Adolescent Health Series: The status of adolescent mental health research, practice and policy in sub-Saharan Africa: A narrative review.

Sub-Saharan Africa (SSA) has the fastest growing adolescent population in the world. In addition to developmental changes, adolescents in SSA face health and socioeconomic challenges that increase their vulnerability to mental ill-health. This paper is a narrative review of adolescent mental health (AMH) in SSA with a focus on past achievements, current developments, and future directions in the areas of research, practice and policy in the region. We describe the status of AMH in the region, critical factors that negatively impact AMH, and the ways in which research, practice and policy have responded to this need. Depression, anxiety and post-traumatic stress disorders are the most common mental health problems among adolescents in SSA. Intervention development has largely been focused on HIV/AIDS service delivery in school or community programs by non-specialist health workers. There is a severe shortage of specialised AMH services, poor integration of services into primary health care, lack of a coordinated inter-sectoral collaboration, and the absence of clear referral pathways. Policies for the promotion of AMH have been given less attention by policymakers, due to stigma attached to mental health problems, and an insufficient understanding of the link between mental health and social determinants, such as poverty. Given these gaps, traditional healers are the most accessible care available to help-seeking adolescents. Sustained AMH research with a focus on the socioeconomic benefits of implementing evidence-based, contextually adapted psychosocial interventions might prove useful in advocating for much needed policies to improve AMH in SSA.

Ketamine plus Alcohol: What We Know and What We Can Expect about This.

Drug abuse has become a public health concern. The misuse of ketamine, a psychedelic substance, has increased worldwide. In addition, the co-abuse with alcohol is frequently identified among misusers. Considering that ketamine and alcohol share several pharmacological targets, we hypothesize that the consumption of both psychoactive substances may synergically intensify the toxicological consequences, both under the effect of drugs available in body systems and during withdrawal. The aim of this review is to examine the toxicological mechanisms related to ketamine plus ethanol co-abuse, as well the consequences on cardiorespiratory, digestive, urinary, and central nervous systems. Furthermore, we provide a comprehensive discussion about the probable sites of shared molecular mechanisms that may elicit additional hazardous effects. Finally, we highlight the gaps of knowledge in this area, which deserves further research.

Contributing to Understand the Crosstalk between Brain and Periphery in Methylmercury Intoxication: Neurotoxicity and Extracellular Vesicles.

Human exposure to methylmercury (MeHg) is currently high in regions such as the Amazon. Understanding the molecular changes associated with MeHg-induced neurotoxicity and the crosstalk with the periphery is essential to support early diagnoses. This work aimed to evaluate cellular and molecular changes associated with behavioral alterations in MeHg acute exposure and the possible changes in extracellular vesicles (EVs) number and S100ß content. Adults male Wistar rats were orally treated with 5 mg/kg for four days. Behavioral performance, molecular and histological changes in the cerebellum, and plasma EVs were assessed. MeHg-intoxicated animals performed significantly worse in behavioral tests. MeHg increased the number of GFAP+ cells and GFAP and S100ß mRNA expression in the cerebellum but no change in NeuN+ or IBA-1+ cells number was detected. The number of exosomes isolated from plasma were decreased by the metal. S100B mRNA was detected in circulating plasma EVs cargo in MeHg exposure. Though preliminary, our results suggest astrocytic reactivity is displaying a protective role once there was no neuronal death. Interestingly, the reduction in exosomes number could be a new mechanism associated with MeHg-induced neurotoxicity and plasma EVs could represent a source of future biomarkers in MeHg intoxication.

Methylmercury plus Ethanol Exposure: How Much Does This Combination Affect Emotionality?

Mercury is a heavy metal found in organic and inorganic forms that represents an important toxicant with impact on human health. Mercury can be released in the environment by natural phenoms (i.e., volcanic eruptions), industrial products, waste, or anthropogenic actions (i.e., mining activity). Evidence has pointed to mercury exposure inducing neurological damages related to emotional disturbance, such as anxiety, depression, and insomnia. The mechanisms that underlie these emotional disorders remain poorly understood, although an important role of glutamatergic pathways, alterations in HPA axis, and disturbance in activity of monoamines have been suggested. Ethanol (EtOH) is a psychoactive substance consumed worldwide that induces emotional alterations that have been strongly investigated, and shares common pathophysiological mechanisms with mercury. Concomitant mercury and EtOH intoxication occur in several regions of the world, specially by communities that consume seafood and fish as the principal product of nutrition (i.e., Amazon region). Such affront appears to be more deleterious in critical periods of life, such as the prenatal and adolescence period. Thus, this review aimed to discuss the cellular and behavioral changes displayed by the mercury plus EtOH exposure during adolescence, focused on emotional disorders, to answer the question of whether mercury plus EtOH exposure intensifies depression, anxiety, and insomnia observed by the toxicants in isolation.

From Molecules to Behavior in Long-Term Inorganic Mercury Intoxication: Unraveling Proteomic Features in Cerebellar Neurodegeneration of Rats.

Mercury is a severe environmental pollutant with neurotoxic effects, especially when exposed for long periods. Although there are several evidences regarding mercury toxicity, little is known about inorganic mercury (IHg) species and cerebellum, one of the main targets of mercury associated with the neurological symptomatology of mercurial poisoning. Besides that, the global proteomic profile assessment is a valuable tool to screen possible biomarkers and elucidate molecular targets of mercury neurotoxicity; however, the literature is still scarce. Thus, this study aimed to investigate the effects of long-term exposure to IHg in adult rats' cerebellum and explore the modulation of the cerebellar proteome associated with biochemical and functional outcomes, providing evidence, in a translational perspective, of new mercury toxicity targets and possible biomarkers. Fifty-four adult rats were exposed to 0.375 mg/kg of HgCl2 or distilled water for 45 days using intragastric gavage. Then, the motor functions were evaluated by rotarod and inclined plane. The cerebellum was collected to quantify mercury levels, to assess the antioxidant activity against peroxyl radicals (ACAPs), the lipid peroxidation (LPO), the proteomic profile, the cell death nature by cytotoxicity and apoptosis, and the Purkinje cells density. The IHg exposure increased mercury levels in the cerebellum, reducing ACAP and increasing LPO. The proteomic approach revealed a total 419 proteins with different statuses of regulation, associated with different biological processes, such as synaptic signaling, energy metabolism and nervous system development, e.g., all these molecular changes are associated with increased cytotoxicity and apoptosis, with a neurodegenerative pattern on Purkinje cells layer and poor motor coordination and balance. In conclusion, all these findings feature a neurodegenerative process triggered by IHg in the cerebellum that culminated into motor functions deficits, which are associated with several molecular features and may be related to the clinical outcomes of people exposed to the toxicant.

Methylmercury intoxication and cortical ischemia: Pre-clinical study of their comorbidity.

Stroke is one of the main causes of human disability worldwide. Ischemic stroke is mostly characterized by metabolic collapse and fast tissue damage, followed by secondary damage in adjacent regions not previously affected. Heavy metals intoxication can be associated with stroke incidence, because of their damaging action in the vascular system. Mercury, in particular, possesses a high tropism by metabolically active regions, such as the brain. In the present study we sought to evaluate whether methylmercury (MeHg) intoxication can aggravate the tissue damage caused by an ischemic stroke induced by microinjections of endothelin-1 (ET-1) into the motor cortex of adult rats. Following MeHg intoxication by gavage (0.04 mg/kg/day) during 60 days, the animals were injected with ET-1 (1 µl, 40 pmol/µl) or vehicle (1 µl). After 7 days, all animals were submitted to behavioral tests and then their brains were processed to biochemical and immunohistochemical analyses. We observed that long-term MeHg intoxication promoted a significant Hg deposits in the motor cortex, with concomitant increase of microglial response, followed by reduction of the neuronal population following ischemia and MeHg intoxication, as well as disturbance in the antioxidant defense mechanisms by misbalance of oxidative biochemistry with increase of both lipid peroxidation and nitrite levels, associated to behavioral deficits. MeHg exposure and cortical ischemia demonstrated that both injuries are able of causing significant neurobehavioural impairments in motor coordination and learning accompanied of an exacerbated microglial activation, oxidative stress and neuronal loss in the motor cortex, indicating that MeHg as a source of metabolic disturbance can act as an important increasing factor of ischemic events in the brain.

Anti-Inflammatory and Antinociceptive Studies of Hydroalcoholic Extract from the Leaves of Phyllanthus brasiliensis (Aubl.) Poir. and Isolation of 5-O-ß-d-Glucopyranosyljusticidin B and Six Other Lignans.

The aim of this study was to investigate the chemical composition and the antiinflammatory/antinociceptive properties of the hydroalcoholic extract derived from the leaves of Phyllanthus brasiliensis (HEPB) in rodents. A new arylnaphthalene lignan glycoside, 5-O-ß-d-glucopyranosyljusticidin B, together with six known lignans, were isolated from HEPB. 1D and 2D NMR experiments and HRMS were used to elucidate the structure of the new compound. HEPB toxicity and antinociceptive activity were evaluated through acute oral toxicity and formalin models in mice, respectively. The anti-inflammatory effects of HEPB were assessed using carrageenan- and dextran-induced paw edema models in rats. HEPB showed low toxicity. Oral administration of HEPB reduced paw edema induced by carrageenan, but not by dextran. HEPB and its fractions from FR6 to FR10 (FR6-10) inhibited the neurogenic and inflammatory phases of formalin-induced linking, demonstrating its antinociceptive activity. These results indicated that lignans from Phyllanthus brasiliensis exerted antinociceptive/anti-inflammatory effects not related to the histaminergic pathway.

Alveolar bone loss induced by chronic ethanol consumption from adolescence to adulthood in Wistar rats.

Though there are literature indicating the bone loss due to alcohol consumption, studies on the association between ethanol consumption and periodontal breakdown in animals are either scarce or have provided conflicting results. Here, we investigated the effects of chronic alcohol exposure from adolescence to adulthood on the alveolar bone in rats. Wistar rats were exposed to ethanol (6.5 g/kg/day) in a solution of 22.5% (w/v) or distilled water (control) by gavage from 35 days of age (adolescent) until 90 days (adulthood). Evaluation of the bone loss was performed using scanning electronic microscopy, in which the distances between the cement-enamel junction and the alveolar bone crest from the palatal side of the first molar mandibular were measured. The measurements obtained were tabulated and analyzed using Student's t-test. Alcohol-treated group revealed greater bone loss in comparison to the control group. These findings indicate that heavy chronic alcohol exposure from adolescent to adulthood can induce alveolar bone loss in rats associated to absence of periodontitis.

Masticatory deficiency as a risk factor for cognitive dysfunction.

Several studies have demonstrated that chewing helps to maintain cognitive functions in brain regions including the hippocampus, a central nervous system (CNS) region vital for memory and learning. Epidemiological studies suggest that masticatory deficiency is associated with development of dementia, which is related to spatial memory deficits especially in older animals. The purpose of this paper is to review recent work on the effects of masticatory impairment on cognitive functions both in experimental animals and humans. We show that several mechanisms may be involved in the cognitive deficits associated with masticatory deficiency. The epidemiological data suggest a positive correlation between masticatory deficit and Alzheimer's disease. It may be concluded that chewing has important implications for the mechanisms underlying certain cognitive abilities.

Erratum: Scaling up the task-sharing of psychological therapies: A formative study of the PEERS smartphone application for supervision and quality assurance in rural India - CORRIGENDUM.

[This corrects the article DOI: 10.1017/gmh.2024.11.].

Scaling up the task-sharing of psychological therapies: A formative study of the PEERS smartphone application for supervision and quality assurance in rural India.

Measurement-based peer supervision is one strategy to assure the quality of psychological treatments delivered by non-mental health specialist providers. In this formative study, we aimed to 1) describe the development and 2) examine the acceptability and feasibility of PEERS (Promoting Effective mental healthcare through peER Supervision)-a novel smartphone app that aims to facilitate registering and scheduling patients, collecting patient outcomes, rating therapy quality and assessing supervision quality-among frontline treatment providers delivering behavioral activation treatment for depression. The PEERS prototype was developed and tested in 2021, and version 1 was launched in 2022. To date, 215 treatment providers (98% female; ages 30-35) in Madhya Pradesh and Goa, India, have been trained to use PEERS and 65.58% have completed the supplemental, virtual PEERS course. Focus group discussions with 98 providers were examined according to four themes-training and education, app effectiveness, user experience and adherence and data privacy and safety. This yielded commonly endorsed facilitators (e.g., collaborative learning through group supervision, the convenience of consolidated patient data), barriers (e.g., difficulties with new technologies) and suggested changes (e.g., esthetic improvements, suicide risk assessment prompt). The PEERS app has the potential to scale measurement-based peer supervision to facilitate quality assurance of psychological treatments across contexts.

Physical training mitigates alveolar bone and blood enzymatic antioxidants defense impairment induced by binge ethanol consumption in rats.

We aimed to investigate the effectiveness of physical training as a protective strategy to mitigate alveolar bone damage and blood antioxidant defense caused by ethanol (EtOH) consumption in a binge-drinking pattern. Male Wistar rats aged approximately 90 days were divided into four groups: control, training, EtOH, and training + EtOH. The physical training protocol was conducted on a treadmill for four consecutive weeks, while the animals in the EtOH group were administered EtOH via orogastric gavage for three consecutive days each week, following the binge drink pattern. After the training period, blood and mandibles were collected for plasma oxidative biochemistry analysis, and the alveolar bone was subjected to physicochemical composition analysis, tissue evaluation, and microtomography evaluation. Our results showed that EtOH induced oxidative stress and physical exercise promoted the recovery of antioxidant action. Physical training minimized the damage to the mineral/matrix composition of the alveolar bone due to EtOH consumption and increased the density of osteocytes in the trained group treated with EtOH than in those exposed only to EtOH. Furthermore, physical training reduced damage to the alveolar bone caused by EtOH consumption. Our findings suggest that physical training can serve as an effective strategy to reduce systemic enzymatic oxidative response damage and alleviate alveolar bone damage resulting from alcohol consumption. Further investigations are warranted to elucidate the underlying mechanisms and explore, in addition to physical training, the potential effects of other activities with varying intensities on managing alcohol-induced bone damage.

Ethanol binge drinking exposure during adolescence displays long-lasting motor dysfunction related to cerebellar neurostructural damage even after long-term withdrawal in female Wistar rats.

Ethanol is one of the psychoactive substances most used by young individuals, usually in an intermittent and episodic manner, also called binge drinking. In the adolescent period, brain structures undergo neuromaturation, which increases the vulnerability to psychotropic substances. Our previous studies have revealed that ethanol binge drinking during adolescence elicits neurobehavioral alterations associated with brain damage. Thus, we explored the persistence of motor function impairment and cerebellum damage in the context of ethanol withdrawal periods (emerging adulthood and adult life) in adolescent female rats. Female Wistar rats (35 days old) received orally 4 cycles of ethanol (3.0 g/kg/day) or distilled water in 3 days on-4 days off paradigm (35th until 58th day of life). Motor behavioral tests (open field, grip strength, beam walking, and rotarod tests) and histological assays (Purkinje's cell density and NeuN-positive cells) were assessed on the 1-, 30-, and 60-days of binge alcohol exposure withdrawal. Our findings demonstrate that the adolescent binge drinking exposure paradigm induced cerebellar cell loss in all stages evaluated, measured through the reduction of Purkinje's cell density and granular layer neurons. The cerebellar tissue alterations were accompanied by behavioral impairments. In the early withdrawal, the reduction of spontaneous movement, incoordination, and unbalance was seen. However, the grip strength reduction was found at long-term withdrawal (60 days of abstinence). The cerebellum morphological changes and the motor alterations persisted until adulthood. These data suggest that binge drinking exposure during adolescence causes motor function impairment associated with cerebellum damage, even following a prolonged withdrawal, in adult life.

Neurotoxicology of alcohol: a bibliometric and science mapping analysis.

Alcohol consumption is common in many societies and has increased considerably, resulting in many socioeconomic and public health problems. In this sense, studies have been carried out in order to understand the mechanisms involved in alcohol consumption and related harmful effects. This study aimed to identify and map the knowledge and to perform bibliometric analysis of the neurotoxicology of alcohol based on the 100 most cited articles. A search was carried out in the Web of Science Core Collection database and information was extracted regarding the journal, authors, keywords, year of publication, number of citations, country and continent of the corresponding author. For each selected manuscript, the study design, alcohol exposure model, dose, period of exposure, and effect on the central nervous system and research hotspots were mapped. The journal with the highest number of publications was Alcoholism: Clinical and Experimental Research (n = 11 papers), the author who contributed the most was Crews FT (n = 8 papers), the studies had a total of 288 keywords and 75% of the publications were from the United States of America. The experimental studies evaluated the effects of prenatal and postnatal exposure and were conducted in rats and mice using doses ranging from 2.5 to 14 g/kg/day, with administration by subcutaneous, intraperitoneal, intragastric, or inhalation route or with free access through drinking bottles. Among the studies mapped, the oldest one (1989) aimed to understand the systemic damage and mechanisms of action involved, while the most recent focused on understanding the receptors and mechanisms involved in addiction, as well as genetic factors. Our results show the panorama of the most widespread scientific production in the scientific community on the neurotoxicology of ethanol, a high prevalence was observed in studies that addressed fetal alcohol syndrome and/or the effects of ethanol on neurodevelopment.

Common strategies in empirically supported psychological interventions for alcohol use disorders: A meta-review.

ISSUES: Despite the large number of effective psychological interventions for alcohol use disorders (AUD), there is still a lack of clarity concerning the strategies that make these interventions effective. APPROACH: The overall goal of this review was to identify, examine and synthesise the information about common strategies from evidence-based psychological interventions for AUDs by conducting a review of systematic reviews, that is, a meta-review. We isolated the relevant primary studies from eligible systematic reviews and extracted information about the interventions from these studies to understand the strategies used. Analysis was restricted to narrative summaries. KEY FINDINGS: Thirteen reviews were eligible for inclusion in our meta-review. Of these, eight demonstrated the effectiveness of a range of psychological interventions-behavioural couples therapy, cognitive behaviour therapy combined with motivational interviewing, brief interventions, contingency management, psychotherapy plus brief interventions, Alcoholics Anonymous and 12-step treatment programs, family-therapy or family-involved treatment, and community reinforcement approach. The most commonly used component strategies in effective interventions for AUDs included assessment, personalised feedback, motivational interviewing, goal setting, setting and review of homework, problem solving skills and relapse prevention/management. IMPLICATIONS: Evidence about commonly used strategies in evidence-based psychological interventions for AUDs offer the possibility of creating menu-driven interventions that can be tailored to respond to individual client needs and preferences in different contexts.

Physical Exercise Mitigates Salivary Gland and Saliva Damages in Rats Exposed to Binge-like Ethanol Pattern.

Heavy episodic ethanol (EtOH) consumption is a typical pattern, especially among younger people. The therapeutic effect of exercise on EtOH damage has not yet been fully elucidated. Therefore, this study aims to investigate whether moderate exercise can reduce the damage generated by ethanol consumption in salivary glands and saliva. Thus, 32 male Wistar rats were divided into four groups: control (sedentary animals treated with water); training (trained animals treated with EtOH); EtOH (sedentary animals treated with EtOH); and EtOH + training (trained animals treated with ethanol). EtOH was administered to the animals at a dose of 3 g/kg/day at a concentration of 20% w/v for three consecutive days per week via intragastric gavage. The training was performed on a treadmill for five successive days. At the end of the 4-week experimental protocol, the animals were euthanized, and salivary glands and saliva were collected for oxidative biochemistry analysis. Our results showed that EtOH consumption generated changes in the oxidative biochemistry of the salivary glands and saliva. Thus, it was possible to conclude that moderate physical exercise can significantly recover antioxidant activity, reducing the damage generated by EtOH.

Aerobic Physical Training Attenuates Oxidative Stress in the Spinal Cord of Adult Rats Induced by Binge-like Ethanol Intake.

Binge drinking is the most frequent consumption pattern among young adults and remarkably changes the central nervous system; thus, research on strategies to protect it is relevant. This study aimed to investigate the detrimental effects of binge-like EtOH intake on the spinal cord of male rats and the potential neuroprotective effects provided by moderate-intensity aerobic physical training. Male Wistar rats were distributed into the 'control group', 'training group', 'EtOH group', and 'training + EtOH'. The physical training protocol consisted of daily 30-min exercise on a treadmill for 5 consecutive days followed by 2 days off during 4 weeks. After the fifth day of each week, distilled water ('control group' and 'training group') or 3 g/kg of EtOH diluted at 20% w/v ('EtOH group' and 'training + EtOH group') was administered for 3 consecutive days through intragastric gavage to simulate compulsive consumption. Spinal cord samples were collected for oxidative biochemistry and morphometric analyses. The binge-like EtOH intake induced oxidative and tissue damage by decreasing reduced glutathione (GSH) levels, increasing lipid peroxidation (LPO), and reducing motor neurons (MN) density in the cervical segment. Even under EtOH exposure, physical training maintained GSH levels, reduced LPO, and prevented MN reduction at the cervical segment. Physical training is a non-pharmacological strategy to neuroprotect the spinal cord against oxidative damage induced by binge-like EtOH intake.

One binge-type cycle of alcohol plus ketamine exposure induces emotional-like disorders associated with oxidative damage in adolescent female rats.

Drug abuse is a global public health problem among adolescents, with alcohol often used in association with other psychotropic drugs, such as ketamine. Considering the scarcity of evidence, this study aimed to investigate emotional behavioral effects induced by ethanol plus ketamine co-abuse, as well as oxidative biochemistry, and neurotrophic mediator in the prefrontal cortex and hippocampus in the early withdrawal of adolescent female rats. Animals were divided into control, ethanol, ketamine, and ethanol plus ketamine groups. The protocol administration was performed for 3 consecutive days (binge-like pattern). Behavioral assays of open field, elevated plus maze, and forced swim test were performed. After that, the prefrontal cortex and hippocampus were collected to evaluate oxidative biochemistry (reactive oxygen species-ROS; Antioxidant capacity against peroxyl radicals-ACAP; and lipid peroxidation). We found that isolated or combined ethanol and ketamine exposure displayed anxiety- and depressive-like profile, in a non-synergistically manner during early withdrawal. However, oxidative damage was aggravated in the co-administered animals than in isolated exposed subjects. We concluded that ethanol plus ketamine co-abuse may intensify oxidative damage in the hippocampus and prefrontal cortex in the early withdrawal of adolescent female rats, which was not reflected in the emotional behavioral phenotype. DATA AVAILABILITY STATEMENT: The datasets used and/or analyzed during the current investigation are available upon reasonable request from the corresponding author.

A Multicentre Study of the Clinical and Epidemiological Profile of Inflammatory Bowel Disease in Northeast Brazil.

Purpose: Ulcerative colitis (UC) and Crohn's disease (CD) are inflammatory bowel diseases (IBDs) with multifactorial causes. They are becoming more prevalent in developing countries such as Brazil; however, relevant studies in poorer regions of the country are limited. Here, we report the clinical-epidemiological profile of patients with IBD treated at reference centers in three states of Northeast Brazil. Patients and Methods: This was a prospective cohort study involving patients at referral outpatient clinics for IBD from January 2020 through December 2021. Results: Of 571 patients with IBD, 355 (62%) had UC, and 216 (38%) had CD. The patients were predominantly women (355, 62%) for both UC and CD. Extensive colitis was the pattern present in 39% of the UC cases. For CD, ileocolonic disease was the predominant manifestation (38%), with 67% of cases showing penetrating and/or stenosing behavior. The majority of patients were diagnosed between the ages of 17 and 40, corresponding to 60.2% in CD and 52.7% in UC. The median time between symptom onset and diagnosis was 12 months for CD and 8 months for UC (p=0.042). Joint involvement was the most frequent extraintestinal manifestation, with arthralgia and arthritis present in 41.9% and 18.6% of the patients, respectively. Biological therapy was prescribed to 73% of CD patients and 26% of UC patients. A progressive increase in new cases was observed in every 5-year interval over the last five decades, with 58.6% being diagnosed in the last 10 years. Conclusion: More extensive disease behavior patterns predominated in UC, while forms associated with complications were prevalent in CD. A prolonged time to diagnosis may have contributed to these findings. A progressive increase in IBD incidence was observed and may be related to greater urbanization and better access to specialized outpatient clinics, resulting in improvements in diagnosis.

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.