Maternal exposure to glyphosate increased the risk of adverse neurodevelopmental outcomes in rodent offspring: A systematic review.

The potential neurotoxicity of environmental contaminants, such as pesticides, is implicated in the etiology of neurodevelopmental disorders, particularly given the heightened vulnerability of the developing brain. Among these contaminants, glyphosate, a widely used herbicide, has been linked to alterations in neurodevelopment, though its precise neurotoxic mechanisms are not fully elucidated. In this context, our systematic review evaluates the impact of maternal exposure to glyphosate alone (GLY) or glyphosate-based-herbicide (GBH) on neurodevelopmental and behavioral outcomes in rodent offspring. This assessment encompasses a comprehensive examination of behavioral, biochemical, morphological, and genetic alterations resulting from perinatal glyphosate exposure. The Systematic review protocol was registered in the platform Open Science Framework (OSF) following the guidelines of the Systematic Review Center for Laboratory Animal Experimentation (SYRCLE). Our analysis demonstrate that glyphosate disrupts redox signaling, metabolic pathways, and neurotransmitter systems, thereby affecting brain architecture and function across genders and developmental stages in rodents. The results of this review elucidate the extensive neurochemical and behavioral disruptions attributed to glyphosate, highlighting the critical need for advanced neurodevelopmental risk assessment methodologies. Such refined evaluations are vital to inform targeted prevention and intervention strategies in the context of environmental neurotoxicants.

What does scientometry tell us about mercury toxicology and its biological impairments?

Mercury is a toxic pollutant that poses risks to both human and environmental health, making it a pressing public health concern. This study aimed to summarize the knowledge on mercury toxicology and the biological impairments caused by exposure to mercury in experimental studies and/or diagnosis in humans. The research was conducted on the main collection of Web of Science, employing as a methodological tool a bibliometric analysis. The selected articles were analyzed, and extracted data such as publication year, journal, author, title, number of citations, corresponding author's country, keywords, and the knowledge mapping was performed about the type of study, chemical form of mercury, exposure period, origin of exposure, tissue/fluid of exposure measurement, mercury concentration, evaluation period (age), mercury effect, model experiments, dose, exposure pathway, and time of exposure. The selected articles were published between 1965 and 2021, with Clarkson TW being the most cited author who has also published the most articles. A total of 38% of the publications were from the USA. These studies assessed the prenatal and postnatal effects of mercury, emphasizing the impact of methylmercury on neurodevelopment, including motor and cognitive evaluations, the association between mercury and autism, and an evaluation of its protective effects against mercury toxicity. In observational studies, the blood, umbilical cord, and hair were the most frequently used for measuring mercury levels. Our data analysis reveals that mercury neurotoxicology has been extensively explored, but the association among the outcomes evaluated in experimental studies has yet to be strengthened. Providing metric evidence on what is unexplored allows for new studies that may help governmental and non-governmental organizations develop guidelines and policies.

Deciphering the Global Proteomic Profile Involved in Methylmercury-Induced Cerebellar Neurodegeneration and Motor Dysfunction in Adult Rats.

Mercury is a ubiquitous pollutant in the environment with potential neurotoxic effects. Several populations are susceptible to mercurial exposure, especially methylmercury (MeHg) at low doses for long periods through food consumption. Given this, the present work aimed to assess the effects of long-term MeHg exposure on the cerebellum of rats from a translational perspective using a representative dose, assessing molecular, biochemical, morphological, and behavioral parameters. The model was produced by administering 40 µg/kg of MeHg for 60 days to adult male Wistar rats by oral gavage. As a result of this exposure, the animals presented motor deficits in open field and rotarod tests which were associated with an increase in total mercury content in cerebellar parenchyma, a reduction in antioxidant competence against peroxyl radicals, and increased nitrite and lipid peroxidation levels. The proteomic approach showed 317 modulated proteins. Such findings were associated with reductions in mature neuron and Purkinje cell densities and glial fibrillary acidic protein immunostained areas and increased microglial density. In addition, decreases in myelin basic protein and synaptophysin immunostaining were also observed. The results thus provided new evidence of the mechanisms underlying complex MeHg-induced neurodegeneration, especially the proteins underlying the biochemical and morphological features associated with motor dysfunction.

Methylmercury exposure during prenatal and postnatal neurodevelopment promotes oxidative stress associated with motor and cognitive damages in rats: an environmental-experimental toxicology study.

The environmental contamination by methylmercury (MeHg) is a major concern for public health. The effects of MeHg in the central nervous system (CNS) of adult animals have been extensively investigated; however, little is known about the effects of MeHg exposure during intrauterine and lactation periods on motor and cognitive functions of adolescent rats. Therefore, this study aimed to investigate the effect of MeHg exposure during intrauterine life and lactation on both motor and cognitive functions of offspring rats. Ten female Wistar rats were exposed to 40 µg/kg/day of MeHg through cookie treats from the first day of pregnancy until the last day of breastfeeding. Both motor and cognitive functions of offspring male rats were assessed by open field, rotarod, and step-down inhibitory avoidance tests. Forty-one days after birth, the hippocampus and cerebellum were collected to determine total Hg content, antioxidant capacity against peroxyl radicals (ACAP), reduced glutathione (GSH) levels, lipid peroxidation (LPO), and nitrite levels. MeHg exposure during CNS development increased Hg levels in both hippocampal and cerebellar parenchymas, triggered oxidative stress throughout ACAP and GSH decrease, increased LPO and nitrite levels. These alterations resulted in reduced spontaneous and stimulated locomotion and short- and long-term memory deficits. Therefore, damages triggered by MeHg exposure during intrauterine life and lactation had detrimental effects on oxidative biochemistry and motor and cognitive functions of offspring rats.

Chronic exposure to environmentally relevant concentrations of guanylurea induces neurotoxicity of Danio rerio adults.

Recent studies have shown guanylurea (GUA) alters the growth and development of fish, induces oxidative stress, and disrupts the levels and expression of several genes, metabolites, and proteins related to the overall fitness of fish. Nonetheless, up to date, no study has assessed the potential neurotoxic effects that GUA may induce in non-target organisms. To fill the current knowledge gaps about the effects of this metabolite in the central nervous system of fish, we aimed to determine whether or not environmentally relevant concentrations of this metabolite may disrupt the behavior, redox status, AChE activity in Danio rerio adults. In addition, we also meant to assess if 25, 50, and 200 µg/L of GUA can alter the expression of several antioxidant defenses-, apoptosis-, AMPK pathway-, and neuronal communication-related genes in the brain of fish exposed for four months to GUA. Our results demonstrated that chronic exposure to GUA altered the swimming behavior of D. rerio, as fish remained more time frozen and traveled less distance in the tank compared to the control group. Moreover, this metabolite significantly increased the levels of oxidative damage biomarkers and inhibited the activity of acetylcholinesterase of fish in a concentration-dependent manner. Concerning gene expression, environmentally relevant concentrations of GUA downregulated the expression GRID2IP, PCDH17, and PCDH19, but upregulated Nrf1, Nrf2, p53, BAX, CASP3, PRKAA1, PRKAA2, and APP in fish after four months of exposure. Collectively, we can conclude that GUA may alter the homeostasis of several essential brain biomarkers, generating anxiety-like behavior in fish.

Metal brain bioaccumulation and neurobehavioral effects on the wild rodent Liomys irroratus inhabiting mine tailing areas.

Ecotoxicological studies are necessary in order to evaluate the effects of environmental exposure of chemicals on wild animals and their ecological consequences. Particularly, neurobehavioral effects of heavy metal elements on wild rodents have been scarcely investigated. In the present study, we analyzed the effect of metal bioaccumulation (Pb, As, Mg, Ni, and Zn) in the brain and in the liver on exploratory activity, learning, memory, and on some dopaminergic markers in the wild rodent Liomys irroratus living inside mine tailings, at Huautla, Morelos, Mexico. We found higher Pb concentration but lower Zn in striatum, nucleus accumbens, midbrain, and hippocampus in exposed animals in comparison to rodents from the reference site. Exposed rodents exhibited anxious behavior evaluated in the open field, while no alterations in learning were found. However, they displayed slight changes in the memory test in comparison to reference group. The neurochemical evaluation showed higher levels of dopamine and 5-hydroxyindolacetic acid in midbrain, while lower levels of metabolites dihydroxyphenyl acetic acid and homovanillic acid in striatum of exposed rodents. In addition, mRNA expression levels of dopaminergic D2 receptors in nucleus accumbens were lower in animals from the mining zone than in animals from the reference zone. This is the first study that shows that chronic environmental exposure to metals results in behavioral and neurochemical alterations in the wild rodent L. irroratus, a fact that may comprise the survival of the individuals resulting in long-term effects at the population level. Finally, we suggest the use of L. irroratus as a sentinel species for environmental biomonitoring of mining sites.

Long-term exposure to lead reduces antioxidant capacity and triggers motor neurons degeneration and demyelination in spinal cord of adult rats.

Lead is a toxic metal found in environment with great neurotoxic potential. The main effect is associated with impairments in hippocampus and cerebellum, driving to cognitive and motor dysfunctions, however, there is a lack of evidences about the effects over the spinal cord. In this way, we aimed to investigate in vivo the effects of long-term exposure to lead acetate in oxidative biochemistry and morphology of rats' spinal cord. For this, 36 male Wistar rats (Rattus norvegicus) were divided into the group exposed to 50 mg/kg of lead acetate and control group, which received only distilled water, both groups through intragastric gavage, for 55 days. After the exposure period, the animals were euthanized and the spinal cords were collected to perform the analyses of lead levels quantification, oxidative biochemistry evaluation by levels of malondialdehyde (MDA), nitrites and the antioxidant capacity against peroxyl radicals (ACAP). Besides, morphological evaluation with quantitative analysis of mature and motor neurons and reactivity to myelin basic protein (MBP). Our results showed high levels of lead in spinal cord after long-term exposure; there was a reduction on ACAP level; however, there was no difference observed in MDA and nitrite levels. Moreover, there was a reduction of mature and motor neurons in all three regions, and a reduction of immunolabeling of MBP in the thoracic and lumbar segments. Therefore, we conclude that long-term exposure to lead is able of increasing the levels of the metal in spinal cord, affecting the antioxidant capacity and inducing morphological impairments in spinal cord parenchyma. Our results also suggest that the tissue impairments triggered by lead may be resultant from others molecular mechanisms besides the oxidative stress.

Diphenyl diselenide dietary supplementation protects against fumonisin B1-induced oxidative stress in brains of the silver catfish Rhamdia quelen.

The trend toward using plant-based ingredients in aquafeeds has raised important concerns for aquaculture owing to the negative impacts of mycotoxins on fish health; with emphasis for contamination by fumonisin B1 (FB1). The brain is an important target of FB1; however, study of the pathways linked to brain damage is limited to an analysis of histopathological alterations. Reports have demonstrated the protective effects of dietary supplementation with diphenyl diselenide (Ph2Se2) in the brains of fish subjected to several environmental insults; nevertheless, its neuroprotective effects in fish fed with diets contaminated with FB1 remain unknown. Therefore, the aim of this study was to evaluate whether oxidative damage may be a pathway associated with FB1-induced neurotoxicity, as well as to evaluate whether dietary supplementation with Ph2Se2 prevents or reduces FB1-mediated brain oxidative damage in silver catfish. Brain reactive oxygen species (ROS), lipid peroxidation (LOOH) and protein carbonylation increased on day 30 post-feeding in animals that received FB1-contaminated diets compared to the control group, while brain antioxidant capacity against peroxyl radicals (ACAP) levels and catalase (CAT), glutathione peroxidase (GPx) and glutathione S-transferase (GST) activities were lower. Diphenyl diselenide dietary supplementation avoid increases in brain ROS levels, as well minimizing the augmentation of LOOH levels. Furthermore, Ph2Se2 prevented impairment of brain ACAP levels, as well as GPx and GST activities elicited by FB1-contaminated diets. These data suggest that dietary supplementation with 3 mg/kg Ph2Se2 prevented FB1-induced brain damage in silver catfish, and this protective effect occurred through avoided of excessive ROS production, as well as via prevention of brain lipid damage. Furthermore, Ph2Se2 exerted its neuroprotective effects via ameliorative effects on the enzymatic and non-enzymatic antioxidant defense systems, and may be an approach to prevent FB1-induced brain oxidative stress; however, is not an alternative to prevent the impairment on performance caused by FB1.

Behavioural, electrocorticographic, and electromyographic alterations induced by Nerium oleander ethanolic extract: Anticonvulsant therapeutics assessment.

Nerium oleander Linn. is an Apocynaceae shrub which is among the most toxic ornamental plants. Although seizures are one of the symptoms associated with N. Oleander poisoning in humans, only a few studies are available on the behavioural and electrophysiological alterations caused by this plant poisoning. This study aimed at providing a thorough description of the electroencephalographic (EEG) and electromyographic (EMG) profiles throughout the experimental poisoning of Wistar rats (200-250 g) using ethanolic extract of N. oleander (EENO). Further, seizure control was assessed using different anticonvulsants. Male Wistar rat's behaviour was assessed upon EENO (150 mg/kg) administration and the animals were evaluated for muscle and neural activities through EMG and EEG recordings, respectively. The behavioural test showed two distinct phases of CNS activity: Phase I - myorelaxation and depression, and Phase II - excitability (agitated behaviour and seizures). Such phases were consistent with the EEG and EMG tracing patterns attained. Within the first 400 s of the recordings, during Phase I, the EMG showed no tracing amplitude variation. Later, the tracing pattern was changed and an intensification of the muscle contraction power in higher frequencies was observed during Phase II. The EEG showed initially a slight flattening in the tracings with a reduction in the intensity of the signal as per spectrogram of frequency attained. Thereafter, during Phase II, much higher amplitude tracings could be noted with an intensification of the signal, compatible with seizures. Seizure control was evaluated using four agents: phenytoin, phenobarbital, diazepam and scopolamine (at 10 mg/kg in all cases). While scopolamine was not effective in the seizure control, diazepam was the most efficient drug for the attenuation of the poisoning. Our results indicate the possibility of including phenytoin, phenobarbital and diazepam, mainly the latter, in the poisoning therapeutic protocol, including for those individuals who could be more susceptible to the poisoning by Nerium oleander as in the case of epileptic patients.

Spinal cord neurodegeneration after inorganic mercury long-term exposure in adult rats: Ultrastructural, proteomic and biochemical damages associated with reduced neuronal density.

Mercury chloride (HgCl2) is a chemical pollutant widely found in the environment. This form of mercury is able to promote several damages to the Central Nervous System (CNS), however the effects of HgCl2 on the spinal cord, an important pathway for the communication between the CNS and the periphery, are still poorly understood. The aim of this work was to investigate the effects of HgCl2 exposure on spinal cord of adult rats. For this, animals were exposed to a dose of 0.375 mg/kg/day, for 45 days. Then, they were euthanized, the spinal cord collected and we investigated the mercury concentrations in medullary parenchyma and the effects on oxidative biochemistry, proteomic profile and tissue structures. Our results showed that exposure to this metal promoted increased levels of Hg in the spinal cord, impaired oxidative biochemistry by triggering oxidative stress, mudulated antioxidant system proteins, energy metabolism and myelin structure; as well as caused disruption in the myelin sheath and reduction in neuronal density. Despite the low dose, we conclude that prolonged exposure to HgCl2 triggers biochemical changes and modulates the expression of several proteins, resulting in damage to the myelin sheath and reduced neuronal density in the spinal cord.

Comparison of Visual Functions of Two Amazonian Populations: Possible Consequences of Different Mercury Exposure.

The present study investigated the visual perimetry and color vision of two Amazonian populations differently exposed to mercury. Ten riverines environmentally exposed to mercury by fish eating and 34 gold-miners occupationally exposed to mercury vapor. The visual perimetry was estimated using the Förster perimeter and the color vision was evaluated using a computerized version of Farnsworth-Munsell test. Riverine and gold-miners' hair mercury concentrations were quantified. Mercury hair concentration of the riverines was significantly higher than that from gold-miners. Riverines had lower perimetric area than the gold-miners. The errors in the hue ordering test of both Amazonian populations were larger than the controls (non-exposed subjects), but there was no difference between themselves. Riverines had significant multiple association between the visual function and hair mercury concentration, while the gold-miners has no significant association with the exposure. We concluded that the different ways of mercury exposure led to similar visual outcomes, with greater impairment in riverines (organic mercury exposed subjects).

Developmental neurotoxic effects of graphene oxide exposure in zebrafish larvae (Danio rerio).

Although graphene oxide (GO), a nanomaterial with hexagonal planar layer, has been widely studied due to its applications in neurobiology that include drug delivery and tissue engineering, additional studies to assess its potential toxic effects are still needed. Thus, this study evaluated the effects of GO exposure (at 5, 10, 50 or 100mg/L) during six consecutive days on mortality, hatching, spontaneous movement, heart rate, morphology, locomotion behavior, acetylcholinesterase (AChE) activity, dopamine levels and relative gene expression of developmental neurology-related genes using zebrafish larvae. In the 5mg/L dose, synapsin IIa expression up-regulation was seen concomitantly with down-regulation of dat expression, showing a potential compensatory mechanism. Moreover, the 10mg/L exposure caused an increase in heart rate, in absolute turn angle, brain cell damage and a decrease in dopamine levels. These alterations may be associated with autophagosome formation found in GO-exposed larval brain. No changes were observed on higher doses of GO exposure, probably due to nanomaterial agglomeration. Taken together, these results show that toxic effects of GO exposure are not dose-dependent, and are preeminent in lower concentrations. Additional studies are needed to deepen the specific mechanisms of GO neurotoxicity and are required to elucidate its potential biomedical use.

Assessment of the developmental and neurotoxicity of the mosquito control larvicide, pyriproxyfen, using embryonic zebrafish.

In 2014, as an attempt to address the Zika health crisis by controlling the mosquito population, Brazil took the unprecedented action of applying a chemical larvicide, pyriproxyfen, to drinking water sources. The World Health Organization has established an acceptable daily intake of pyriproxyfen to be 100 µg per kg of body weight per day, but studies have demonstrated that at elevated doses (>5000 mg/kg), there are adverse effects in mice, rats and dogs. To better understand the potential developmental toxicity of pyriproxyfen, we utilized the embryonic zebrafish. Our results demonstrate that the concentration resulting in 50% of animals presenting adverse morphological effects (EC50), including craniofacial defects, was 5.2 µM for daily renewal exposure, and above this concentration, adverse behavioral effects were also observed in animals that followed a static exposure regimen. Thus, zebrafish data suggest that the developmental toxicity of pyriproxyfen may not be limited to insects.

Saxitoxins induce cytotoxicity, genotoxicity and oxidative stress in teleost neurons in vitro.

The aim of this study was establish a protocol for isolation and primary culture of neurons from tropical freshwater fish species Hoplias malabaricus for assessment of the effects of neurotoxic substances as saxitoxins (STXs). Cells from brain of H. malabaricus were treated with different concentrations of trypsin, dispase and papain for tissue dissociation. Cells type was separated by cellular gradient and basic fibroblast growth factor (bFGF) supplement nutrition media were added. The dissociated cells were plated with medium and different STXs concentrations and the toxic cellular effects such as oxidative stress, neurotoxicity, and genotoxicity and apoptosis process were evaluated. Cultures treated with bFGF showed the greatest adherence, survival and cellular development. STXs increased specific activity of glutathione peroxidase and lipoperoxidation levels, were cytotoxic and genotoxic indicated by the comet assay. Although the STXs effects due the blockage of sodium channels is reported to be reversible, the time exposure and concentration of STXs suggested cellular injuries which can lead to neuropathology. The establishment of primary neuronal culture protocol enables new applications for neurotoxicological assessments.

Abordagem inicial no atendimento ambulatorial em distúrbios neurotoxicológicos: parte III - solventes orgânicos / Initial approach to outpatient treatment of neurotoxicological disorders: Part III – organic solvents

Introdução: Milhões de pessoas são expostas diariamente aos solventes. Inúmeros solventes podem causar intoxicação aguda. Menos clara é a associação da exposição crônica e em baixas doses poder produzir alteração neurológica. Diversas atividades ocupacionais estão envolvidas com a sua exposição. Condição bastante diferente é o seu uso inadvertido com intuito alucinógeno. Método: Trata-se de revisão atualizada da literatura a partir de pesquisa na base de dados MEDLINE e LILACS. Também utilizou-se livros e documentos publicados em formato eletrônico.Discussão: Distúrbios neuromusculares, distúrbios do movimento, alterações cognitivo-comportamentais e neurofisiológicas têm sido relacionados a inúmeros agentes tóxicos nos últimos anos. A proposta deste artigo é revisar os principais distúrbios neurológicos associados à exposição crônica por solventes orgânicos. A fim de facilitar a abordagem inicial no atendimento ambulatorial aos distúrbios neurotoxicológicos foram confeccionadas tabelas descrevendo os principais agentes tóxicos, as fontes de exposição envolvidas e suas principais manifestações neurológicas. Conclusão: Tolueno, bissulfeto de carbono e n-Hexano são alguns solventes envolvidos nos distúrbios neurotoxicológicos, Contudo, fica evidente nesta revisão que são necessários novos estudos a fim de determinar a real associação destes e outros solventes nos distúrbios crônicos do sistema nervoso central e periférico.

Introduction: Millions of peoples are exposed to solvents every day. Most solvents cause acute intoxication. Less evident is the association of chronic exposure and in low doses in producing neurological disorders. Innumerable occupational activities are involved in the exposure to solvents. Their inadvertent use with hallucinogenous intention is an entirely different condition. Method: The method consists of an updated review of the literature based on research in the MEDLINE and LILACS databases, as well as books and documents published online. Discussion: Neuromuscular disorders, movement disorders, cognitive-behavioral and neurophysiological changes have been attributed to innumerable toxic agents in recent years. This article proposes to review the main neurological disorders associated with chronic exposure to organic solvents. To facilitate the initial approach to treatment of neurotoxicological disorders of outpatient, tables were devised to describe the main toxic agents, the sources of exposure involved and their main neurological manifestations. Conclusions: Toluene, carbon bisulfate and n-hexane are some of the solvents involved in neurotoxicological disorders. However, this review reveals the need for new studies to determine the real association of these and other solvents in chronic disorders of the central and peripheral nervous systems.

Abordagem inicial no atendimento ambulatorial em distúrbiosneurotoxicológicos. Parte II - agrotóxicos / Initial approach to outpatient treatment of neurotoxicological disorders. Part II – pesticides

Introdução: A venda de agrotóxicos no Brasil representa 86% do mercado consumidor da América Latina, com um faturamento anual que chega a US$ 7 bilhões. O desconhecimento e a falta de percepção dos riscos inerentes a utilização dessas substâncias é constatada com frequência aumentando as chances de intoxicação por tais agentes. Métodos: Trata-se de revisão atualizada da literatura a partir de pesquisa na base de dados MEDLINE e LILACS. Também utilizaram-se livros e documentos publicados em formato eletrônico. Resultados e discussão: Distúrbios neuromusculares, distúrbios do movimento, alterações cognitivo-comportamentais e neurofisiológicas têm sido relacionados a inúmeros agentes tóxicos nos últimos anos. A proposta deste artigo é revisar os principais distúrbios neurológicos associados à exposição crônica por agrotóxicos. A fim de facilitar a abordagem inicial no atendimento ambulatorial aos distúrbios neurotoxicológicos foram confeccionadas tabelas descrevendo os principais agentes tóxicos, as fontes de exposição envolvidas e suas principais manifestações neurológicas. Conclusão: Inseticidas, herbicidas, fungicidas e fumigantes são alguns agrotóxicos envolvidos nos distúrbios neurotoxicológicos. Contudo, fica evidente nesta revisão que são necessários novos estudos a fim de determinar a real associação destes e outros agrotóxicos nos distúrbios crônicos do sistema nervoso central e periférico.

Introduction: The sale of pesticides in Brazil represents 86% of the Latin American consumer market, with annual revenues reachingup to US$ 7 billion. Lack of knowledge and unawareness of the risks inherent to the use of these substances is frequently found, increasingthe possibility of intoxication by these agents. Methods: The method consists of an updated review of the literature based on research in theMEDLINE and LILACS databases, as well as books and documents published online. Results and discussion: Neuromusculardisorders, movement disorders, cognitive-behavioral and neurophysiologic alterations have been attributed to innumerable toxic agents in recentyears. This article proposes to review the main neurological disorders associated with chronic exposure to pesticides. To make easy the initialapproach to outpatient treatment of neurotoxicological disorders, tables were devised to describe the main toxic agents, the sources of exposureinvolved and their main neurological manifestations. Conclusion: Insecticides, herbicides, fungicides and fumigants are some of the pesticides involved in neurotoxicological disorders. However, this review reveals the need for new studies to determine the real association of these and other pesticides in chronic disorders of the central and peripheral nervous systems.

Abordagem inicial no atendimento ambulatorial em distúrbios neurotoxicológicos. Parte I - metais / Initial approach to outpatient treatment of neurotoxicological disorders. Part I – metals

Introdução: A toxicologia é uma ciência que envolve inúmeros sistemas necessitando de uma equipe multiprofissional e interdisciplinar. A indistinção clínica entre as doenças ocupacionais e não ocupacionais dificulta o seu diagnóstico. Nesse contexto, a neurotoxicologia ocupacional e ambiental estuda os distúrbios do sistema nervoso central (SNC) e periférico (SNP) decorrente da intoxicação dos mais variados agentes. Método: Trata-se de revisão atualizada da literatura a partir de pesquisa na base de dados MEDLINE e LILACS. Também utilizou-se livros e documentos publicados em formato eletrônico. Resultados e Discussão: Distúrbios neuromusculares, distúrbios do movimento, doença do neurônio motor, alterações cognitivocomportamentais e neurofisiológicas têm sido relacionados a inúmeros agentes tóxicos nos últimos anos. A proposta deste artigo é revisar os principais distúrbios neurológicos associados à exposição crônica por metais. A fim de facilitar a abordagem inicial no atendimento ambulatorial aos distúrbios neurotoxicológicos foram confeccionadas tabelas descrevendo os principais agentes tóxicos, as fontes de exposição envolvidas e suasprincipais manifestações neurológicas. Conclusão: Arsênio, chumbo, mercúrio, manganês, cádmio e estanho são alguns metais envolvidos nos distúrbios neurotoxicológicos. Contudo, fica evidente nesta revisão que são necessários novos estudos a fim de determinar a real associação destes e outros metais nos distúrbios crônicos do sistema nervoso central e periférico.

Introduction: Toxicology is a science that involves innumerable systems and requires a multiprofessional and interdisciplinary team. The clinical indistinctiveness of occupational and non-occupational disorders makes their diagnosis difficult. In this context, occupational and environmental toxicology studies the disorders of the central nervous system (CNS) and the peripheral nervous system (PNS) resulting from intoxication by a wide variety of agents. Method: The method consists of an updated review of the literature based on research in the MEDLINE and LILACS databases, as well as books and documents published online. Results and Discussion: Neuromuscular disorders, movement disorders, motor neuron disease, cognitive-behavioral and neurophysiological alterations have been attributed to innumerable toxic agents in recent years. This article proposes to review the main neurological disorders associated with chronic exposure to metals. To facilitate the initial approach to outpatient treatment of neurotoxicological disorders, tables were devised to describe the main toxic agents, the sources of exposure involved and their main neurological manifestations. Conclusions: Arsenic, lead, mercury, manganese, cadmium and tin are some of the metals involved in neurotoxicological disorders. However, this review reveals the need for new studies to determine the real association of these and other metals in chronic disorders of the central and peripheral nervous systems.

Impairment of color spatial vision in chronic alcoholism measured by psychophysical methods

We used psychophysical tests to evaluate spatial vision in 15 subjects with a clinical history of chronic alcoholism by measuring luminance contrast sensitivity and color discrimination. The subjects were initially subjected to clinical inquiry and ophthalmological exam. Subjects then performed psychophysical tests to measure spatial contrast thresholds using sine wave gratings of different spatial frequencies and contrasts and chromatic discrimination thresholds using the Mollon-Reffin test. For the analysis, subjects were divided into three groups according to age and compared with age-matched controls. Ten subjects had some degree of color vision loss, which was quite severe in seven cases. All subjects had normal luminance contrast sensitivity. The results suggest that color vision changes related to chronic alcoholism can occur in the absence of impairment of spatial luminance contrast sensitivity and thus is an important aspect to be considered in the clinical evaluation of this condition.(AU)

Impairment of color spatial vision in chronic alcoholism measured by psychophysical methods

We used psychophysical tests to evaluate spatial vision in 15 subjects with a clinical history of chronic alcoholism by measuring luminance contrast sensitivity and color discrimination. The subjects were initially subjected to clinical inquiry and ophthalmological exam. Subjects then performed psychophysical tests to measure spatial contrast thresholds using sine wave gratings of different spatial frequencies and contrasts and chromatic discrimination thresholds using the Mollon-Reffin test. For the analysis, subjects were divided into three groups according to age and compared with age-matched controls. Ten subjects had some degree of color vision loss, which was quite severe in seven cases. All subjects had normal luminance contrast sensitivity. The results suggest that color vision changes related to chronic alcoholism can occur in the absence of impairment of spatial luminance contrast sensitivity and thus is an important aspect to be considered in the clinical evaluation of this condition.

Atividade colinesterásica cerebral e comportamento de ratos após exposição perinatal ao diclorvós

The organophosphate dichlorvos impregnated into plastic collars (8.37%) is used in veterinary practice as an alternative for the control of ectoparasites in dogs and cats. The aim of this work was to determine the possible toxic effects of these collars in female Wistar rats during pregnancy and lactation, as a possible cause of alterations in brain cholinesterase activity and behavior of offspring. At weaning, there was no difference in brain cholinesterase activity between control and treated dams, nor between their respective offspring as well. The treatment did not affect the general behavior of the offspring, when evaluated in the open field, nor anxiety in the elevated plus-maze, both evaluated on the 35th postnatal day.

O organofosforado diclorvós impregnado em coleiras plásticas é um recurso utilizado em medicina veterinária que visa ao controle de ectoparasitas de cães e gatos. O objetivo deste trabalho foi avaliar os efeitos do uso de coleiras plásticas impregnadas com diclorvós (8,37%) em ratas Wistar durante o período de gestação e lactação, como possível fonte de alterações comportamentais e da atividade colinesterásica cerebral dos filhotes. Na desmama, não houve diferença na atividade colinesterásica cerebral entre as mães tratadas com diclorvós e o grupo controle, bem como entre os respectivos filhotes. O tratamento com diclorvós também não influenciou no comportamento geral dos animais, avaliado no campo aberto, nem no nível de ansiedade testado no labirinto em cruz elevado, ambos aos 35 dias pós-natal.