Aluminum Exposure Research Articles

Benefits of rutin on mitochondrial function and inflammation in an aluminum-induced neurotoxicity rat model: Potential interest for the prevention of neurodegeneration

Rutin, a phenolic compound, exhibits a diverse range of biological properties, including antioxidant, anti-inflammatory, and antimicrobial effects. In this study, we aimed to investigate the potential of rutin, a naturally occurring plant bioactive molecule, to mitigate the neurotoxic effects induced by aluminum chloride (AlCl3). Over a period of 6 weeks, rats were intraperitoneally injected with AlCl3 at a weekly dose of 60 mg/kg, while rutin treatment was administered orally via gavage at a daily dose of 30 mg/kg. AlCl3 exposure resulted in a significant increase lipid peroxidation (LPO) by 316.24%, nitrate levels by 504.14%, and tumor necrosis factor-alpha (TNF-α) levels by 93.82% in brain mitochondria. Additionally, AlCl3 exposure led to a reduction in glutathione levels and the activity of antioxidant enzymes, including superoxide dismutase (SOD) by 19.74%, glutathione peroxidase (GPx) by 44.76%, and catalase by 50.50%. There was also a significant decline in the activity of mitochondrial complex enzymes. In contrast, rutin treatment significantly enhanced the activity of antioxidant enzymes while concurrently reducing lipid peroxidation levels in rats. Specifically, rutin administration exerted a modulatory effect on the inflammatory response triggered by aluminum exposure, effectively suppressing the excessive production of nitrate and TNF-α. These findings highlight the potential of rutin as an effective therapeutic strategy in mitigating and combating neuro-inflammation and oxidative stress associated with aluminum-induced toxicity, thereby effectively restoring mitochondrial function.

Prospective findings from the Dongfeng-Tongji cohort: Exposure to various metals, the expression of microRNA-4286, and the incidence of acute coronary syndrome

Mounting evidence suggests that metal/metalloid exposure is related to the adverse health effects. Our prior investigation revealed a positive relation between the plasma level of microRNA-4286 (miR-4286) and an increased risk of developing acute coronary syndrome (ACS). However, it is a lack of studies evaluating the connection between metal/metalloid exposure and miRNA expression on ACS. In the prospective Dongfeng-Tongji cohort, we performed a nested case-control study. A total of 480 ACS and 480 controls were carefully selected based on similar age, sex, and blood collection time. Using inductively coupled plasma mass spectrometry, we assessed the plasma concentrations of 24 different metals. Quantitative real-time polymerase chain reaction was used to analyze the plasma miR-4286. We examined the relations of plasma metals with miR-4286 levels, the incidence of ACS, and the potential interactions. Using the multivariate conditional logistic regression models, we observed that the adjusted odds ratios (95% confidence intervals [CI]) for incident ACS were 1.79 (1.03, 3.12; P-trend = 0.03), 0.60 (0.41, 0.87; P-trend = 0.008), and 0.66 (0.46, 0.93; P-trend = 0.02), when comparing the extreme tertiles of aluminum, rubidium, and selenium, respectively. There was a relation between the concentration of rubidium in plasma and a decrease in the level of plasma miR-4286 (percent difference [95% CI]: −13.36% [-22.74%, −2.83%]; P-trend = 0.01). Both multiplicative (P interaction = 0.009) and additive interactions (relative excess risk due to interaction [95% CI]: 0.82 [0.59, 1.06]) were noted in our observation regarding the relationship between plasma aluminum and miR-4286 in incident ACS. The findings indicated that plasma aluminum was positively while plasma rubidium and selenium were negatively linked to an increased risk of developing ACS. Plasma aluminum exposure and plasma miR-4286 expression might synergistically affect the incident ACS risk. Controlling aluminum exposure was important for ACS prevention, especially for individuals with high expression of plasma miR-4286.

How do different concentrations of aluminum and zinc affect the survival, body size, morphology and immune system of Physalaemus cuvieri (Fitzinger, 1826) tadpole?

ABSTRACT The assessment of amphibian responses as bioindicators of exposure to chemical pollutants is an important tool for conservation of native species. This study aimed to investigate the effects of chronic aluminum (Al) and zinc (Zn) exposure on survival, body size, morphology (malformations), and immune system (leukocyte profile) in P. cuvieri tadpoles. Ecotoxicological analyses were performed utilizing chronic toxicity tests in which 210 tadpoles at the 25th Gosner developmental stage were exposed to Al and Zn. Individuals of P. cuvieri were maintained in glass containers containing various concentrations of aluminum sulfate (0.1, 0.2, or 0.3 mg/L) and zinc sulfate (0.18, 0.27 or 0.35 mg/L), and tests were performed in triplicate. After 14 days, amphibians were weighed, measured and survival rate, malformations in the oral and intestine apparatus, leukocyte profile, and ratio between neutrophils and lymphocytes determined. The differing concentrations of Al and Zn did not produce lethality in P. cuvieri where 95% of the animals survived 326 hr following metal exposure. Individuals exposed to Zn achieved greater body growth and weight gain compared to controls. Aluminum increased weight gain compared controls. These metals also produced malformations of the oral and intestine apparatus and enhanced occurrence of hemorrhages, especially at the highest doses. Lymphocytes were the predominant cells among leukocytes, with lymphopenia and neutrophilia observed following Al and Zn treatment, as evidenced by elevated neutrophil/lymphocyte ratio, an important indicator of stress in animals. Data suggest that further studies need to be carried out, even with metal concentrations higher than those prescribed by CONAMA, to ensure the conservation of this species.

Association between aluminum and iron exposure in maternal blood and umbilical cord blood and congenital heart defects in children.

Congenital heart disease (CHDs) is the major cause of mortality from birth defects, affecting up to 1% of live births worldwide. However, the relationship between aluminum (Al) and iron (Fe) levels and the risk of CHDs has yielded inconsistent results. We conducted a pair-matched case-control study that included 97 CHDs and 194 non-CHDs to investigate the association and interaction between Al/Fe exposure and the risk of CHDs in a birth cohort study in Lanzhou, China. Higher concentrations of cord blood Al were associated with a greater risk of total CHDs (aOR = 2.826, 95% CI [1.009-7.266]) and isolated CHDs (aOR = 10.713, 95% CI [1.017-112.851]) compared to the lowest Al level. Both in maternal blood and cord blood, a significant dose-effect was observed between Al level and total CHDs (Ptrend < 0.05), but a similar pattern was not observed for Fe. High Al in addition to high Fe appeared to elicit a stronger association with CHDs than both lowest tertile of Al and Fe level in umbilical cord blood, particularly for multiple CHDs, septal defects and patent ductus arteriosus. Our study suggests that exposure to Al during pregnancy (≥2,408 μg/L) is significantly associated with an increased risk of CHDs in offspring, especially septal defects, and that high levels of Al and Fe are strongly correlated with fetal heart development. Further research is needed to understand the underlying mechanisms.

Post-exposure self-recovery reverses oxidative stress, ameliorates pathology and neurotransmitters imbalance and rescues spatial memory after time-dependent aluminum exposure in rat brain.

Aluminum is a potent neurotoxin, responsible for memory impairment and cognitive dysfunction. The neurotoxic effect of aluminum on cognitive impairment is well documented, however, exposure to aluminum in a time-dependent manner and post-exposure self-recovery still needs to be elaborated. This research aimed to (1) study the time-dependent effect of aluminum exposure by administering a total dose of 5850mg/kg of Al over two different time periods: 30 and 45days (130 and 195mg/kg of AlCl3 respectively), and (2) study 20days post-exposure self-recovery effect in both aluminum-exposed groups by giving distilledwater. Cognitive abilities were investigated through Morris water maze test and hole board test and compared in both exposure and recovery groups. Oxidative stress markers and neurotransmitter levels were measured for both exposure and recovery groups. To understand the mechanism of aluminum exposure and recovery, immunohistochemical analysis of synaptophysin (Syp) and glial fibrillary acidic protein (GFAP) was performed. Results showed cognitive dysfunction, oxidative stress-induced damage, reduced neurotransmitter levels, decreased immunoreactivity of Syp, and increased GFAP. However, these parameters showed a larger improvement in the recovery group where rats were given aluminum for 30days period in comparison to recovery group followed by 45days of aluminum exposure. These results suggest that restoration of cognitive ability is affected by the duration of aluminum exposure. The study findings provide us with insight into the adverse effects of aluminum exposure and can be utilized to guide future preventive and therapeutic strategies against aluminum neurotoxicity.

MiR-128-3p is involved in aluminum-induced cognitive impairment by regulating the Sirt1-Keap1/Nrf2 pathway

Aluminum (Al) is a common neurotoxicant in the environment, but the molecular mechanism of its toxic effects is still unclear. Studies have shown that aluminum exposure causes an increase in neuronal apoptosis. The aim of this study was to investigate the mechanism and signaling pathway of neuronal apoptosis induced by aluminum exposure. The rat model was established by intraperitoneal injection of maltol aluminum for 90 days. The results showed that the escape latency of the three groups exposed to maltol aluminum was higher than that of the control group on the 3rd, 4th and 5th days of the positioning cruise experiment (P < 0.05). On the 6th day of the space exploration experiment, compared with the control group(6.00 ± 0.71,15.33 ± 1.08) and the low-dose group(5.08 ± 1.69,13.67 ± 1.09), the number of times that the high-dose group crossed the platform(2.25 ± 0.76) and the platform quadrant(7.58 ± 1.43) was significantly reduced (P < 0.01). The relative expression levels of Sirt1 and Nrf2 in hippocampal tissues of all groups decreased gradually with increasing maltol aluminum exposure dose the relative expression levels of Sirt1 and Nrf2 in high-dose group (0.261 ± 0.094,0.325 ± 0.108) were significantly lower than those in control group (1.018 ± 0.222,1.009 ± 0.156)(P < 0.05). The relative expression level of Keap1 increased gradually with increasing maltol aluminum exposure dose (P < 0.05). The relative expression level of miR-128–3p in the high-dose group(1.520 ± 0.280) was significantly higher than that in the control group(1.000 ± 0.420) (P < 0.05). The content of GSH-Px in the hippocampus of rats decreased with increasing dose. ROS levels gradually increased. We speculated that subchronic aluminum exposure may lead to the activation of miR-128–3p in rat hippocampus of rats, thereby inhibiting the Sirt1-Keap1/Nrf2 pathway so that the Sirt1-Keap1/Nrf2 pathway could not be activated to exert antioxidant capacity, resulting in an imbalance in the antioxidant system of rats and the apoptosis of neurons, which caused reduced cognitive impairment in rats.

Exploring the Combined Effect of Exercise and Apigenin on Aluminium-Induced Neurotoxicity in Zebrafish.

Aluminium (AL) is a strong environmental neurotoxin linked to neurodegenerative disorders. Widespread industrial use leads to its presence in water systems, causing bioaccumulation in organisms. This, in turn, results in the bioaccumulation of AL in various organisms. Several studies have highlighted the benefits of enhanced physical activity in combating neurodegenerative diseases. Meanwhile widespread presence of apigenin in aquatic environment has been largely overlooked, in terms of its potential to counter AL-induced neurotoxicity. The combined impact of exercise and apigenin in mitigating the effects of AL-induced neurotoxicity in aquatic animals remains unexplored. Hence, the objective of this study is to determine whether the combined treatment of exercise and apigenin can effectively alleviate the chronic neurotoxicity induced by AL. Zebrafish that were exposed to AL showed behaviours resembling anxiety, increased aggression, unusual swimming pattern, and memory impairment, which are typical features observed in Alzheimer's disease (AD)-like syndrome. Combined treatment of exercise and apigenin protects zebrafish from AL-induced neurotoxicity, which was measured by improvements in memory, reduced anxiety and aggression, and increased levels of antioxidant enzymes and acetylcholinesterase (AChE) activity. Furthermore, AL exposure is associated with increased expression of genes related to neuroinflammation and AD. However, synergistic effect of exercise and apigenin counteract this effect in AL-treated zebrafish. These findings suggest that AL is involved in neurodegenerative diseases in fish, which could affect the integrity of aquatic ecosystem. Hence, there is a strong correlation between enhanced physical activity, apigenin, and the well-being of the ecosystem.

Assessment of Histopathological Alterations and Oxidative Stress in the Liver and Kidney of Male Rats following Exposure to Aluminum Chloride.

The study aims to investigate the residual and histopathological effects of chronic aluminum chloride (AlCl3) toxicity in the kidney and liver of male rats. After 30-, 60-, and 90-day exposure period, analyses were conducted to assess the toxicity in the kidney and liver. The results showed that the concentration of AlCl3 in the kidney and liver increased significantly in 30-, 60-, and 90-day periods. The effects of oxidative stress on the kidneys and liver were dose- and time-dependent. Levels of malondialdehyde (MDA) significantly increased when exposed to AlCl3 groups. Conversely, the activity of antioxidant parameters, including reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD), significantly decreased in the AlCl3 exposed groups, indicating compromised oxidant mechanisms. Both the kidney and liver exhibited severe tissue damage, including necrosis, fibrosis, and inflammatory cell infiltration, in rats exposed to AlCl3. Kidney sections showed hyperplasia of the epithelial cells lining the renal tubules, resembling finger-like structures. Liver sections displayed severe lobular hyperplasia and an increase in mitotic figures. Our study suggests that AlCl3 has a detrimental impact on these vital organs and emphasizes the importance of monitoring and mitigating aluminum exposure, particularly where it is present in high concentration.

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.

An Assessment of aluminum contamination in neonatal parenteral nutrition solutions based on measured versus labeled content

Aluminum can potentially cause toxicity in pediatrics and neonates receiving parenteral nutrition. Some PN solutions and ingredients in Saudi Arabia do not comply with US FDA regulations regarding aluminum exposure. This study aims to determine the aluminum concentration in samples of PN solutions and ingredients used to feed infants in Saudi Arabia. The aluminum in the samples was determined using inductively coupled plasma mass spectrometry. The concentration of metal contaminants in each sample was determined in triplicate. The aluminum content of 38 samples was investigated, 15 of which originated from components included in the prepared PN solutions. Among the 15 samples, the least measurable aluminum content was detected in potassium chloride solutions (0.81 mcg/L). In contrast, the greatest amount of aluminum was detected in potassium phosphate and calcium gluconate (141,64 mcg/L and 462.7 mcg/L), respectively. The results showed that the final PN solution (PNS) product contained more aluminum levels than the content ingredients; in addition, the study found a statistically significant relationship among 18 pediatric patients at KFMC who had intestinal failure and needed long-term parenteral nutrition. Specifically, their high aluminum levels, exceeding the normal range of 0.6 ng/ml, indicate that the current use of PN solutions will likely cause toxicity due to aluminum contamination in additives. Hence, reducing aluminum in PN solutions is imperative to ensure patient safety.

METTL3-mediated m6A RNA methylation was involved in aluminum-induced neurotoxicity

Aluminum (Al) exposure has been linked to the development of a variety of neurodegenerative diseases. However, whether m6A RNA methylation participated in Al-induced neurotoxicity remain to be defined. In this study, mice were administrated with aluminum-lactate at dose of 220 mg/kg. bw by gavage for 3 months. Meanwhile, the primary hippocampal neurons were isolated and treated with 0, 50, 100, 150 μM aluminum-lactate, respectively for 7 days. Al exposure caused neuronal shrinkage, decreased Nissl bodies, and increased apoptosis. In accordance, in vitro studies also showed that Al exposure led to neuronal apoptosis in a dose-dependent manner, together with the decline in m6A RNA methylation levels. Moreover, the mRNA expression of Mettl3, Mettl14, Fto, and Ythdf2 were decreased upon Al exposure. Notably, the protein expression of METTL3 was dramatically down-regulated by 42% and 35% in Al-treated mice and neurons, suggesting METTL3 might exert a crucial role in Al-induced neurotoxicity. We next established a mouse model with hippocampus-specific overexpressing of Mettl3 gene to confirm the regulatory role of RNA methylation and found that METTL3 overexpression relieved the neurological injury induced by Al. The integrated MeRIP-seq and RNA-seq analysis elucidated that 631 genes were differentially expressed at both m6A RNA methylation and mRNA expression. Notably, EGFR tyrosine kinase inhibitor resistance, Rap1 signaling pathway, protein digestion and absorption might be involved in Al-induced neurotoxicity. Moreover, VEGFA, Thbs1, and PDGFB might be the central molecules. Collectively, our findings provide the novel sight into the role of m6A RNA methylation in neurodegenerative disease induced by Al.

Aluminum-maltol induced oxidative stress and reduced AMPK activity via BCK-related energy supply failure in C6 cell

Aluminum (Al) exposure significantly interferes with the energy supply in astrocytes, which may be a potential mechanism of Al-induced neurotoxicity. This study was designed to explore the mechanisms of Al-induced energy supply impairment in rat C6 astroglioma cell line. Aluminum-maltolate (Al(mal)3) (0.1 mM, 24 h) exposure significantly decreased brain-type creatine kinase (BCK) co-localization with the endoplasmic reticulum (ER) and resulted in mitochondrial dysfunctions, accompanied by a decrease in AMPK phosphorylation. The results of molecular docking showed that Al(mal)3 increased BCK’s hydrophobicity and hindered the localization movement of BCK between subcells·H2O2 co-administration was found to exacerbate mitochondrial dysfunction, Ca2+ dyshomeostasis, and apoptosis. After treated with Al(mal)3, additional oxidative stress contributed to BCK activity inhibition but did not promote a further decrease in AMPK phosphorylation. The activation of p-AMPK by its agonist can partially restore mitochondrial function, BCK activity, and ER-localized-BCK levels in Al(mal)3-treated astrocytes. In summary, Al exposure resulted in a sustained depletion of the mitochondrial and antioxidant systems, which was associated with reduced p-AMPK activity and decreased ER-localized-BCK levels in astrocytes. This study provides a theoretical basis for exploring the mechanisms of neurotoxicity induced by Al exposure.

Ameliorative effects of Aqueous Fruit Pulp Extracts of Adansonia digitata on the Hippocampus of Aluminium Chloride‐treated Adult Wistar Rats

AbstractBackgroundThis study evaluated the effects of aqueous extract of Adansonia digitata fruit pulp (AEAD) on the hippocampus of Aluminium chloride Alzheimer model Wistar rats.MethodThirty Wistar rats (110‐150g) were randomly divided into six groups (n = 5). The animals in Group 1 were administered 2ml/kg distilled water. Group 2 were administered 100mg/kg AlCl3. Groups 3 were administered 595mg/kg ascorbic acid. Group 4 and 5 were administered 100mg/kg AlCl3 + 500mg/kg AEAD and 100mg/kg AlCl3 + 1500mg/kg AEAD respectively. Group 6 were administered 100mg/kg AlCl3 + 595mg/kg ascorbic acid. Once daily, for four consecutive weeks, behavioral tests for spatial memory using the Morris water maze test were carried out. Experimentation lasted for 28 days after which the animals were humanely sacrificed.ResultAnimals treated with A. digitata and Ascorbic acid following Aluminium exposure showed significant decrease (11.67±1.74) in the time taken for the experimental rats to locate the escape platform. The result of the oxidative stress study showed a significant increase Malondialdehyde concentration and decrease in Superoxide dismutase (SOD) and reduced glutathione (GSH) in groups exposed to aluminium chloride, however, treatment with A. digitata and Ascorbic acid following Aluminium exposure did not show any significant difference when compared to the control group. Histopathological studies revealed degenerating pyramidal cells, Karyolysis, Pkynosis, were observed in the hippocampus of the aluminium treated group. Treatment with Adansonia digitata and Ascorbic acid ameliorated the changes observed in groups exposed to aluminium. The histoarchitecture of the aqueous extracts treated groups were preserved, particularly the 1500mg/kg doses.ConclusionA. digitata fruit pulp possess vital antioxidant properties that could ameliorate the toxic effects of aluminium on the Hippocampus of adult Wistar rats and as such could be used as a treatment of aluminium toxicity.

Effects of miR-204-5p and Target Gene EphB2 on Cognitive Impairment Induced by Aluminum Exposure in Rats.

Aluminum is a common environmental neurotoxin. Aluminum ions can cross the blood-brain barrier and accumulate in different brain regions, damage brain tissue, and cause cognitive impairment, but the molecular mechanism of aluminum neurotoxicity is not precise. This study investigated the effects of miR-204-5p, target gene EphB2, and downstream signaling pathway NMDAR-ERK-CREB-Arc on cognitive dysfunction induced by aluminum exposure. The results showed that the learning and memory of the rats were impaired in behavior. The accumulation of aluminum in the hippocampus resulted in the damage of nerve cell morphology in the CA1 region of the hippocampus. The expression level of miR-204-5p was increased, and the mRNA and protein expressions of EphB2, NMDAR2B, ERK1/2, CREB, and Arc were decreased. The results indicated that the mechanism of impaired learning and memory induced by aluminum exposure might promote the expression of miR-204-5P and further inhibit the expression of the target gene EphB2 and its downstream signaling pathway NMDAR-ERK-CREB-Arc.

Dietary solutions for aluminum embryotoxicity: A study in Danio rerio using spirulina and okra-spirulina diets

Aluminum (Al) is a versatile element commonly employed in various industries and water treatment processes. However, its presence in aquatic ecosystems can elicit adverse effects on organisms, particularly the Danio rerio fish species. Aluminum exposure has been associated with a spectrum of issues, ranging from oxidative stress to behavioral anomalies, reproductive disruptions, and morphological alterations in these organisms. This research aimed to assess the impact of aluminum chloride (AlCl3) on D. rerio embryos and explore strategies to mitigate its effects. Three dietary groups (commercial, okra-spirulina, and spirulina) were studied, focusing on embryonic development, oxidative damage, and gene expression changes. The study revealed that diets enriched with spirulina and okra-spirulina effectively reduced aluminum-induced embryotoxicity, oxidative stress, and gene expression alterations, surpassing the commercial diet. However, all AlCl3-exposed groups experienced adverse effects on embryonic development, including hatching anomalies, structural deformities, and cardiac delays. The okra-spirulina group showed milder toxic responses. In conclusion, this study highlights the potential of spirulina and okra-spirulina diets in mitigating aluminum-triggered oxidative stress and apoptosis in D. rerio. It underscores the need for future research on embryonic development and carries significant implications for environmental conservation and the well-being of aquatic organisms in aluminum-contaminated environments.

Experimental investigation on the explosion characteristics and flame propagation behavior of aluminum hydride dust

Aluminum hydride (AlH3) dust is a high-capacity hydrogen storage material but is prone to explosion. In this paper, explosion characteristics and flame propagation behavior of AlH3 dust are investigated. The results indicate that the exposure of bare aluminum and the increase of specific surface area lead to the maximum explosion pressure of AlH3 dust being 4 times higher than that of Al dust. The enhancement of heat transfer by hydrogen combustion causes a higher combustion rate, leading to a higher maximum explosion pressure rise rate and flame propagation velocity of AlH3 dust. The thermo-diffusive instabilities and the evolution of hydrogen result in a pulsation flame propagation velocity of AlH3 dust. Combining the explosion temperature calculated by NASA CEA with the explosion residues analysis, the explosion mechanism of AlH3 dust is further revealed. The break of the oxide film and the combustion of hydrogen result in a different explosion mechanism.

Innovative covalently modified Al‐MOF as a highly selective fluorescent sensor for Al (III) detection in tap water, human serum, and tea samples

Generally, aluminum exposure is not a risk; however, long‐term and high‐intensity exposure can have a negative impact on health. The ligand‐embedded MOF was developed for high sensitivity in the detection and removal of Al (III) ions in aqueous solutions. Novel selective metal–organic framework was synthesized via strong covalent attachment of NH2‐MIL‐53(Al) and 2‐hydroxy naphthaldehyde (2‐HNA) for selective and efficient fluorometric sensing of Al (III) ions. The elemental structure and morphology of the fabricated sensor (2‐HNA = N‐MIL‐53[Al]) were thoroughly evaluated to understand the high selectivity and considerable fluorescence stability in the water. The intensity of the sensor fluorescence increased linearly as the concentration of Al (III) increased from 0.19 to 2.0 ppm with a detection limit of 33.1 ppb (1.23 × 10−6 M) and 5 s of response time at pH 7. The potential mechanism is discussed. The high selectivity of the developed chemosensor was achieved against various competing environmentally relevant metal ions. Furthermore, Al (III) ions were successfully quantified in tap water, wastewater, human serum, and tea samples. The high precision (RSD percent, 0.009–1.76) and excellent accuracy (recovery percent, 99.96–101.56) of the 2‐HNA = N‐MIL‐53 (Al) sensor indicated that it holds great promise for the ultrafast and highly selective determination of Al (III) ions in wastewaters, with high reproducibility and reversibility.

Transcriptional analysis in four wild and cultivated rice genotypes identifies aluminum-induced genes

Differential gene expression analysis is a widely used approach to identify relevant genes and functional mechanisms that influence plant tolerance to abiotic stresses. In this study, we evaluated the transcriptional responses of contrasting rice genotypes to prolonged aluminum (Al) exposure, in cultivated (Oryza sativa) and wild (Oryza glumaepatula) rice species, through RNA-Seq experiments. After comparing transcriptional responses under control and Al treatment conditions, differentially expressed genes (DEGs) were identified for each genotype. Additionally, the transcription levels of six DEGs were validated by quantitative real-time PCR. Functional analyses of the identified DEGs provided insights into the coordinated action of both exclusion and detoxification mechanisms associated with Al responses in rice. Furthermore, we report a group of 28 genes that were differentially expressed in all analyzed species and genotypes, pinpointing a core set of mechanisms that are triggered by Al exposure. Likewise, 14 DEGs were identified only in Al-tolerant genotypes, representing potential key elements for the understanding of the successful adaptive response to toxic conditions adopted by tolerant genotypes. Given that many of these identified genes have not been previously reported or characterized, they could be considered novel regulators linked with Al tolerance responses, and promising candidates for the generation of agronomically improved rice varieties.

Aluminum exposure and cognitive performance: A meta-analysis

BackgroundAluminum is increasingly used in various industrial processes due to its beneficial properties. Occupational exposure to aluminum, however, has been linked to several adverse health effects. The impact of occupational aluminum exposure on worker's cognitive performance and its contribution in developing neurodegenerative diseases is highly discussed with competing results. MethodWe conducted a literature search via online databases until June 2023. Applicable studies fulfilling inclusion criteria investigating the effects of occupational aluminum exposure on cognitive functions were gathered. Results were aggregated using random effects meta-analysis and the effect size g. We further explored types of publication biases, moderating variables and exposure-effect relationships using meta-regressions. ResultsThe final sample consisted of 18 studies with 87 effect sizes for seven cognitive functions. We found significant worse performances in workers occupationally exposed to aluminum regarding processing speed, working memory, attention, and reaction time after exclusion of outliers. Additionally, we found increased blood plasma aluminum significantly predicting decreased cognitive performance in exposed workers. ConclusionOur results show decreased performance levels in processing speed, working memory, attention and reaction time in workers occupationally exposed to aluminum compared to controls. Furthermore, we found that aluminum in blood plasma was the only biomarker as significant predictor of cognitive performance. We discuss recommendations for further research in relation to occupational health and safety. Finally, we extend the discourse between occupational aluminum exposure and development of neurodegenerative diseases like Alzheimer's disease.

Aluminum Exposure and Health

Alüminyum günlük diyetle düzenli olarak alınan, antiperspirantlarda, aşılarda adjuvan olarak kullanılan bir elementtir. Alüminyumun kaynakları, vücuda alınımı ve insan sağlığı üzerindeki zararlı etkileri hakkında bilgi vermek amacıyla PubMed ve SCOPUS veri tabanlarından elde edilen yayınlara dayanan bu derlemede yazarların mesleki ve kişisel deneyimleri ele alınmıştır. Alüminyum, çevrede, gıda maddelerinde ve içme suyunda doğal olarak bulunur. Alüminyum için referans değerleri aşma olasılığı özellikle mesleki maruziyeti olan kişilerde daha yüksektir. Buna bağlı olarak alüminyum kaynakçıları ve alüminyum endüstrisindeki işçilerin idrarlarında alüminyum konsantrasyonları yüksek seviyelerde bulunmuştur. Ancak, işçiler üzerinde yapılan nöropsiko mantıksal (dikkat, öğrenme, hafıza) testlerinde demansla tezahür eden ensefalopati bulunamamıştır. Alzheimer hastalığı olan kişilerin beyinlerinde yüksek alüminyum içeriği bulunmasına rağmen, bunun hastalığın bir nedeni veya etkisi olup olmadığı belirsizliğini korumaktadır. Alüminyumun kanserojenlik etkisi konusunda da çelişkili sonuçlar vardır. Alüminyum içeren antiperspiranların meme kanserini teşvik ettiği iddiası bilimsel verilerle desteklenememiştir. Alüminyumun kritik yan etkisi ancak insanlarda ve hayvanlarda nörotoksisite gösterilerek belirlenebilir. Buna Alzheimer tipi demansın patofizyolojisi ile aynı olmayan demans sendromlu ensefalopati dahildir. Alüminyum içeren ter önleyiciler ile meme riski arasındaki ilişki, geniş çaplı epidemiyolojik kanser çalışmalarından elde edilebilir.