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The knowledge about a potential in vivo uptake and subsequent toxicological effects of aluminum (Al), especially in the nanoparticulate form, is still limited. This paper focuses on a three day oral gavage study with three different Al species in Sprague Dawley rats. The Al amount was investigated in major organs in order to determine the oral bioavailability and distribution. Al-containing nanoparticles (NMs composed of Al 0 and aluminum oxide (Al 2 O 3 )) were administered at three different concentrations and soluble aluminum chloride (AlCl 3 ·6H 2 O) was used as a reference control at one concentration. A microwave assisted acid digestion approach followed by inductively coupled plasma mass spectrometry (ICP-MS) analysis was developed to analyse the Al burden of individual organs. Special attention was paid on how the sample matrix affected the calibration procedure. After 3 days exposure, AlCl 3 ·6H 2 O treated animals showed high Al levels in liver and intestine, while upon treatment with Al 0 NMs significant amounts of Al were detected only in the latter. In contrast, following Al 2 O 3 NMs treatment, Al was detected in all investigated organs with particular high concentrations in the spleen. A rapid absorption and systemic distribution of all three Al forms tested were found after 3-day oral exposure. The identified differences between Al 0 and Al 2 O 3 NMs point out that both, particle shape and surface composition could be key factors for Al biodistribution and accumulation.

Currently prescribed medications for the treatment of Alzheimer's disease (AD) that are based on acetylcholinesterase inhibition only offer symptomatic relief but do not provide protection against neurodegeneration. There appear to be an intense need for the development of therapeutic strategies that not only improve brain functions but also prevent neurodegeneration. The oxidative stress is one of the main causative factors of AD. Various antioxidants are being investigated to prevent neurodegeneration in AD. The objective of this study was to investigate the neuroprotective effects of naringenin (NAR) against AlCl3+D-gal induced AD-like symptoms in an animal model. Rats were orally pre-treated with NAR (50 mg/kg) for two weeks and then exposed to AlCl3+D-gal (150 mg/kg + 300 mg/kg) intraperitoneally for one week to develop AD-like symptoms. The standard drug, donepezil (DPZ) was used as a stimulator of cholinergic activity. Our results showed that NAR pre-treatment significantly protected AD-like behavioral disturbances in rats. In DPZ group, rats showed improved cognitive and cholinergic functions but the neuropsychiatric functions were not completely improved and showed marked histopathological alterations. However, NAR not only prevented AlCl3+D-gal induced AD-like symptoms but also significantly prevented neuropsychiatric dysfunctions in rats. Results of present study suggest that NAR may play a role in enhancing neuroprotective and cognition functions and it can potentially be considered as a neuroprotective compound for therapeutic management of AD in the future.

A sufficient quantitative understanding of aluminium (Al) toxicokinetics (TK) in man is still lacking, although highly desirable for risk assessment of Al exposure. Baseline exposure and the risk of contamination severely limit the feasibility of TK studies administering the naturally occurring isotope 27Al, both in animals and man. These limitations are absent in studies with 26Al as a tracer, but tissue data are limited to animal studies. A TK model capable of inter-species translation to make valid predictions of Al levels in humans—especially in toxicological relevant tissues like bone and brain—is urgently needed. Here, we present: (i) a curated dataset which comprises all eligible studies with single doses of 26Al tracer administered as citrate or chloride salts orally and/or intravenously to rats and humans, including ultra-long-term kinetic profiles for plasma, blood, liver, spleen, muscle, bone, brain, kidney, and urine up to 150 weeks; and (ii) the development of a physiology-based (PB) model for Al TK after intravenous and oral administration of aqueous Al citrate and Al chloride solutions in rats and humans. Based on the comprehensive curated 26Al dataset, we estimated substance-dependent parameters within a non-linear mixed-effect modelling context. The model fitted the heterogeneous 26Al data very well and was successfully validated against datasets in rats and humans. The presented PBTK model for Al, based on the most extensive and diverse dataset of Al exposure to date, constitutes a major advancement in the field, thereby paving the way towards a more quantitative risk assessment in humans.

The application of the coagulation/flocculation process is very important due to its simplicity in removing turbidity. Due to the disadvantages of using chemical coagulants in water and the lack of sufficient effect of natural materials alone in removing turbidity for proper performance, the simultaneous use of chemical and natural coagulants is the best way to reduce the harmful effects of chemical coagulants in water. In this study, the application of poly aluminum chloride (PAC) as a chemical coagulant and rice starch as a natural coagulant aid to remove turbidity from aqueous solutions was investigated. Effects of the above coagulants on the four main factors, coagulant dose (0–10 mg/L), coagulant adjuvant dose (0–0.1 mg/L), pH (5–9), turbidity (NTU 0–50), and each five levels were assessed using a central composite design (CCD). Under the optimized conditions, the maximum turbidity elimination efficiency was found to be 96.6%. The validity and adequacy of the proposed model (quadratic model) were confirmed by the corresponding statistics (i.e., F -value of 23.3, p -values of 0.0001, and lack of fit of 0.877 for the model, respectively, R 2  = 0.88, R 2 adj . = 0.84, R 2 pred  = 0.79, AP = 22.04). Graphical Abstract

A common heavy metal in many facets of daily life is aluminum (AlCl 3 ), which can be found in food, toothpaste, cosmetics, food additives, and numerous pharmaceutical items. The hippocampus, liver, and kidneys have the highest concentrations of this powerful neurotoxin, which also accumulates over time and contributes to the development of a number of cognitive disorders. Long-term overconsumption of AlCl 3 results in hepatic and renal toxicity as well as neuronal inflammation. The purpose of the research is to assess the potential protective effects of various L-carnitine dosages as an antioxidant against hebato, renal, and neuronal toxicity in rats caused by aluminum chloride (AlCl 3 ) (20 mg/kg, 1/20 LD 50). Six groups (n = 6), consisting of 36 adult albino rats, were randomly assigned. Saline was administered to the control group (GI) by injection. (GII) had given an injection of L-carnitine at a low-dose of 75 mg/kg body weight. An injections of L-carnitine at a high-dose (150 mg/kg) were given to (GIII), and AlCl 3 (20 mg/kg) was given to (GIV). (GV) administered with L-carnitine (75 mg/kg) and AlCl 3 (20 mg/kg) by injection. For 60 days, AlCl 3 (20 mg/kg) and L-carnitine (150 mg/kg) were administered to GVI by injection. Furthermore, the histological structure of the cortex, hippocampus, and hepatic renal tissues appeared to change in response to AlCl 3 . L-carnitine therapy lessened the negative effects of AlCl 3 . The observable improvement in the tissues of the brain, liver, and kidneys further supported this histopathologically. It is possible to draw the conclusion that L-carnitine holds promise as a corrective measure for AlCl 3 , which causes renal toxicity and neural hepatotoxicity in rats. When it comes to adult albino rats, L-carnitine has a negative impact and exhibits ameliorative effects against aluminum chloride.

Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases leading to dementia. Despite research efforts, currently there are no effective pharmacotherapeutic options for the prevention and treatment of AD. Recently, numerous studies highlighted the beneficial effects of curcumin (CUR), a natural polyphenol, in the neuroprotection. Especially, its dual antioxidant and anti-inflammatory properties attracted the interest of researchers. In fact, besides its antioxidant and anti-inflammatory properties, this biomolecule is not degraded in the intestinal tract. Additionally, CUR is able to cross the blood–brain barrier and could therefore to be used to treat neurodegenerative pathologies associated with oxidative stress, inflammation and apoptosis. The present study aimed to assess the ability of CUR to induce neuronal protective and/or recovery effects on a rat model of neurotoxicity induced by aluminum chloride (AlCl3), which mimics the sporadic form of Alzheimer’s disease. Our results showed that treatment with CUR enhances pro-oxidant levels, antioxidant enzymes activities and anti-inflammatory cytokine production and decreases apoptotic cells in AlCl3-exposed hippocampus rats. Additionally, histopathological analysis of hippocampus revealed the potential of CUR in decreasing the hallmarks in the AlCl3-induced AD. We also showed that CUR post-treatment significantly improved the behavioral, oxidative stress and inflammation in AlCl3-exposed rats. Taken together, our data presented CUR as a nutraceutical potential through its protective effects that are more interesting than recovery ones in sporadic model of AD.

This paper determines the effect of calcination temperature on the activity of polymerized aluminum chloride (PAC) waste residue. The effect of the calcination temperature of PAC waste residue on the compressive strength of cement mortar was studied using the slurry substitution method. The compressive strength data of cement mortar mixed with different temperatures of calcined PAC waste residue were analyzed by fitting. A compressive strength prediction model of PAC waste residue calcination temperature on the compressive strength of cement mortar can be built. The effect of PAC waste residue on the volume stability of cement mortar was also studied. The results showed that calcination increased the activity index of PAC waste residue by 5 to 10%, and 600[degrees]C was the optimal calcination temperature. Compared with the uncal-cined PAC waste residue cement mortar, the calcined samples showed complete hydration, smaller micropores, and a denser overall structure. The fitting curve provided a good fit for the development of the compressive strength of cement mortar mixed with different temperatures of calcined PAC waste residue. A model of the calcination temperature of PAC waste residue on the compressive strength of cement mortar was derived based on the fitting curve. The volume stability of cement mortar mixed with PAC waste residue calcined at 600[degrees]C was improved. Keywords: activity index; calcination temperature; compressive strength; micro-morphology; polymerized aluminum chloride (PAC) waste residue; volume stability.

The male reproductive system is negatively influenced by Al exposure. Al represented a considerable hazard to men’s reproduction capabilities. Amygdalin (AMG) and spirulina platensis (SP) have been considered to have a strong antioxidant and repro-protective activity; also, targeted drug delivery systems called niosomes improve the distribution of water-soluble medications like amygdalin and spirulina. Current study targeted to determine the effectiveness of AMG and SP against negative reproductive impact resulted by aluminum chloride (AlCl 3 ) toxicity. Sixty adult male albino rats were separated into 6 groups, including the control group, which received distilled water; AlCl 3 group, which received AlCl 3 ; AMG+AlCl 3 group, which received AlCl 3 +AMG; AMGLN+AlCl 3 group, which received AlCl 3 +amygdalin-loaded niosomes; SP+AlCl 3 group, which received AlCl 3 +SP; and SPLN+AlCl 3 group, which received AlCl 3 +spirulina-loaded niosomes. All treatments were orally gavaged daily for 5 weeks, and rats were weighed weekly. At the termination of the experiment, some males (three from each group) were used for fertility traits via mating thirty virgin rat females (in a ratio of 1:2 and 2:3 male:female, respectively) followed by recording of birth weights and litter size (number of pups per each female) at birth to assess males’ reproductive capability. Other males were euthanized for collection of serum, epididymal semen samples, and tissue samples for biochemical, sperm evaluation, gene expression, and histopathological measurements. There are a considerable number of negative impacts of AlCl 3 on male fertility clarified by declined serum testosterone levels; an increased oxidative stress (MDA, TAC); deteriorated semen quality; down-regulation of CYP11A1, StAR, and HSD-3b gene expressions; and testicular tissue degenerative changes. In addition, litter size (number of pups per each female) and birth weights of pups obtained from mated females were affected. AMG and SP treatments, either in niosomal or conventional form, alleviated the AlCl 3 negative effects by reducing oxidative stress; increasing testosterone levels; improving semen quality; upregulating of CYP11A1, StAR, and HSD-3b gene expressions; and reducing degenerative changes of testicular tissue. Besides, negative reproductive effect was diminished as observed by changes in the litter size (number of pups per each female) and birth weights of pups obtained from mated females. AMG and SP treatments (either in niosomal or conventional form), ameliorated the AlCl 3 negative effects as they possess powerful antioxidant activity, as well as they have the ability to improve the reproductive activity of affected males. Graphical abstract

Dysregulation of protein homeostasis, proteostasis, is a distinctive hallmark of many neurodegenerative disorders and aging. Deleteriously, the accumulation of aberrant proteins in Alzheimer’s disease (AD) is accompanied with a marked collapse in proteostasis network. The current study explored the potential therapeutic effect of vardenafil (VAR), a phosphodiesterase-5 inhibitor, in AlCl 3 / d -galactose ( d -gal)-induced AD in rats and its possible underlying mechanisms. The impact of VAR treatment on neurobehavioral function, hippocampal tissue architecture, and the activity of the cholinergic system main enzymes were assessed utilizing VAR at doses of 0.3 mg/kg and 1 mg/kg. Additionally, the expression level of amyloid-beta and phosphorylated tau proteins in the hippocampus were figured out. Accordingly, VAR higher dose was selected to contemplate the possible underlying mechanisms. Intriguingly, VAR elevated the cyclic guanosine monophosphate level in the hippocampus and averted the repressed proteasome activity by AlCl 3 / d -gal; hence, VAR might alleviate the burden of toxic protein aggregates in AD. In addition, a substantial reduction in the activating transcription factor 6-mediated endoplasmic reticulum stress was demonstrated with VAR treatment. Notably, VAR counteracted the AlCl 3 / d -gal-induced depletion of nuclear factor erythroid 2-related factor 2 level. Moreover, the anti-senescence activity of VAR was demonstrated via its ability to restore the balance of the redox circuit. The modulation of phosphatidylinositol-3-kinase/protein kinase B/p53 pathway and the reduction of nuclear factor kappa B level, the key regulator of senescence-associated secretory phenotype mediators release, with VAR treatment were also elucidated. Altogether, these findings insinuate the possible therapeutic benefits of VAR in AD management. Graphic abstract

Aluminum chloride is an inorganic polymeric coagulant commonly found in daily life and various materials. Although male reproductive toxicity has been associated with AlCl3 exposure, the underlying mechanism remains unclear. This study aimed to examine the impact of AlCl3 exposure on mitophagy and mitochondrial apoptosis in testicular tissue and mouse spermatocytes. Reactive oxygen species (ROS) and ATP levels were measured in GC-2spd after AlCl3 exposure using a multifunctional enzyme labeler. The changes in mitochondrial membrane potential (MMP) and TUNEL were observed through confocal laser microscopy, and the expression of proteins associated with mitophagy and apoptosis was analyzed using Western blot. Our results demonstrated that AlCl3 exposure disrupted mitophagy and increased apoptosis-related protein expression in testicular tissues. In the in vitro experiments, AlCl3 exposure induced ROS production, suppressed cell viability and ATP production, and caused a decrease in MMP, leading to mitophagy and cell apoptosis in GC-2spd cells. Intervention with N-acetylcysteine (NAC) reduced ROS production and partially restored mitochondrial function, thereby reversing the resulting mitophagy and cell apoptosis. Our findings provide evidence that ROS-mediated mitophagy and cell apoptosis play a crucial role in the toxicity of AlCl3 exposure in GC-2spd. These results contribute to the understanding of male reproductive toxicity caused by AlCl3 exposure and offer a foundation for future research in this area.