Mercury is a toxic metal that can be found in the environment in three different forms – elemental, organic and inorganic. Inorganic mercury has a lower liposolubility, which results in a lower organism absorption and reduced passage through the blood–brain barrier. For this reason, exposure models that use inorganic mercury in rats in order to evaluate its effects on the central nervous system are rare, especially in adult subjects. This study investigated if a chronic exposure to low doses of mercury chloride (HgCl2), an inorganic form of mercury, is capable of promoting motor alterations and neurodegenerative in the motor cortex of adult rats. Forty animals were exposed to a dose of 0.375 mg/kg/day, for 45 days. They were then submitted to motor evaluation and euthanized to collect the motor cortex. Measurement of mercury deposited in the brain parenchyma, evaluation of oxidative balance, quantification of cellular cytotoxicity and apoptosis and density of mature neurons and astrocytes of the motor cortex were performed. It was observed that chronic exposure to inorganic mercury caused a decrease in balance and fine motor coordination, formation of mercury deposits and oxidative stress verified by the increase of lipoperoxidation and nitrite concentration and a decrease of the total antioxidant capacity. In addition, we found that this model of exposure to inorganic mercury caused cell death by cytotoxicity and induction of apoptosis with a decreased number of neurons and astrocytes in the motor cortex. Our results provide evidence that exposure to inorganic mercury in low doses, even in spite of its poor ability to cross biological barriers, is still capable of inducing motor deficits, cell death by cytotoxicity and apoptosis, and oxidative stress in the motor cortex of adult rats.

Mercury (Hg) is a highly toxic metal, which can be found in its inorganic form in the environment. This form presents lower liposolubility and lower absorption in the body. In order to elucidate the possible toxicity of inorganic Hg in the hippocampus, we investigated the potential of low doses of mercury chloride (HgCl₂) to promote hippocampal dysfunction by employing a chronic exposure model. For this, 56 rats were exposed to HgCl₂(0.375 mg/kg/day) via the oral route for 45 days. After the exposure period, the animals were submitted to the cognitive test of fear memory. The hippocampus was collected for the measurement of total Hg levels, analysis of oxidative stress, and evaluation of cytotoxicity, apoptosis, and tissue injury. It was observed that chronic exposure to inorganic Hg promotes an increase in mercury levels in this region and damage to short‐ and long‐term memory. Furthermore, we found that this exposure model provoked oxidative stress, which led to cytotoxicity and cell death by apoptosis, affecting astrocytes and neurons in the hippocampus. Our study demonstrated that inorganic Hg, even with its low liposolubility, is able to produce deleterious effects in the central nervous system, resulting in cognitive impairment and hippocampal damage when administered for a long time at low doses in rats.

Background: Physical exercise is a systematic sequence of movements executed with a predefined purpose. This muscular activity impacts not only on circulatory adaptations, but also neuronal integration with the potential to influence cognition. The aim of this review was to determine whether the literature supports the idea that physical exercise promotes cognitive benefits in healthy adults. Methods: A systematic search for relevant articles was performed according to the Preferred Reporting Items for Systematic Review and Meta-Analysis criteria using available databases (PubMed, LILACS, Scopus, Web of Science, The Cochrane Library, OpenGrey, Google Scholar and CENTRAL). The search terms included “humans” or “adults” or “cognition” or “awareness” or “cognitive dissonance” or “cognitive reserve” or “comprehension” or “consciousness” and “motor activity” or “exercise” or “physical fitness,” and not “aged” or “nervous system diseases,” with the purpose of finding associations between moderate physical exercise and cognition. A methodological quality and risk of bias unit assessed the eligibility of articles. Results: A total of 7179 articles were identified. Following review and quality assessment, three articles were identified to fulfill the inclusion criteria. An association between moderate physical exercise and cognition was observed. Improvements in cognitive parameters such as reduced simple reaction time, improved response precision and working memory were identified among the included articles. Conclusion: This systematic review found that moderate physical exercise improves cognition.

Background: Atherosclerosis is a multifactorial inflammatory disease of the cardiovascular system. It has been suggested that periodontitis, an infectious disease of oral cavity caused by gram-negative anaerobic bacteria, could be linked to atherosclerosis. Objective: The objective of this systematic review was to assess the evidence between the association of periodontitis and atherosclerosis in adults. Methods: A systematic literature search was conducted in 7 databases up to January 2017, according to the Preferential Reports for Systematic Review and Meta-analysis (PRISMA) guidelines. Studies in humans with atherosclerosis were considered eligible when considering a group exposed to periodontitis and a control group (absence of periodontitis), in which the primary outcome was the association between the 2 diseases (atherosclerosis and periodontitis). The synthesis of the qualitative studies included was evaluated using previously validated checklist for assessing the risk of bias. Results: Among the 2138 studies found, 4 observational studies met the eligibility criteria and were included in the qualitative synthesis. All articles were considered adequate, presenting consistent and valid information. The results of the selected studies show the expected effects, being considered as low risk of bias. Conclusion: The available evidence indicates an association between the 2 diseases, with elevated levels of inflammatory markers, mainly C-reactive protein and interleukin 6.

This study investigates morphological and biochemistry effects of binge ethanol consumption in parotid (PG) and submandibular (SG) salivary glands of rats from adolescence to adulthood. Female Wistar rats (n = 26) received ethanol at 3 g/kg/day (20% w/v) for 3 consecutive days/week from the 35th until the 62nd day of life. Animals were treated in two periods: 1 week (G1) and 4 weeks (G2), with a control (treated with distilled water) and an ethanol group to each period. In morphological analysis, morphometric and immunohistochemistry evaluation for smooth muscle actin (αSMA), cytokeratin‐18 (CK‐18), and vimentin (VIM) were made. Biochemical changes were analyzed by concentration of nitrites and levels of malondialdehyde (MDA). The difference between groups in each analysis was evaluated by Mann‐Whitney U test or Student’s t‐test (p ≤ 0.05). PG showed, at one week of ethanol exposure, lower CK‐18 and α‐SMA expression, as well as MDA levels. After four weeks, lower CK‐18 and higher MDA levels were observed in PG exposed to ethanol, in comparison to control group. SG showed lower α‐SMA expression after 1 and 4 weeks of ethanol exposure as well as higher MDA levels after 1 week. Ethanol binge consumption during adolescence promotes tissue and biochemical changes with only one‐week binge in acinar and myoepithelial PG cells.