דו״ח מאומת

Packaging has become an essential component of food production and distribution. It plays a vital role in preserving food quality and safety, while also helping to reduce food waste. However, the widespread use of packaging has led to increased chemical migration, posing significant risks to food safety and public health. Migration occurs when low molecular weight compounds from packaging materials, printing inks, or adhesives transfer to food under certain conditions, potentially introducing harmful substances. This contamination can degrade food quality through unwanted changes and expose consumers to serious health risks, highlighting the need for stringent controls. This review examines various packaging materials, explores the factors influencing the migration of chemical substances from packaging into food, compiles data on the presence of migrants in foods, identifies those posing risks to public health, and underlines measures to minimize migration from a food safety perspective.…

PMID: 40401309

The widespread use of aluminum in industry, medicine and everyday life is associated with the risk of its bioaccumulation and toxic effects, including neurotoxicity, trace element metabolism disorders and osteopathy. Cooking and storing food in aluminum cookware, especially with acidic products, promotes metal migration into food matrices. Despite the proven role of aluminum in the induction of oxidative stress and cellular damage, the mechanisms of its influence on the expression of metal transporter genes and subclinical effects remain poorly understood. The aim of the research was to study the effect of oral administration of various doses of aluminum hydroxide on biochemical parameters, gene expression and homeostasis of essential elements in experimental animals.<h4>Material and methods</h4>A prospective study was conducted on 40 white outbred rats with an initial body weight of 180-200 g, which received aluminum hydroxide orally at doses of 0, 0.015, 0.15, 1.5, and 15 mg per 1 kg of body weight for 120 days. The content of elements in the kidneys, liver, brain, and blood was determined using atomic absorption spectrometry. Gene expression was analyzed by real-time polymerase chain reaction. The activity of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and alkaline phosphatase in blood serum was measured using test kits on a semi-automated biochemical analyzer.<h4>Results</h4>The study revealed a dose-dependent effect of oral administration of aluminum hydroxide on the rats' organism, simulating alimentary intake. Aluminum accumulation was found mainly in the brain and blood, which confirms its neurotropic properties. Violation of element homeostasis was characterized by a two-phase change in calcium levels: its increase in the liver and kidneys under the influence of low doses and a decrease in blood under the influence of high doses. In addition, an imbalance of magnesium (increased level in the brain) and iron (increased concentration in the blood) was observed. The expression of metal transporter genes (ZIP8, Mt1a, Mt2a) was activated even at minimal doses of aluminum hydroxide, which indicates their role in adaptation to toxic effects. Traditional biochemical markers (AST, ALT) did not show significant changes, in contrast to LDH, the activity of which increased at high oral doses of aluminum hydroxide.<h4>Conclusion</h4>Regular intake of aluminum with food can lead to its bioaccumulation, especially in the nervous tissue, and provoke subclinical disturbances in the homeostasis of minerals and trace elements, oxidative stress and cellular adaptive responses. The identified changes in gene expression (ZIP8, Mt1a, Mt2a) are proposed as early biomarkers of toxic effects. The findings highlight the need for stricter control over the use of aluminum-containing materials in the food industry and the development of preventive strategies for vulnerable populations.…

PMID: 41263352

Aluminum intoxication is common in patients with chronic renal failure because of absorption of aluminum during dialysis from aluminum-containing dyalysate water and ingestion of phosphate binders containing aluminum. Aluminum accumulation in the body is followed by bone disease, encephalopathy and anemia. Bone diseases can be recorded in 44% of the patients treated with long-term dialysis. Two early histologic types of retarded bone turnover can be seen, i.e. osteomalacia and aplastic bone disease. In dialyzed patients, osteomalacia is usually followed by low PTH level in human serum. On the contrary, studies on uremic rats have shown that previous parathyroidectomy can prevent aluminum intoxication, because hyperparathyroidism in an early phase of chronic renal failure increases aluminum absorption from the gut and its accumulation in the body. As the pathogenesis of aluminum-induced alterations is unclear, the prevention of bone disease should be provided through lowering the aluminum intake in dialyzed patients. Bone biopsy is unavoidable for the early detection and diagnosis of the disease. Promising results in the treatment of aluminum intoxication have been obtained using deferoxamine, a chelating agent.…

PMID: 2671563

Aluminum, as an abundant metal, has gained widespread use in human life, entering the body predominantly as an additive to various foods and drinking water. Other major sources of exposure to aluminum include medical, cosmetic, and occupational routes. As a common environmental toxin, with well-known roles in several medical conditions such as dialysis encephalopathy, aluminum is considered a potential candidate in the causality of Alzheimer's disease. Aluminum mostly accumulates in the bone, which makes bone an indicator of the body burden of aluminum and an ideal organ as a proxy for the brain. Most of the techniques developed for measuring aluminum include bone biopsy, which requires invasive measures, causing inconvenience for the patients. There has been a considerable effort in developing non-invasive approaches, which allow for monitoring aluminum levels for medical and occupational purposes in larger populations. In vivo neutron activation analysis, a method based on nuclear activation of isotopes of elements in the body and their subsequent detection, has proven to be an invaluable tool for this purpose. There are definite challenges in developing in vivo non-invasive techniques capable of detecting low levels of aluminum in healthy individuals and aluminum-exposed populations. The following review examines the method of in vivo neutron activation analysis in the context of aluminum measurement in humans focusing on different neutron sources, interference from other activation products, and the improvements made in minimum detectable limits and patient dose over the past few decades.…

PMID: 26890739

The widespread use of aluminum in industry, medicine and everyday life is associated with the risk of its bioaccumulation and toxic effects, including neurotoxicity, trace element metabolism disorders and osteopathy. Cooking and storing food in aluminum cookware, especially with acidic products, promotes metal migration into food matrices. Despite the proven role of aluminum in the induction of oxidative stress and cellular damage, the mechanisms of its influence on the expression of metal transporter genes and subclinical effects remain poorly understood. The aim of the research was to study the effect of oral administration of various doses of aluminum hydroxide on biochemical parameters, gene expression and homeostasis of essential elements in experimental animals.<h4>Material and methods</h4>A prospective study was conducted on 40 white outbred rats with an initial body weight of 180-200 g, which received aluminum hydroxide orally at doses of 0, 0.015, 0.15, 1.5, and 15 mg per 1 kg of body weight for 120 days. The content of elements in the kidneys, liver, brain, and blood was determined using atomic absorption spectrometry. Gene expression was analyzed by real-time polymerase chain reaction. The activity of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and alkaline phosphatase in blood serum was measured using test kits on a semi-automated biochemical analyzer.<h4>Results</h4>The study revealed a dose-dependent effect of oral administration of aluminum hydroxide on the rats' organism, simulating alimentary intake. Aluminum accumulation was found mainly in the brain and blood, which confirms its neurotropic properties. Violation of element homeostasis was characterized by a two-phase change in calcium levels: its increase in the liver and kidneys under the influence of low doses and a decrease in blood under the influence of high doses. In addition, an imbalance of magnesium (increased level in the brain) and iron (increased concentration in the blood) was observed. The expression of metal transporter genes (ZIP8, Mt1a, Mt2a) was activated even at minimal doses of aluminum hydroxide, which indicates their role in adaptation to toxic effects. Traditional biochemical markers (AST, ALT) did not show significant changes, in contrast to LDH, the activity of which increased at high oral doses of aluminum hydroxide.<h4>Conclusion</h4>Regular intake of aluminum with food can lead to its bioaccumulation, especially in the nervous tissue, and provoke subclinical disturbances in the homeostasis of minerals and trace elements, oxidative stress and cellular adaptive responses. The identified changes in gene expression (ZIP8, Mt1a, Mt2a) are proposed as early biomarkers of toxic effects. The findings highlight the need for stricter control over the use of aluminum-containing materials in the food industry and the development of preventive strategies for vulnerable populations.…

PMID: 41263352

Early reviews identified over 20 risk factors associated with Alzheimer's disease (AD) including age, familial inheritance, exposure to aluminium, traumatic brain injury (TBI), and associated co-morbidities such as vascular disease and infection. In the light of recent evidence, this review reconsiders these risk factors, identifies those currently regarded as important, and discusses various hypotheses to explain how they may cause AD. Rare forms of early-onset familial AD (EO-FAD) are strongly linked to causal gene mutations, viz. mutations in amyloid precursor protein (APP) and presenilin (PSEN1/2) genes. By contrast, late-onset sporadic AD (LO-SAD) is a multifactorial disorder in which age-related changes, genetic risk factors, such as allelic variation in apolipoprotein E (Apo E) and many other genes, vascular disease, TBI and risk factors associated with diet, the immune system, mitochondrial function, metal exposure, and infection are all implicated. These risk factors may act collectively to cause AD pathology: 1) by promoting the liberation of oxygen free radicals with age, 2) via environmental stress acting on regulatory genes early and later in life ('dual hit' hypothesis), or 3) by increasing the cumulative 'allostatic load' on the body over a lifetime. As a consequence, life-style changes which reduce the impact of these factors may be necessary to lower the risk of AD.…

PMID: 31556570

Aluminum (Al) is a widespread environmental contaminant with suspected links to neurodegenerative diseases, particularly Alzheimer's disease (AD). This systematic review and meta-analysis aimed to evaluate the association between environmental Al exposure and the risk of AD by synthesizing evidence from diverse sources and study designs. A systematic review was conducted following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Literature searches were performed in PubMed, Scopus, Web of Science, EMBASE, and the gray literature up to June 2024. After duplicate removal and screening of 6504 records, 54 eligible studies on Al exposure and dementia/AD were included. Data extraction focused on exposure media, Al concentrations, Al and AD/dementia correlation, and geographic context. Screening was independently conducted by two reviewers, with good inter-rater reliability (Kappa = 0.75). Meta-analysis was conducted on the studies that reported sufficient quantitative data, using Hedges' g to estimate the effect size of Al exposure on AD. The included studies demonstrated considerable spatial and temporal variation. Of the 54 studies, 26 reported a positive association between Al exposure and AD or dementia, while 24 found no or negative associations. Major exposure sources included contaminated water, soil, diet, occupational settings, and medical interventions. Although few studies confirmed Al-induced brain pathology as a direct cause of dementia, meta-analysis of four eligible studies revealed a strong association between Al exposure and AD (Hedges' g = 2.451), despite high heterogeneity across data sources and outcome measures. Our findings suggest that environmental Al exposure may contribute to the development of AD, though it is likely one of several interacting risk factors. Environmental conditions appear to influence both Al bioaccumulation and its neurotoxic effects related to cognitive decline.…

PMID: 40749395

Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by cognitive decline, neuronal loss and abnormal tau phosphorylation. Although aluminum exposure has been suggested as a risk factor, no causal link to AD has been confirmed. The combination of D-galactose and aluminum chloride (AlCl₃) is widely used to model aging-related neurotoxicity, including oxidative stress, cognitive impairment and tau hyperphosphorylation. Ficus deltoidea (FD), a Southeast Asian plant rich in flavonoids like vitexin, exhibits antioxidant and anti-inflammatory properties, but its role in tau pathology remains unclear. In this study, male Wistar rats received D-galactose/AlCl₃ to induce AD-like pathology and were co-treated with FD extract (50, 100, or 200 mg/kg) and donepezil. The results showed that FD significantly improved spatial memory, reduced hippocampal neuronal loss and attenuated p-tau T181 levels. The apparent decrease in p-tau levels may have led to reduced neurodegeneration and improved learning and memory. These findings support FD's neuroprotective potential against aluminum-induced tauopathy and warrant further studies in translational AD-like models.…

PMID: 41921869