Search

Lead poisoning is a global public health concern. Maternal exposure during intrauterine and lactational periods can present a higher susceptibility of harm to the offspring. Thus, pregnant female Wistar rats (Rattus norvegicus) were randomly divided in two experimental groups: control group and Lead group. The animals were exposed to 50 mg/kg of Lead Acetate daily for 42 days (21 days of gestational period + 21 days of lactational period). After the exposure period, the mandibles of the offspring were collected for lead quantification, Raman spectroscopy analysis, micro-CT, morphometric e histochemical analysis. Lead exposure altered the physical-chemical composition of alveolar bone and caused histological damage associated with a reduction in osteocyte density and collagen area fraction, increase in collagen maturity, as well as a reduction in bone volume fraction. An increase in trabecular spaces with anatomical compromise of the vertical dimensions of the bone was observed. Thus, the results suggest that developing alveolar bone is susceptible to toxic effects of lead when organisms are exposed during intrauterine and lactation periods., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Human environment is highly contaminated with aluminum, and aluminum is toxic to majority of tissues, particularly to neurons. In previous decades, aluminum exposure was frequently linked with the onset of Alzheimer's disease (AD), and increased levels of Al were detected in the brains of individuals with AD. People who live in a certain area are exposed to aluminum in a similar way (they eat the same vegetable and other foodstuffs, use similar cosmetics, and buy medications from the same manufacturer), nevertheless not all of them develop Alzheimer's disease. Majority of known risk factors for AD promote atherosclerosis and consequently reduce brain blood supply. In this review, we highlighted the significance of local (carotid disease and atherosclerosis of intracranial blood vessels) and systemic hypoxia (chronic obstructive pulmonary disease and anemia) in the development of AD. Nerve tissue is very sophisticated and sensitive to hypoxia and aluminum toxicity. As a side effect of compensatory mechanisms in case of hypoxia, neurons start to uptake aluminum and iron to a greater extent. This makes perfect a background for the gradual onset and development of AD., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

This study aimed to identify the landscape of current aluminum toxicity based on knowledge mapping of the 100 most-cited articles on toxicological aspects of aluminum in biological organisms. The research was searched in the Web of Science Core Collection (WoS-CC) with publications between 1945 and 2022. Data regarding authorship, title, journal, year of publication, citation count, country, keywords, study design, and research hotspots were extracted and all elected articles were analyzed. Our results showed that among the articles selected, literature review and in vivo studies were the most common study designs. The USA and England were found as the countries with most publications. Alzheimer's disease (AD), aluminum, and neurotoxicity were found as the most frequent keywords. The articles most cited in world literature suggested that aluminum exposure is associated with Alzheimer's disease, Parkinson's disease (PD), dialysis encephalopathy, amyotrophic lateral sclerosis, neurodegeneration changes, cognitive impairment, such as bone damage, oxidative alterations, and cytotoxicity., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

The central nervous system is the main target of MeHg toxicity and glial cells are the first line of defense; however, their true role remains unclear. This study aimed to identify the global map of human glial-like (U87) cells transcriptome after exposure to a non-toxic and non-lethal MeHg concentration and to investigate the related molecular changes. U87 cells were exposed upon 0.1, 0.5, and 1 µM MeHg for 4 and 24 h. Although no changes were observed in the percentage of viable cells, the metabolic viability was significantly decreased after exposure to 1 µM MeHg for 24 h; thus, the non-toxic concentration of 0.1 µM MeHg was chosen to perform microarray analysis. Significant changes in U87 cells transcriptome were observed only after 24 h. The expression of 392 genes was down regulated while 431 genes were up-regulated. Gene ontology showed alterations in biological processes (75%), cellular components (21%), and molecular functions (4%). The main pathways showed by KEGG and Reactome were cell cycle regulation and Rho GTPase signaling. The complex mechanism of U87 cells response against MeHg exposure indicates that even a low and non-toxic concentration is able to alter the gene expression profile., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Mercury (Hg) is a toxic metal that became a public health problem due to environmental contamination caused by anthropogenic activity. In this sense, oral homeostasis can undergo changes due to the toxic effects of metal on the salivary glands. Therefore, our objective was to investigate the proteomic and genotoxic changes in salivary glands after exposure to inorganic mercury (IHg). Forty Wistar rats that were divided into a control group, which received distilled water, and an exposed group, which received 0.375 mg/kg of mercury chloride for 45 days via orogastric gavage. After that, the animals were euthanized, and the parotid and submandibular glands were collected for analysis of the genotoxic effects, using the comet assay and proteome global profile assessment. The results showed that IHg promoted damage to cellular DNA associated with proteomic changes that showed events such as oxidative stress, mitochondrial dysfunction, changes in the cytoskeleton, and apoptosis. Therefore, these findings show a profile of molecular changes due to the interactions of IHg with several proteins and mechanisms inherent to the cell, which consequently may result in dysfunction of the salivary glands and impaired homeostasis of the oral cavity., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

The alveolar bone is an important mineralized structure of the periodontal support apparatus, and information about the methylmercury (MeHg) effects on the structural integrity is scarce. Therefore, this study aimed to investigate whether systemic, chronic, and low-dose exposure to MeHg can change the alveolar bone microstructure of rats. Adult Wistar rats (n = 30) were exposed to 0.04 mg/kg/day of MeHg or vehicle through intragastric gavage. The animals were euthanized after 60 days, and blood samples were collected for trolox equivalent antioxidant capacity (TEAC), glutathione (GSH), lipid peroxidation (LPO), and comet assays. The mandible of each animal was collected and separated into hemimandibles that were used to determine the total Hg level in the bone and to analyze microstructural damage and alveolar bone loss in terms of trabecular number (Tb.N), trabecular thickness (Tb.Th), bone volume fraction (BV/TV), and exposed root area of the second molars. MeHg exposure triggered oxidative stress in blood represented by lower levels of GSH and TEAC and the increase in LPO and DNA damage of the blood cells. High total Hg levels were found in the alveolar bone, and the microstructural analyses showed a reduction in Tb.N, Tb.Th, and BV/TV, which resulted in an increase in the exposed root area and a decrease in bone height. Long-term MeHg exposure promotes a systemic redox imbalance associated with microstructural changes and alveolar bone loss and may indicate a potential risk indicator for periodontal diseases., (© 2021. Springer Science+Business Media, LLC, part of Springer Nature.)

Intoxication by heavy metals such as methylmercury (MeHg) is recognized as a global health problem, with strong implications in central nervous system pathologies. Most of these neuropathological conditions involve vascular, neurotransmitter recycling, and oxidative balance disruption leading to accelerated decline in fine balance, and learning, memory, and visual processes as main outcomes. Besides neurons, astrocytes are involved in virtually all the brain processes and perform important roles in neurological response following injuries. Due to astrocytes' strategic functions in brain homeostasis, these cells became the subject of several studies on MeHg intoxication. The most heterogenous glial cells, astrocytes, are composed of plenty of receptors and transporters to dialogue with neurons and other cells and to monitor extracellular environment responding tightly through fluctuation of cytosolic ions. The overall toxicity of MeHg might be determined on the basis of the balance between MeHg-mediated injury to neurons and protective responses from astrocytes. Although the role of neurons in MeHg intoxication is relatively well-established, the role of the astrocytes is only beginning to be understood. In this review, we update the information on astroglial modulation of the MeHg-induced neurotoxicity, providing remarks on their protective and deleterious roles and insights for future studies., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Mercury chloride (HgCl 2 ) is a compound found in the environment that presents low risk due to low liposolubility. Considering the importance of blood as access rout to the systemic distribution of this toxicant to the organism as well as functions performed by it, this study aimed to investigate the effects of HgCl 2 on the peripheral blood of rats, evaluating the oxidative biochemistry, blood count, and morphology of cell populations. For this, 20 adult Wistar male rats were divided into control (n = 10) and exposed (n = 10) groups and received distilled water or HgCl 2 at a dose of 0.375 mg/kg for 45 days, respectively, through intragastric gavage. Then, the animals were euthanized and the blood was collected for total mercury (Hg) levels determination, complete blood and reticulocyte count, oxidative biochemistry by Trolox Equivalent Antioxidant Capacity (TEAC), reduced glutathione (GSH) levels, superoxide dismutase activity (SOD), thiobarbituric acid reactive substances (TBARS), and nitric oxide (NO), in blood cells and plasma. Long-term exposure increased total Hg in plasma and blood cells. In blood cells, only TEAC has decreased; in plasma, the HgCl 2 increased TBARS and NO levels, followed by a decrease in TEAC and GSH levels. There were no quantitative changes in reticulocytes, erythrocytes, and hemoglobin; however, the number of leukocytes have increased and platelets have decreased. Our results suggest that even in the face of low toxicity when compared with other mercury species, HgCl 2  at low doses is able to modulate the systemic redox balance and affect some blood cell populations.

Methylmercury (MeHg) is one of the main global pollutants. The vulnerability of fetus and newborn to MeHg-induced changes is extensively reported, making relevant investigation possible for alternative sample matrix for human biological monitoring for at this stage of life. This study aimed to characterize tissue change effects of environmental-experimental MeHg on salivary glands of offspring rats after pre- and postnatal exposure. For this, pregnant Wistar rats were orally exposed to MeHg (40 μg/kg BW/day) or only vehicle (control group), from the gestational period to the end of the lactation period. Salivary glands (SG) were collected from the offspring to analyze possible Hg levels and main findings by histopathological evaluations and CK19 and α-SMA immunostaining. The results indicated that Hg levels in SG of intoxicated offspring were associated with histologic abnormalities, such as acinar atrophy and an increase in the intercellular matrix among the acini, as well as damages in the architecture of epithelium and myoepithelial cells, evidenced by a decrease in immunostaining area. Thus, this is the first study to show in the literature the toxicopathologic findings on SG of offspring after pre- and postnatal exposure to MeHg. Moreover, it presents the SG as an attractive target to futures studies, mainly in children exposed to environmentally relevant doses.

High amounts of aluminum (Al) are found in soil and water. It is highly bioavailable, which makes it an important agent of environmental imbalance. Moreover, Al is considered a neurotoxic agent that is associated with several neurodegenerative diseases. Thus, this study investigated the effects of long-term Al chloride (AlCl 3 ) exposure on motor behavior, oxidative biochemistry, and cerebellar tissue parameters. For this, adult Wistar rats were divided into three groups: Al-D1 (8.3 mg kg -1  day -1 ), Al-D2 (5.2 mg kg -1  day -1 ), and control (distilled water); all groups were orally exposed for 60 days by intragastric gavage. After the exposure period, animals performed the open field, elevated plus maze, rotarod, and beam walking tests. Then, the blood and cerebellum were collected to evaluate Al levels and biochemical and morphological analyses, respectively. Our results demonstrate that animals exposed to Al doses presented a higher Al level in the blood. In the spontaneous locomotor activity, Al exposure groups had traveled a lower total distance when compared with the control group. There was no statistically significant difference (p > 0.05) between exposed and control groups when anxiogenic profile, forced locomotion, fine motor coordination/balance, pro-oxidative parameter, and density Purkinje cells were compared. Thus, aluminum exposure in equivalent doses to human consumption in urban regions did not promote significant changes in the cerebellum or motor parameters.

Several studies indicate aluminum (Al) as a potent toxicant, mainly related to central nervous system disorders. However, investigations about the Al effects over salivary glands are still scarce. In this way, the present study aimed to investigate whether the Al chloride (AlCl 3 ) is able of triggering oxidative stress in parotid and submandibular glands of mice and also, if any morphological impairment is observed. For this, twenty mice were divided into two groups: Exposed group (EG), which received 18.5 mg/kg of AlCl 3 by intragastric gavage for 60 days and control group (CG), which received distilled water by intragastric gavage during the same period of time. After that, levels of reduced glutathione (GSH) and malonaldehyde (MDA) were analyzed and we performed morphological analyses by evaluating the area of parenchyma, stroma, acini, and ducts in both glands. Statistical analyses were performed by Student's t test and two-way ANOVA, adopting p < 0.05. No abnormal body weight was observed and data indicates that although both major salivary glands are susceptible to Al-induced oxidative stress, by increasing MDA and reducing GSH, only submandibular glands decreased the parenchyma and increased stroma area. Moreover, the submandibular glands showed smaller total area of acini and higher total area of ducts, in comparison with the control group. Notably, AlCl 3 induces oxidative stress in both glands, however, submandibular glands showed to be more susceptible to Al effects than parotid glands. Our study gives evidences about Al toxicity in parotid and submandibular glands and claims for new investigations to understand more mechanisms of Al-induced toxicity.

Environmental and occupational mercury exposure is considered a major public health issue. Despite being well known that MeHg exposure causes adverse effects in several physiologic functions, MeHg effects on salivary glands still not completely elucidated. Here, we investigated the cellular MeHg-induced damage in the three major salivary glands (parotid, submandibular, and sublingual) of adult rats after chronic, systemic and low doses of MeHg exposure. Rats were exposed by 0.04 mg/kg/day over 60 days. After that, animals were euthanized and all three glands were collected. We evaluated total Hg accumulation, metallothionein I/II (MT I/II), α-smooth muscle actin (α-SMA), and cytokeratin 18 (CK18) immune expression. Our results have showed that MeHg is able to disrupt gland tissue and to induce a protective mechanism by MT I/II expression. We also showed that cell MT production is not enough to protect gland tissue against cellular structural damage seen by reducing marking of cytoskeletal proteins as CK18 and α-SMA. Our data suggest that chronic MeHg exposure in low-daily doses is able to induce cellular damage in rat salivary glands.