Mercury in the Amazon: The danger of a single story.

Amazon conservation is essential for the global future. Mercury is currently among the worst global pollutants and most (78.5%) of the South-American emissions are from the Amazon. Current Brazilian legislation on mining activities and trade of gold, and economic interests in soy, beef and large-scale projects such as dams, are key influences in mercury mobilization and emissions in the Amazon with the potential to affect the global environment. However, banning mercury in mining, while desirable, is not an efficient strategy if no other action is taken. The interconnected issues, such as exports (soy, beef and gold) and energy generation, must be addressed together to provide effective protection for human health and the environment. Realistically, to improve mercury emissions in the Amazon, we must stop looking solely at "the single story" (a limited view of reality) of supposedly "artisanal and small-scale gold mining" in the region and understand the complex economic, social, political, and international aspects of this problem. We propose some recommendations for international agencies, governments, communities and the private sector.

Gene Expression Profile in Immortalized Human Periodontal Ligament Fibroblasts Through hTERT Ectopic Expression: Transcriptome and Bioinformatic Analysis.

Human periodontal ligament fibroblast (hPLF) cells play an important role in maintaining oral cavity homeostasis with special function in tissue regeneration and maintenance of dental alveoli. Although their primary cell cultures are considered a good experimental model with no genetic changes, the finite life span may limit some experimental designs. The immortalization process increases cell life span but may cause genetic changes and chromosomal instability, resulting in direct effects on physiological cell responses. In this way, we aimed to investigate the global gene expression of hPLFs after the immortalization process by the ectopic expression of the catalytic subunit of the enzyme telomerase reverse transcriptase (hTERT) through transcriptome analysis. The embryonic origin of the primary culture of hPLF cells and immortalized hPLF-hTERT was also tested by vimentin staining, hTERT synthesis evaluated by indirect immunocytochemistry, analysis of cell proliferation, and morphology. The results indicated that hPLFs and hPLF-hTERT were positive for vimentin. On the 20th cell passage, hPLFs were in senescence, while hPLF-hTERT maintained their proliferation and morphology characteristics. At the same passage, hPLF-hTERT presented a significant increase in hTERT synthesis, but transcriptome did not reveal overexpression of the hTERT gene. Fifty-eight genes had their expression altered (11 upregulated and 47 downregulated) with the absence of changes in the key genes related to these cell types and in the main cancer-associated genes. In addition, the increase in hTERT protein expression without the overexpression of its gene indicates posttranscriptional level regulation. Successful immortalization of hPLFs through the ectopic expression of hTERT encourages further studies to design experimental protocols to investigate clinical questions from a translational perspective.

Human neurotoxicity of mercury in the Amazon: A scoping review with insights and critical considerations.

Human exposure to mercury is a major public health concern, causing neurological outcomes such as motor and visual impairment and learning disabilities. Currently, human exposure in the Amazon is among the highest in the world. A recent systematic review (doi:10.1016/j.jtemb.2018.12.001), however, highlighted the lack of high-quality studies on mercury-associated neurotoxicity. There is, therefore, a need to improve research and much to still learn about how exposure correlates with disease. In this review, we discuss studies evaluating the associations between neurological disturbances and mercury body burden in Amazonian populations, to generate recommendations for future studies. A systematic search was performed during July 2020, in Pubmed/Medline, SCOPUS and SCIELO databases with the terms (mercury*) and (Amazon*). Four inclusion criteria were used: original article (1), with Amazonian populations (2), quantifying exposure (mercury levels) (3), and evaluating neurological outcomes (4). The extracted data included characteristics (as year or origin of authorship) and details of the research (as locations and type of participants or mercury levels and neurological assessments). Thirty-four studies, most concentrated within three main river basins (Tapajós, Tocantins, and Madeira) and related to environmental exposure, were found. Mercury body burden was two to ten times higher than recommended and main neurological findings were cognitive, vision, motor, somatosensory and emotional deficits. Important insights are described that support novel approaches to researching mercury exposure and intoxication, as well as prevention and intervention strategies. As a signatory country to the Minamata Convention, Brazil has the opportunity to play a central role in improving human health and leading the research on mercury intoxication.

Mercury: What can we learn from the Amazon?

Mercury is among the ten most dangerous chemicals for public health, and is a priority concern for the 128 signatory countries of the Minamata Convention. Mercury emissions to the atmosphere increased 20% between 2010 and 2015, with South America, Sub-Saharan Africa and Southeast Asia as the main contributors. Approximately 80% of the total mercury emissions in South America is from the Amazon, where the presence of the metal is ubiquitous and highly dynamic. The presence of this metal is likely increasing, with global consequences, due to events of the last two years including extensive biomass burning and deforestation, as well as mining activities and the construction of large-scale projects, such as dams. Here we present a concise profile of this mobilization, highlighting the human exposure to this metal in areas without mining history. Mercury reaches the food chain in its most toxic form, methylmercury, intoxicating human populations through the intake of contaminated fish. Amazonian populations present levels over 6 ppm of hair mercury and, according to the 175:250:5:1 ratio for methylmercury intake : mercury hair : mercury brain : mercury blood, consume 2-6 times the internationally recognized reference doses. This exposure is alarmingly higher than that of other populations worldwide. A possible biphasic behavior of the mercury-related phenomena, with consequences that may not be observed in populations with lower levels, is hypothesized, supporting the need of improving our knowledge of this type of chronic exposure. It is urgent that we address this serious public health problem in the Amazon, especially considering that human exposure may be increasing in the near future. All actions in this region carry the potential to have global repercussions.

Influence of Prolonged Dental Bleaching on the Adhesive Bond Strength to Enamel Surfaces.

The objective of this in vitro study was to assess the influence of prolonged bleaching pre- and postrestoration on the bond strength (microshear) to enamel using 4% hydrogen peroxide (PH4). In the postrestorative bleached specimens evaluation, the composite cylinders were assembled after bleaching, while in the prebleached specimens, the cylinders were assembled before. Therefore, in the postbleached specimens, 60 bovine teeth were randomly assigned as follows: G1: control; G2: 14 days bleaching before bond strength (BS) testing; G3: 21 days; and G4: 28 days. In prebleached specimens, 180 bovine teeth were randomly assigned as follows: G1: control; G5: 14 days bleaching, storage in artificial saliva (AS) for 24 h before BS testing; G6: 14 days beaching, AS storage for 7 days before BS testing; G7: 21 days bleaching, AS storage for 24 h before BS testing; G8: 21 days bleaching, AS storage for 7 days before BS testing; G9: 28 days bleaching, AS storage for 24 hours before BS testing; and G10 : 28 days bleaching, AS storage for 7 days before BS testing. The results were submitted to ANOVA one-way (postrestoration bleaching) and two-way (prerestoration bleaching) and Tukey's post hoc test (p ≤ 0.05). In the postrestoration bleaching, no statistical difference between times was found. However, when bleached groups were compared to the control (G1), an expressive difference was detected (p ≤ 0.0001). For prerestoration bleaching, all experimental groups were statistically different from G1 (p ≤ 0.05), except G6 (p ≥ 0.01), and for G5 and G6, statistical differences were found (p ≤ 0.01). There were no significant differences between G7 and G8 and between G9 and G10, regardless of the AS storage times (p ≥ 0.05). It was concluded that prolonged bleaching with PH4 decreased adhesion resistance regardless of the moment of the bleaching (post- and prerestoration bleaching).

Association between Psychological Stress and Periodontitis: A Systematic Review.

This systematic review aims to investigate the association between psychological stress and periodontitis through analysis of cortisol levels and periodontal clinical parameters. This review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guide and based on PECO (Participants, Exposure, Comparators, Outcomes) question and registered at PROSPERO under the code CRD42017076670. As eligibility criteria, observational studies performed in adult humans presenting periodontitis (P), which evaluated patients exposed (E) and nonexposed to psychological stress (C) and to verify the association between this type of stress and periodontitis (O) were included. The searches were performed until March 2018. The following databases were used: PubMed, Scopus, Web of Science, The Cochrane Library, LILACS, OpenGrey, and Google Scholar. After searches, the duplicate results were removed. The remaining citations were selected according to eligibility criteria in two phases. In the first phase, the title/abstract was evaluated. In the second phase, the articles were chosen previously were assessed by full text. After selection, the studies were submitted to data extraction and risk of bias evaluation by Fowkes and Fulton. A total of 1,386 citations were retrieved. After duplicates removal and selection process, three articles were selected by full text. Among them, two articles reported a positive association between psychological stress and periodontitis. All articles were classified as low risk of bias. Even though two articles highlighted an association between psychological stress and the presence of a possible modulatory pattern of cortisol levels in clinical parameters of periodontitis, more studies are necessary to elucidate this question.

Oxidative Damage in Human Periodontal Ligament Fibroblast (hPLF) after Methylmercury Exposure.

Human exposure to mercury (Hg) is primary associated with its organic form, methylmercury (MeHg), through the ingestion of contaminated seafood. However, Hg contamination is also positively correlated with the number of dental restorations, total surface of amalgam, and organic mercury concentration in the saliva. Among the cells existing in the oral cavity, human periodontal ligament fibroblast (hPLF) cells are important cells responsible for the production of matrix and extracellular collagen, besides sustentation, renewal, repair, and tissue regeneration. In this way, the present study is aimed at investigating the potential oxidative effects caused by MeHg on hPLF. Firstly, we analyzed the cytotoxic effects of MeHg (general metabolism status, cell viability, and mercury accumulation) followed by the parameters related to oxidative stress (total antioxidant capacity, GSH levels, and DNA damage). Our results demonstrated that MeHg toxicity increased in accordance with the rise of MeHg concentration in the exposure solutions (1-7 µM) causing 100% of cell death at 7 µM MeHg exposure. The general metabolism status was firstly affected by 2 µM MeHg exposure (43.8 ± 1.7%), while a significant decrease of cell viability has arisen significantly only at 3 µM MeHg exposure (68.7 ± 1.4%). The ratio among these two analyses (named fold change) demonstrated viable hPLF with compromised cellular machinery along with the range of MeHg exposure. Subsequently, two distinct MeHg concentrations (0.3 and 3 µM) were chosen based on LC50 value (4.2 µM). hPLF exposed to these two MeHg concentrations showed an intracellular Hg accumulation as a linear-type saturation curve indicating that metal accumulated diffusively in the cells, typical for metal organic forms such as methyl. The levels of total GSH decreased 50% at exposure to 3 µM MeHg when compared to control. Finally, no alteration in the DNA integrity was observed at 0.3 µM MeHg exposure, but 3 µM MeHg caused significant damage. In conclusion, it was observed that MeHg exposure affected the general metabolism status of hPLF with no necessary decrease on the cell death. Additionally, although the oxidative imbalance in the hPLF was confirmed only at 3 µM MeHg through the increase of total GSH level and DNA damage, the lower concentration of MeHg used (0.3 µM) requires attention since the intracellular mercury accumulation may be toxic at chronic exposures.

Antidepressant and Antiaging Effects of Açaí (Euterpe oleracea Mart.) in Mice.

Depression is a mental disorder that affects 300 million people of all ages worldwide, but fewer than half of those with the condition receive adequate treatment. In addition, the high pharmacological refractoriness (affecting 30%-50% of patients) and toxicity of some classical antidepressants support the pursuit of new therapies. People with this condition show depressed mood, loss of pleasure, high levels of oxidative stress, and accelerated biological aging (decreased telomere length and expression of the telomerase reverse transcriptase (TERT), the enzyme responsible for telomere maintenance). Because of the close relationship between depression and oxidative stress, nutraceuticals with antioxidant properties are excellent candidates for therapy. This study represents the first investigation of the possible antidepressant and antiaging effects of commercial samples of clarified açaí (Euterpe oleracea) juice (EO). This fruit is rich in antioxidants and widely consumed. In this study, mice were treated with saline or EO (10 µL/g, oral) for 4 days and then with saline or lipopolysaccharide (0.5 mg/kg, i.p.) to induce depressive-like behavior. Only four doses of EO were enough to abolish the despair-like and anhedonia behaviors and alterations observed in electromyographic measurements. The antidepression effect of EO was similar to that of imipramine and associated with antioxidant and antiaging effects (preventing lipid peroxidation and increasing TERT mRNA expression, respectively) in three major brain regions involved in depression (hippocampus, striatum, and prefrontal cortex). Additionally, EO significantly protected hippocampal cells, preventing neuronal loss associated with the depressive-like state and nitrite level increases (an indirect marker of nitric oxide production). Moreover, EO alone significantly increased TERT mRNA expression, revealing for the first time a potent antiaging action in the brain that suggests neuroprotection against long-term age-related consequences.

Influence of Prolonged Bleaching with 4% Hydrogen Peroxide Containing Calcium and Different Storage Times on the Bond Strength to Enamel.

AIMS: To assess the influence of different bleaching protocols on the bond strength to enamel. MATERIALS AND METHODS: In this laboratory experiment were used forty sound bovine incisors were divided into five groups. G1: No bleaching (control). G2: 14 days bleaching with 4% hydrogen peroxide containing calcium (4% HP+Ca2+) (2 hours/ day) and 24 hours of artificial saliva (AS) storage. G3: 14 days bleaching with 4% HP+Ca2+ (2 hours/day) and 7 days storage in AS. G4: 28 days bleaching with 4% HP+Ca2+(2 hours/day) and 24 hours storage in AS. G5: 28 days bleaching with 4% HP+Ca2+ (2 hours/day) and 7 days storage in AS. Following storage times, composite resin cylinders were built upon the enamel surfaces and tested for micros hearing. For statistical analysis, two-way ANOVA and Tukey's test was applied to the data (p≤0.05), for it was evaluated different times of bleaching and stored in artificial saliva. RESULTS: The highest mean was observed in G1 (14.61 MPa), and the lowest in G4 (9.22 MPa). Compared to the negative control (G1), no differences were found in 14 days bleaching and the same between G2 and G3 (p ≥0.01). However, in 28 days bleaching, the effects of the storage periods (24 hours and 7 days) were significantly different (p ≤0.05), besides G4 and G5 were statistically different from G1. CONCLUSIONS: Extended bleaching time (28 days) decreased the bond strength, independently of storage time in AS. CLINICAL SIGNIFICANCE: If adhesive procedures are required after extended at-home bleaching they may need to be delayed for at least for 7 days for the enamel adhesion ability to recover.

Physical Exercise Attenuates Oxidative Stress and Morphofunctional Cerebellar Damages Induced by the Ethanol Binge Drinking Paradigm from Adolescence to Adulthood in Rats.

Ethanol (EtOH) binge drinking is characterized by high EtOH intake during few hours followed by withdrawal. Protection strategies against the damages generated by this binge are poorly explored. Thus, this study is aimed at investigating the protective role of treadmill physical exercise (PE) on the damage caused after repeated cycles of binge-like EtOH exposure in the oxidative biochemistry, morphology, and cerebellar function of rats from adolescence to adulthood. For this, animals were divided into four groups: control group (sedentary animals with doses of distilled water), exercised group (exercised animals with doses of distilled water), EtOH group (sedentary animals with doses of 3 g/kg/day of EtOH, 20% w/v), and exercised+EtOH group (exercised animals with previous mentioned doses of EtOH). The PE occurred on a running treadmill for 5 days a week for 4 weeks, and all doses of EtOH were administered through intragastric gavage in four repeated cycles of EtOH in a binge-like manner. After the EtOH protocol and PE, animals were submitted to open field and beam walking tests. In sequence, the cerebellums were collected for the biochemical and morphological analyses. Biochemical changes were analyzed by measurement of Trolox equivalent antioxidant capacity (TEAC), reduced glutathione content measurements (GSH), and measurement of nitrite and lipid peroxidation (LPO). In morphological analyses, Purkinje cell density evaluation and immunohistochemistry evaluation were measured by antimyelin basic protein (MBP) and antisynaptophysin (SYP). The present findings demonstrate that the binge drinking protocol induced oxidative biochemistry misbalance, from the decrease of TEAC levels and higher LPO related to tissue damage and motor impairment. In addition, we have shown for the first time that treadmill physical exercise reduced tissue and functional alterations displayed by EtOH exposure.

Exposure to Inorganic Mercury Causes Oxidative Stress, Cell Death, and Functional Deficits in the Motor Cortex.

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.

Heavy Chronic Ethanol Exposure From Adolescence to Adulthood Induces Cerebellar Neuronal Loss and Motor Function Damage in Female Rats.

Over the last years, heavy ethanol consumption by teenagers/younger adults has increased considerably among females. However, few studies have addressed the long-term impact on brain structures' morphology and function of chronic exposure to high ethanol doses from adolescence to adulthood in females. In line with this idea, in the current study we investigated whether heavy chronic ethanol exposure during adolescence to adulthood may induce motor impairments and morphological and cellular alterations in the cerebellum of female rats. Adolescent female Wistar rats (35 days old) were treated with distilled water or ethanol (6.5 g/kg/day, 22.5% w/v) during 55 days by gavage. At 90 days of age, motor function of animals was assessed using open field (OF), pole, beam walking and rotarod tests. Following completion of behavioral tests, morphological and immunohistochemical analyses of the cerebellum were performed. Chronic ethanol exposure impaired significantly motor performance of female rats, inducing spontaneous locomotor activity deficits, bradykinesia, incoordination and motor learning disruption. Moreover, histological analysis revealed that ethanol exposure induced atrophy and neuronal loss in the cerebellum. These findings indicate that heavy ethanol exposure during adolescence is associated with long-lasting cerebellar degeneration and motor impairments in female rats.

The Effects of Moderate Physical Exercise on Adult Cognition: A Systematic Review.

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.

Repeated cycles of binge-like ethanol exposure induce immediate and delayed neurobehavioral changes and hippocampal dysfunction in adolescent female rats.

Binge-like ethanol intake (BEI) is a socioeconomical problem among adolescents and increasingly affects women. BEI can leave a long-term imprint in the brain, but it is unknown if its effect on cognition and anxiety is cumulative on repeated binge-ethanol episodes. We now submitted female Wistar rats to repeated cycles of binge-like ethanol treatment by intragastrically administering ethanol (3.0 g/kg/day, 20% w/v ethanol; 3 days on/4 days off) starting at postnatal day 35 (PND35). To investigate the short-term effects of BEI during adolescence, rats underwent 1 or 4 cycles of BEI, being evaluated at PND37 and PND58, respectively: both groups displayed anxiety-like behavior in the open field and elevated plus-maze tests, as well as short-term memory deficits in the object recognition task; this was associated with transient decreases of BDNF levels and increases of GFAP levels in the hippocampus. To evaluate the short- and long-lasting effects of BEI in adulthood, rats were subjected to 8 cycles of BEI and evaluated after 7.5 h (PND86) or after 14 days of ethanol withdrawal (PND100). This caused a persistent anxiogenic profile whereas recognition memory was impaired on the short-term, but not 14 days post-administration. The reduced BDNF level observed shortly after BEI recovered upon withdrawal, whereas increased GFAP immunoreactivity was persistent up to 14 days post-administration in adulthood. These findings show that repeated binge-like ethanol episodes from adolescence to adulthood in female rats cause consistent and long-term alterations of anxiety and hippocampal astrogliosis, whereas they trigger a recognition memory deficit paralleled by lower hippocampal BDNF levels, both recovering upon ethanol withdrawal.

Is there an Association Between Periodontitis and Atherosclerosis in Adults? A Systematic Review.

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 gramnegative 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.

Periodontitis and Alzheimer's Disease: A Possible Comorbidity between Oral Chronic Inflammatory Condition and Neuroinflammation.

Periodontitis is an oral chronic infection/inflammatory condition, identified as a source of mediators of inflammation into the blood circulation, which may contribute to exacerbate several diseases. There is increasing evidence that inflammation plays a key role in the pathophysiology of Alzheimer's disease (AD). Although inflammation is present in both diseases, the exact mechanisms and crosslinks between periodontitis and AD are poorly understood. Therefore, this article aims to review possible comorbidity between periodontitis and AD. Here, the authors discuss the inflammatory aspects of periodontitis, how this oral condition produces a systemic inflammation and, finally, the contribution of this systemic inflammation for worsening neuroinflammation in the progression of AD.

Neurodegeneration and Glial Response after Acute Striatal Stroke: Histological Basis for Neuroprotective Studies.

Stroke is a leading cause of death and neurological disability worldwide and striatal ischemic stroke is frequent in humans due to obstruction of middle cerebral artery. Several pathological events underlie damage progression and a comprehensive description of the pathological features following experimental stroke in both acute and chronic survival times is a necessary step for further functional studies. Here, we explored the patterns of microglial activation, astrocytosis, oligodendrocyte damage, myelin impairment, and Nogo-A immunoreactivity between 3 and 30 postlesion days (PLDs) after experimental striatal stroke in adult rats induced by microinjections of endothelin-1 (ET-1). The focal ischemia induced tissue loss concomitant with intense microglia activation between 3 and 14 PLDs (maximum at 7 PLDs), decreasing afterward. Astrocytosis was maximum around 7 PLDs. Oligodendrocyte damage and Nogo-A upregulation were higher at 3 PLDs. Myelin impairment was maximum between 7 and 14 PLDs. Nogo-A expression was higher in the first week in comparison to control. The results add important histopathological features of ET-1 induced stroke in subacute and chronic survival times. In addition, the establishment of the temporal evolution of these neuropathological events is an important step for future studies seeking suitable neuroprotective drugs targeting neuroinflammation and white matter damage.

Chronic ethanol exposure during adolescence through early adulthood in female rats induces emotional and memory deficits associated with morphological and molecular alterations in hippocampus.

There is increasing evidence that heavy ethanol exposure in early life may produce long-lasting neurobehavioral consequences, since brain structural maturation continues until adolescence. It is well established that females are more susceptible to alcohol-induced neurotoxicity and that ethanol consumption is increasing among women, especially during adolescence. In the present study, we investigated whether chronic ethanol exposure during adolescence through early adulthood in female rats may induce hippocampal histological damage and neurobehavioral impairments. Female rats were treated with distilled water or ethanol (6.5 g/kg/day, 22.5% w/v) by gavage from the 35(th)-90(th) day of life. Ethanol-exposed animals displayed reduced exploration of the central area and increased number of fecal boluses in the open field test indicative of anxiogenic responses. Moreover, chronic high ethanol exposure during adolescence induced marked impairments on short-term memory of female rats addressed on social recognition and step-down inhibitory avoidance tasks. These neurobehavioral deficits induced by ethanol exposure during adolescence through early adulthood were accompanied by the reduction of hippocampal formation volume as well as the loss of neurons, astrocytes and microglia cells in the hippocampus. These results indicate that chronic high ethanol exposure during adolescence through early adulthood in female rats induces long-lasting emotional and memory deficits associated with morphological and molecular alterations in the hippocampus.

Evaluation of the effects of chronic intoxication with inorganic mercury on memory and motor control in rats.

The aims of this study were to evaluate whether chronic intoxication with mercury chloride (HgCl2), in a low concentration over a long time, can be deposited in the central nervous tissue and to determine if this exposure induces motor and cognitive impairments. Twenty animals were intoxicated for 45 days at a dose of 0.375 mg/kg/day. After this period, the animals underwent a battery of behavioral tests, in a sequence of open field, social recognition, elevated T maze and rotarod tests. They were then sacrificed, their brains collected and the motor cortex and hippocampus dissected for quantification of mercury deposited. This study demonstrates that long-term chronic HgCl2 intoxication in rats promotes functional damage. Exposure to HgCl2 induced anxiety-related responses, short- and long-term memory impairments and motor deficits. Additionally, HgCl2 accumulated in both the hippocampus and cortex of the brain with a higher affinity for the cortex.