Aluminum Intake Research Articles

Tea (Camellia sinensis) leaves accumulate higher levels of Aluminum: Potential Health Risk- Alzheimer’s disease (AD): An updated review of evidence

This review paper of literature highlights the role of accumulation of aluminum in tea leaves and its toxic effects on human health. Tea is the most consumed beverage in the world after water and contains heavy metals and trace elements that may cause potential negative effects on health. Tea is known to be a metal accumulator. However, drinking even a very high dietary amount of black tea or green tea would be unlikely to cause these adverse effects in humans. Thus, for the majority of heavy tea drinkers around the world, tea is likely to be the largest single source of aluminum intake. Addition of milk to tea can decrease or completely inhibit tea antioxidant properties. According to the literature survey, it is well known that the tea plant accumulates aluminum in its leaves to a greater extent than most other edible plants, and would be a potentially important source of dietary aluminum. Aluminum can be transferred into tea infusions through brewing tea, then enter the human body via tea drinking, thereby causing potential harm to human health. On the basis of literature survey, even though some epidemiological reports were contradictory, there was mounting scientific evidence suggesting a relationship between the neurotoxicity of aluminum and the pathogenesis of Alzheimer’s disease. In particular, the link between aluminum and Alzheimer’s disease has been the subject of scientific debate for several decades. The literature survey confirmed that aluminum hypothesis has been the subject of much debate and criticism for several decades. Evidence from human clinical trials suggested that moderate (1–6 cups/day) rather than excessive consumption of tea could bring diverse health benefits. The relationship between tea consumption and dementia has not been well established yet and other studies reported no significant association. The cause of Alzheimer's disease and any association with aluminum is still unknown. There have been conflicting findings in the scientific literature.

Hygienic assessment of aluminum intake in the adult population of Western Siberia

BACKGROUND: In recent decades, research has demonstrated the potential for adverse effects of aluminium on human health. However, there has been a lack of information regarding aluminum intake among different population groups in Western Siberia, thus emphasizing the significance of this study.
 AIM: To estimate aluminum intake by food consumption in the adult population of Western Siberia.
 MATERIAL AND METHODS: The study was conducted in 2019–2020 in the Omsk region. Dietary aluminum intake was assessed in 421 adult residents (177 men and 244 women) of the region using a food frequency questionnaire. The sample was similar to the general population of the region in terms of gender, age, and place of residence. The aluminum content in 160 food samples was determined earlier.
 RESULTS: The median daily intake of aluminum was 4.77 mg/day (3.679; 6.118). No differences in the aluminum intake was observed either by age (р=0.619) or by gender (р=0.334). The main dietary sources of aluminum were beverages (48.5%), vegetables (18.4%), and bakery (11.1%). Among single food products the main sources of aluminium were tea (45.5%), bread (6.7%) and cucumbers (5.3%).
 The proportion of aluminum consumed through vegetables tends to increase with age, whereas the opposite trend is observed for confectionery consumption.
 CONCLUSION: The dietary consumption of aluminum among the adult population in the Omsk region did not exceed the permissible levels. There were no variations in aluminum intake between men and women across different age groups. The primary source of aluminum in the diet of the Omsk region population is plant-based food.

Assessment of Aluminum Levels in the Milk Supply of Tiruvallur district of Tamil Nadu

Introduction: Aluminium is a predominant heavy metal found in everyday products like perfumes, antiperspirants, medication, milk, vaccinations, etc. Biologically available Aluminum is non-essential and toxic to the body. Excessive intake of Aluminum can lead to various negative consequences such as neurodegeneration of the brain, age-related changes, etc. Most of the aluminium exposure is through food and its products. Hence, this study aims to determine the Aluminium levels in milk. Materials and Methods: Twenty samples were collected and stored in the Tiruvallur district area, Chennai. They were broken down into nitric and perchloric acid (4:1 v/v) until a transparent solution was obtained. This was then filtered using Whatman filter paper and diluted. Aluminum content was estimated using a flame absorption spectrophotometer. Results: This study shows that the mean aluminum levels in the milk supply in Tiruvallur district are . The current study also showed that the values are significant (p=0.000) Conclusion: Hence, the Aluminium levels of milk are within permissible levels, and care should be taken not to intake excessive amounts.

Memory impairment induced by aluminum nanoparticles is associated with hippocampal IL-1 and IBA-1 upregulation in mice

ABSTRACT Objectives Increasing evidence indicates a link between aluminum (Al) intake and Alzheimer’s disease (AD). The main entry of Al into the human body is through oral route, and in the digestive tract, under the influence of the pH change, Al can be transformed into Al nanoparticles (Al-NP). However, studies related to the effect of Al-NP on the brain are limited and need further investigation. Neuro-inflammation is considered as one of the principal features of AD. Microglial activation and expression of the inflammatory cytokine IL-1β (interleukin-1β) in the brain have been used as hallmarks of brain inflammation. Therefore, in the present study, the hippocampal levels of ionized calcium-binding adaptor molecule 1 (IBA-1), as the marker of microglia activation, and IL-1β were assessed. Methods Adult male NMRI mice were treated with Al-NP (5 or 10 mg/kg) for 5 days. A novel object recognition (NOR) test was used to assess memory. Following cognitive assessments, the hippocampal tissues were isolated to analyze the levels of IL-1β and IBA-1 as well as beta actin proteins using western blot technique. Results Al-NP in both doses of 5 and 10 mg/kg impaired NOR memory in mice. In addition, Al-NP increased IL-1β and IBA-1 in the hippocampus. Discussion These findings indicate that the memory impairing effect of Al-NP coincides with hippocampal inflammation. According to the proposed relationship between AD and Al toxicity, this study can increase the knowledge about the toxic effects of Al-NP and highlight the need to limit the use of this nanoparticle.

The Research of Influence Factors that Possibly Lead to Alzheimer's Disease

In known studies it has been shown that the prevalence of Alzheimer's disease is related to factors such as heredity, aluminum intake, lifestyle, and gender, but there are still many factors that have not been considered and studied. Therefore, this study focused on the effect of other factors on the prevalence of Alzheimer's disease. The study used multiple linear regression models to process the data from the Alzheimer's Disease Prediction System, an online web-based system that publishes test data from 373 individuals, and visual graphs to analyze the independent variables. The study concluded that Alzheimer's disease was not significantly associated with age, but was significantly associated with gender, years of education, and socioeconomic status, and positively associated with the latter two. However, there was a significant relationship with gender, level of education and socioeconomic status, and a positive relationship with the latter two. These factors such as years of education and socioeconomic status have not appeared in previous studies, so this study provides a new perspective on Alzheimer's disease medical research and a new direction for predicting the disease.

Остеодистрофія в умовах експериментальної інтоксикації алюмінієм як наслідок порушень у травному тракті щурів

Relevance. The growing level of aluminum content in the environment: in the atmosphere, soil, water causes concern due to its toxic properties. The central nervous system, bones, kidneys and other are the target-organs for excessive intake of aluminum in the body. The mechanism by which aluminum induces changes in bone tissue has not been fully deciphered and, according to the authors, can be carried out not only due to its antagonistic action in relation to calcium, but also indirectly – due to pathological changes in the digestive tract and inhibition of the absorption of essential substances, which are necessary for bone tissue remodeling. The aim of the work is an experimental study of the effect of long-term intoxication with aluminum chloride on the condition of the mucous membranes of the digestive tract and bone tissue of rats. Materials and methods. The experiment was conducted on 16 male white rats weighing 239–268 g, which were divided into groups: group 1 – intact animals (n=8); group 2 – injection of 0.5 ml of 12 % AlCl3×6H2O solution (80 mg Al/kg) (n=8). On the 60th day of the study, the rats were removed from the experiment, blood serum was collected, the mandible and mucous membranes of the oral cavity, stomach, small and large intestine were isolated. In the mucous membranes of the digestive tract of rats, the activity of acid phosphatase, elastase, urease, catalase and the content of malonic dialdehyde were determined, in the mandibles – atrophy of the alveolar process, the content of aluminum, calcium and biochemical indexes of bone tissue remodeling (activity of elastase, acid and alkaline phosphatase), in blood serum – «liver» markers and calcium content. Results and conclusions. Long-term intoxication with aluminum chloride caused increase the activity of elastase, acid phosphatase, urease and decrease the activity of catalase in the mucous membranes of the digestive tract of rats against the background of increase the level of malonic dialdehyde. The most significant pathological changes were registered in the mucous membranes of the small and large intestines. Enter of aluminum chloride to rats for two months caused a hepatotoxic effect: increased the activity of aminotransaminases, the content of bilirubin and cholesterol in the blood serum of animals. Increased atrophy of the alveolar process of the mandibles of rats simulated aluminum intoxication, accumulation of aluminum in bone tissue and simultaneous decreased calcium level, and increased activity of acid phosphatase against the background of decreased activity of elastase and alkaline phosphatase were established. The extremely wide range of toxic effects of aluminum on the body requires the development of effective approaches to the prevention of intoxication.

Protective effects of L-arginine on Alzheimer's disease: Modulating hippocampal nitric oxide levels and memory deficits in aluminum chloride-induced rat model

There is evidence that high daily intake of aluminum (Al) is associated with an increased risk of dementia or cognitive decline. We injected L-arginine into the dorsal hippocampus (DH) of an AlCl3-induced Alzheimer's model and studied memory deficit, β-amyloid (βA) accumulation, neurodegeneration, and molecular changes. Male Wistar rats were cannulated unilaterally in the DH under a stereotaxic apparatus and a dose of AlCl3 (1–200 μg/rat) was injected into the CA1. After recovery, L-arginine and L-NAME (0.05–25 μg/rat) were injected into CA1 and animals were tested in novelty seeking task. One group received βA (2 μg/rat, intra CA1) as a reference group. Control groups received saline (1 μL/rat, intra-CA1) and galantamine (25 μg/rat, intra-CA1), respectively. Finally, rats were anesthetized and hippocampal tissues were isolated on ice. Levels of neuronal NO synthase (nNOS), β-secretase and soluble guanylyl cyclase (sGC) were measured by western blotting. βA formation and the number of CA1 neurons were assessed by Congo red and Nissl staining. NOS activation by NADPH-diaphorase (NADPH-d) was investigated. All data were analyzed using analysis of variance (ANOVA) at α = 0.05 level. Like βA, AlCl3 (25 μg/rat) caused accumulation of βA in the DH and increased stopping of the animal on the novel side (indicating a recall deficit). CA1 neurons decreased, and nNOS and β-secretase, but not sGC, showed a change consistent with Alzheimer's. However, prophylactic intervention of L-arginine at 3–9 μg/rat was protective, probably by nNOS stimulation in DH, as shown by NADPH-d assay. L-arginine may protect against Alzheimer's by increasing hippocampal NO levels.

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.

First data on the effect of Aluminium intake in Chamelea gallina of exploited stocks in the Southern Adriatic Sea (Central Mediterranean Sea)

The striped venus clam Chamelea gallina is an important shellfish resource in coastal area of Mediterranean Basin, playing a fundamental role in the ecosystems. In the last two decades there has been a reduction in the stocks of this bivalve with several mortality events along Adriatic Sea due to pollutants. Aiming to evaluate the effects on clams of the anthropogenic increase of some metals in the sea, we focused on aluminium. In particular, we tested whether Al could affect mucus secretion, since mucins are involved in protection from pathogens and toxicants and transport of alimentary particles and pseudofeces. Aluminium was administered in the form of aluminium chloride at concentrations of 25, 50 and 200 μM. Histochemical and lectin-histochemical - analyses were used to evaluate in situ qualitative and quantitative variation of the muciparous secretions produced by both the gills and foot epithelia. Treatments resulted in quali-quantitative alterations in the secretions of both gills and foot epithelia, in particular reduction of glycosylation resulting in a general decrease of acidic residuals and of mannosylated, glycosaminylated and fucosylated chains. This can result in a decrease of acidity and viscosity of mucus and thus it could affect its functionality and the survival of the animals.

Anatomical and Histological Evidence of Aluminum Bone Toxicity: An Experimental Study

Objectives: Aluminum has may be cytotoxic to animals and humans. It is mainly stored in bone and unfortunately, its absorption is increased with age. This study is done to define possible aluminum pathological changes in bone of aging albino rats. Methods: Twenty male albino rats aged 24 months was divided into two groups, control experimental. Experimental group received aluminum chloride for 10 weeks orally. The femur of both control and experimental group is investigated by light and electron microscope. Plain X-ray to the femur as an example to bone is also done. Results: Plain X-ray of femurs of the experimental group showed medullary bone trabeculae destruction, cortical bone resorption and sclerosis. Sections of the shaft of the femur stained with H&E confirmed X-ray gross picture and the bony cortex appeared very thin in comparison with control and showed multiple erosion cavities that may leads to bone fractures. Bone cells appeared few and highly degenerated while the periosteum was very thin and detached from the bone cortex. The bone trabeculae were highly destroyed, and the wide bone marrow spaces were filled by fat cells in some bones. At the level of electron microscope, both osteocytes and osteoblasts revealed severe degenerative changes and showed few irregular collagenous matrices. Conclusion: The degenerative changes observed in the bone of this study are most probably due to aluminum ingestion.

Exposure to tolerable concentrations of aluminum triggers systemic and local oxidative stress and global proteomic modulation in the spinal cord of rats

The tolerable aluminum (Al) intake levels for humans are constantly under review by regulatory agencies due to novel pre-clinical evidence on the neurotoxicity of prolonged Al exposure; however, little is known about the effects of Al on the spinal cord. This study aimed to investigate potential adverse effects on both spinal cord and systemic biochemical balance after prolonged exposure to a low dose of Al. Twenty adult rats were distributed in the control (distilled water) and exposed group (8.3 mg of AlCl3/kg/day). After 60 days, both blood and spinal cord samples were collected for oxidative stress and proteomic analyses. In plasma and erythrocytes, glutathione level was not different between groups; however, exposure to AlCl3 significantly decreased glutathione level in the spinal cord. Thiobarbituric acid reactive substances levels in the plasma and spinal cord of animals from the control group were significantly lower than those animals exposed to AlCl3. Exposure to AlCl3 significantly modulated the expression of proteins associated with the cell cycle, stimulus-response, cytoskeleton, nervous system regulation, protein activity, and synaptic signaling. Therefore, prolonged exposure to a low dose of Al triggered oxidative stress and proteomic changes that may affect spinal cord homeostasis.

Effects of Subchronic Aluminum Exposure on Learning, Memory, and Neurotrophic Factors in Rats.

Aluminum (Al) is a neurotoxin that gradually accumulates in the brain in human life, resulting in oxidative brain injury related to Alzheimer's disease (AD) and other diseases. In this study, the learning and memory of rats exposed to different aluminum concentrations (0.0 g/L, 2.0 g/L, 4.0 g/L, and 8.0 g/L) were studied, and the learning and memory of rats were observed by shuttle box experiment. With hematoxylin and eosin staining, Western blot, immunofluorescence, and RT-PCR, the morphology of nerve cells in the hippocampus of rat brain were observed, and the levels of activator protein-1 (AP-1) gene and protein, nerve growth factor (NGF), neurotrophin-3 (NT3), glial cell line-derived neurotrophic factor (GDNF), and brain-derived neurotrophic factor (BDNF) gene and protein level, etc. The experimental results showed that subchronic aluminum exposure damaged learning and memory in rats. The cognitive function damage in rats was more evident after increasing the aluminum intake dose. The more aluminum intake, the more pronounced the histological changes in the hippocampus will be. The expression level and protein content of neurotrophic factors in the hippocampus of rats showed a negative correlation with aluminum intake. In this experiment, we explored the mechanism of aluminum exposure in learning and memory disorders, and provided some data reference for further elucidation of the damage mechanism of aluminum on the nervous system and subsequent preventive measures.

Aluminium intake through the consumption of selected baby foods and risk characterization in a population of Brazilian infants aged 0 to 36 months

Aluminium (Al) dietary intake from selected baby foods was estimated for Brazilian infants from the São Paulo State by means of a deterministic and a probabilistic estimation. The deterministic exposure assessment was carried out by combining mean levels of Al in 171 samples of baby foods (infant formula, meat/vegetable purees, fruit purees, petit-suisse and cereals), analytically determined by inductively coupled plasma optical emission spectrometry method, with individual food consumption data. Data on food consumption were generated using a duplicated 24 h recall applied to the parents of 158 infants aged from 0–36 months. The mean Al intakes for the total population, calculated using mean Al concentrations, were estimated to be 0.184 mg/kg body weight (bw) per week, whilst at 95th percentile, the obtained value was 0.474 mg/kg bw per week. In addition, distributions were fitted on the concentration and consumption data for further probabilistic intake estimations. The results corroborated well with the deterministic approach. The highest frequency and daily food consumption (in g/day) were observed for infant formulas and meat/vegetable purees, respectively. Boys presented higher frequency consumption of infant formulas, while meat/vegetable purees intake by girls was higher compared to boys. The baby food that most contributed to Al exposure in the total population, considering mean Al concentration values, was meat/vegetable purees, followed by infant formulas. This study suggests potential concern regarding consumers of highly Al contaminated products and may be used as a basis for the establishment of risk management actions.

Dietary aluminium intake disrupts the overall structure of gut microbiota in Wistar rats.

Approximately, 40% of ingested dietary aluminium accumulates in the intestine, which has been considered a target organ for dietary aluminium exposure. The gut microbiota may be the first protective barrier against the toxic metal aluminium and a crucial mediator of the bioavailability of metal aluminium. We previously evaluated dietary aluminium intake and its health risks in a population from Jilin Province, China, and found that the average daily intake of aluminium in the diet of residents in Jilin Province was 0.163 mg/kg after the total diet survey. In the present study, the equivalent concentration of aluminium in rats was extrapolated by the average dietary aluminium intake in the population of Jilin Province based on body surface area. Furthermore, healthy adult Wistar rats were randomly divided into four groups (n=15 for each group): a control group and three groups treated with aluminium solution (1, 10, and 100 mg/kg/day, intragastrically) for 28 days. Following treatment, necrosis of renal tubular epithelial cells, hyperplasia of bile ducts and hyperplasia of heart tissue, as well as fiber in the liver, kidney, and heart tissues of aluminium-treated rats were observed, although there were no significant changes in the spleen and brain. Subsequently, fecal samples were withdrawn for 16S rRNA gene sequence analysis. It was found that aluminium decreased the microbiota diversity and changed the overall community structure of the gut microbiota, including three phyla and four genera, together with the regulation of 12 signaling pathways. Collectively, treatment with aluminium markedly altered the structure of the gut microbiota, suggesting that the disorders of intestinal flora induced by aluminium may be an important mechanism for aluminium toxicity.

Heavy metals and aluminium intake from stored canned tomato, sardines and tuna in Algeria

This study assessed heavy metals intake and their impacts on healthcare in Algeria. Peculiar attention was given to heavy metals found in largely consumed canned foods in Algeria such as double concentrated tomato, tuna crumbs and sardines. Chemical analyses of the metal and aluminium containers (foil, tray) were performed by X-Ray Fluorescence (XRF) and EDS spectrometry (Energy Dispersive Spectrometry). The determination of the trace metal content in canned food (element metal trace EMT) was achieved by Atomic Absorption Spectrometry (AAS). The approach proposed in this study aimed to highlight the interaction of the product and packaging material, and thus to identify and quantify heavy metals traces that were able to undergo specific or overall migration to food. The morphology of the contact surface food / packaging was observed by Scanning Electron Microscope (SEM) and showed a slight degradation of the base metal (Black Iron). There was an obvious increase in EMTs during tuna, sardines and tomatoes storage and artificial aging. A special interest was given to cooking modes using aluminium foil and trays. ‎‎The respective dosages of aluminium, in baked food (fresh tuna) were obtained. Specific Aluminium migration was noticed and was strong for the flame cooking mode.

Research progress of epigenetic regulation in the pathogenesis of aluminum exposure

Aluminum is one of the most abundant elements on earth. Aluminum compounds are widely used in food additives, antacids, cooking utensils and so on. Human exposure to aluminum is mainly through diet and drinking water, while excessive intake of aluminum can accumulate in tissues and cause toxic reactions. In the central nervous system, aluminum exposure is closely related to a series of nervous system diseases such as Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis. Epigenetic modification refers to the regulation of gene expression without changing the DNA sequence, and its regulatory disorders can lead to abnormalities and diseases of the central nervous system. This paper describes the regulation of epigenetics and its components, including DNA methylation, histone modification and non-coding RNA, in aluminum-induced neurotoxicity, in order to provide insights into the epigenetic mechanism of aluminum-induced neurotoxicity.

Aluminum intake in the neonatal phase disrupts endochondral ossification in rodents

ObjectiveThis study evaluated the effects of aluminum (Al) intake on endochondral ossification during the neonatal phase. MethodTwelve male newborn Gerbils (Meriones unguiculatus) were randomly divided into control (C) and aluminum (Al) groups (n = 6 animals/group). From the 1st to 15th day of life, gerbils received an AlCl3 solution (10 mg/kg/day) via gavage. The control group received only the saline solution. On the 16th day, their tibias were processed for paraffin embedding and were submitted to histomorphometric, histochemical, and immunohistochemical analyses. ResultsIn the epiphyseal cartilage Al did not affect the proteoglycan content or cell proliferation; however, it increased matrix metalloprotease-2 (MMP-2) immunostaining and the hypertrophic layer thickness. In bone, Al decreased trabeculae number, trabecular width, cortical bone width, and proliferation. Furthermore, the relative frequency of bone matrix and fibrillar collagen decreased 3.9% and 16.2%, respectively. The number of osteoclasts and osteocalcin digital optical density (D.O.D) remained the same. ConclusionThe results suggest that Al intake during the neonatal period impairs endochondral ossification by affecting epiphyseal cartilage and bone architecture.

Elevated IgG Antibody to Aluminum Bound to Human Serum Albumin in Patients with Crohn’s, Celiac and Alzheimer’s Disease

Aluminum is in our water and food, and is used as an adjuvant in vaccines. About 40% of the ingested dose accumulates within the intestinal mucosa, making the gut the main target of inflammation and autoimmunity; about 1% accumulates in the skeletal system and brain, inducing the cross-linking of amyloid-β-42 peptide and the formation of amyloid aggregates associated with Alzheimer’s disease. To examine whether the accumulation of aluminum in the gut and brain tissues results in neoantigen formation, we bound aluminum compounds to human serum albumin. We used ELISA to measure IgG antibody in 94 different sera from healthy controls and 47 sera from each group of patients: anti-Saccharomyces cerevisiae antibody-positive (Crohn’s), and positive for deamidated α-gliadin and transglutaminase-2 IgA antibodies (celiac disease), autoimmune disorders associated with intestinal tissue antigens. Because earlier studies have shown that aluminum exposure is linked to Alzheimer’s disease etiology, and high aluminum content is detected in Alzheimer’s patients’ brain tissue, we also measured aluminum antibody in the blood of these patients. Additionally, we measured aluminum antibody in the sera of mixed connective tissue disease patients who were positive for antinuclear antibodies, and used them as disease controls. We found significant IgG antibody elevation against all three aluminum compounds in the sera of patients with Crohn’s, celiac and Alzheimer’s disease, but not in patients with mixed connective tissue disease. We concluded that aluminum ingestion and absorption from the GI tract and brain may contribute to Crohn’s, celiac and Alzheimer’s disease, but not to mixed connective tissue disease.

Aluminium Induced Neurodegeneration in Rat Cerebrum in Presence of Ethanol Co-exposure

Introduction: Aluminium (AL) exposure leads to neurotoxicity and many problems in the body. AL role in Alzheimer's Disease (AD) is unknown and controversial to the scientists. According to World Health Organisation (WHO) provisional tolerable weekly intake of AL is 2 mg/kg body weight. Moderate intake of alcohol may favour body in coronary heart disease and diabetes mellitus, etc. Aluminium being cheaper along with increased consumption of alcohol, mixed with each other may induce neurotoxicity. Aim: The study was designed to identify the effects of AL in cerebrum of rats in presence of ethanol co-exposure. Materials and Methods: An experimental study was carried out at Dr. RP Government Medical College, Kangra and Government Medical College, Amritsar, India after due approval from the Institute Animal Ethics Committee. Thirty-two wistar rats were divided into one vehicle control and three experimental groups. Group I received the normal saline water as vehicle control group. Group II received AL chloride 4.2 mg/kg body weight as experimental group. Group III received ethanol 1 gm/kg body weight as experimental group. Group IV received both AL chloride 4.2 mg/kg body weight and ethanol 1 gm/kg body weight as experimental group. After treatment, brain cortex was processed for histopathological observation under microscope. Results: Cerebral cortex showed normal architecture of the brain with haematoxylin and eosin staining and cresyl violet staining and modified Bielchowsky silver staining in low and high magnification in vehicle control group. Experimental group treated with AL and ethanol separately showed reduction in the count of pyramidal cells with moderate neuronal degeneration with pyknotic nuclei. Vacuolar changes and pericellular spaces around the necrotic neurons were also seen. Combined AL and ethanol treated group showed acute neurodegeneration and necrosis of cortex indicating chromatolysis and loss of substances and Neurofibrillary Tangle (NFT) and plaque. Conclusion: It has been concluded that the ethanol induced the effects of AL on the cerebrum and plays a significant role in AD pathogenesis.

Élelmiszerek ásványi anyag tartalma : Alumínium az élelmiszerekben

The paper deals with questions of aluminium, which concentration can be significant in plants, although it is not an essential element. The concentration of aluminium of tea leaves is extremely high. The concentration of aluminium of plants strongly depends on the pH-value of the soil, if the level of acidity in the soil is high, the Al-content of the soil-solution is also high, causing P-deficiency for plants. The intake of aluminium of the humans is a function of the ratio of consumption of plant and animal origin foodstuffs. The aluminium content of animal origin foodstuffs – because of low level absorption rate of aluminium is rather low – so the concentration range of milk of aluminium is low. After the macroelements the aluminium is the metallic micro element which it’s daily intake generally the highest in the human diet, approximately between 30 and 50 mg. The too high aluminium uptake in the diet can produce various healthy disorders in the human body, and probably there is a connection between Al-intake and Alzheimer-disease and the old age dementia, as well (The association between aluminium uptake and Alzheimer’s disease is disputed by several sources in the literature; the Editor).