) over 28 days. Half the crayfish in each group were then killed and the remainder fed control pellets for a further 10 days (clearance period). Concentrations of aluminium plus the essential metals calcium, copper, potassium and sodium were measured in the gill, hepatopancreas, flexor muscle, antennal gland (kidney) and haemolymph. Histopathological analysis of tissue damage and sub-cellular distribution of aluminium were examined in the hepatopancreas. Haemocyte number and protein concentration in the haemolymph were analysed as indicators of toxicity. The hepatopancreas of aluminium-fed crayfish contained significantly more aluminium than controls on days 28 and 38, and this amount was positively correlated with the amount ingested. More than 50% of the aluminium in the hepatopancreas of aluminium-fed crayfish was located in sub-cellular fractions thought to be involved in metal detoxification. Aluminium concentrations were also high in the antennal glands of aluminium-fed crayfish suggesting that some of the aluminium lost from the hepatopancreas is excreted. Aluminium exposure via contaminated food caused inflammation in the hepatopancreas but did not affect the number of circulating haemocytes, haemolymph ion concentrations or protein levels. In conclusion, crayfish accumulate, store and excrete aluminium from contaminated food with only localised toxicity.

Aluminium in the human brain

An inevitable consequence of humans living in the Aluminium Age is the presence of aluminium in the brain. This non-essential, neurotoxic metal gains entry to the brain throughout all stages of human development, from the foetus through to old age. Human exposure to myriad forms of this ubiquitous and omnipresent metal makes its presence in the brain inevitable, while the structure and physiology of the brain makes it particularly susceptible to the accumulation of aluminium with age. In spite of aluminium’s complete lack of biological essentiality, it actually participates avidly in brain biochemistry and substitutes for essential metals in critical biochemical processes. The degree to which such substitutions are disruptive and are manifested as biological effects will depend upon the biological availability of aluminium in any particular physical or chemical compartment, and will under all circumstances be exerting an energy load on the brain. In short, the brain must expend energy in its ‘unconscious’ response to an exposure to biologically available aluminium. There are many examples where ‘biological effect’ has resulted in aluminium-induced neurotoxicity and most potently in conditions that have resulted in an aluminium-associated encephalopathy. However, since aluminium is non-essential and not required by the brain, its biological availability will only rarely achieve such levels of acuity, and it is more pertinent to consider and investigate the brain’s response to much lower though sustained levels of biologically reactive aluminium. This is the level of exposure that defines the putative role of aluminium in chronic neurodegenerative disease and, though thoroughly investigated in numerous animal models, the chronic toxicity of aluminium has yet to be addressed experimentally in humans. A feasible test of the ‘aluminium hypothesis’, whereby aluminium in the human brain is implicated in chronic neurodegenerative disease, would be to reduce the brain’s aluminium load to the lowest possible level by non-invasive means. The simplest way that this aim can be fulfilled in a significant and relevant population is by facilitating the urinary excretion of aluminium through the regular drinking of a silicic acid-rich mineral water over an extended time period. This will lower the body and brain burden of aluminium, and by doing so will test whether brain aluminium contributes significantly to chronic neurodegenerative diseases such as Alzheimer’s and Parkinson’s.

Up-regulation in the expression of renin gene by the influence of aluminium

The excretion of aluminium in urine was significantly increased after intake of analgesics containing aluminium, confirming increased absorption and hence exposure to aluminium with such medication. The effect of aluminium on the kidney was further investigated by study of gene expression in mice. After a single dose of aluminium, an up-regulation of renin gene was found by DNA sequencing of the products of differential display analysis. The up-regulation of renin was confirmed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting experiments in the dose dependent treatments and the time course observation after aluminium citrate injection. The up-regulation of the renin expression by aluminium is a strong indication of the influence of aluminium on the renin-angiotensin-aldosterone-system, resulting in possible induction of essential hypertension.