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BACKGROUND: The prevalence of marijuana use and its derivatives has surged over the past century, largely due to increasing legalization globally. Despite arguments advocating its benefits, marijuana smoking exposes the lungs to harmful combustion byproducts, leading to various respiratory issues such as asthma, pneumonia, emphysema, and chronic obstructive pulmonary disease. METHODS: We embarked on an extensive literature search, utilizing PubMed/Medline, Scopus, Web of Science, and Google Scholar databases, identifying 200 studies. After the elimination of duplicates, and meticulous review of abstracts and full texts, 55 studies were included in our analysis. RESULTS: Current literature demonstrates that marijuana use negatively impacts lung function, triggering symptoms like chronic cough, sputum production, and wheezing, and diminishing FEV1/FVC ratio in spirometry tests. Moreover, prolonged or chronic marijuana use augments the risk of respiratory function impairment. While the carcinogenic effects of marijuana are still contested, a weak correlation between marijuana use and lung cancer has been observed in some studies. Additionally, instances of other pathologies linked to marijuana use have been reported, including the development of COPD, pulmonary bullae, spontaneous pneumothorax, pleuritic pain, chronic pulmonary aspergillosis, hemoptysis, and pulmonary Langerhans cell histiocytosis. CONCLUSIONS: The evidence underscores that marijuana use is detrimental to respiratory health. In light of the escalating trend of marijuana use, particularly among the youth, it is imperative to advocate public health messages discouraging its consumption.

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Neotropical fish Cnesterodon decemmaculatus were exposed to different sublethal concentrations (0.5, 1.0 and 5.0 mg As/L) of sodium arsenite (As III) to determine the median lethal concentration (LC50; 96 h) and to evaluate the response of a set of biomarkers (genotoxic, behavioral, biochemical, and metabolic). At the end of the exposure (96 h), fish were video-recorded for behavior assessment. We used the micronucleus and nuclear abnormality tests and the comet assay in peripheral blood as genotoxicity biomarkers. In regard to biochemical and metabolic biomarkers, we dissected the brain for acetylcholinesterase (AChE) activity; the liver for glutathione-S-transferase (GST) and catalase (CAT) activity and glutathione content (GSH); the gills for GSH content; and muscle for AChE, energy metabolism of lipids, carbohydrates, and proteins, and the electron transport system activity of the mitochondrial chain. We calculated an index using metabolic biomarkers, to determine the cellular energy allocation. The LC50 value was 7.32 mg As/L. The As affected some swimming parameters in females. No significant differences in micronucleus were found compared with the control, whereas nuclear aberrations increased significantly at 1.0 and 5.0 mg As/L. The genomic damage index and the percentage of cells with DNA damage (measured by the comet assay) showed a significant increase in the As-treated groups, and this technique was the most sensitive for detecting genotoxic damage. The As affected the antioxidant system (mainly GSH, CAT, and GST) and reduced the lipid content. A preliminary baseline was generated for the response of C. decemmaculatus exposed to sublethal concentrations of As, when it alters swimming behavior and the antioxidant system, has genotoxic effects, and reduces lipid content. Environ Toxicol Chem 2022;41:1246-1259. © 2022 SETAC.

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The surface of a biomedical implant can be a potential endogenous source of release of microparticles (MPs) and nanoparticles (NPs) into the biological environment. In addition, titanium particles from exogenous sources can enter the body through inhalation, ingestion, or dermal contact. The aim of this work was to evaluate the biological response of the lung, liver, and kidneys to acute exposure to titanium dioxide (TiO2 ). Male Wistar rats were intraperitoneally injected with a suspension of 45 µm or 5 nm TiO2 particles. One month post-exposure, titanium concentration was determined spectrometrically (ICP-MS) in plasma and target organs. Blood smears and organ tissue samples were examined histopathologically, and oxidative metabolism was analyzed (superoxide anion by nitro blue tetrazolium (NBT) test; superoxide dismutase (SOD) and catalase (CAT); lipid peroxidation; paraoxonase 1). Liver (aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase) and kidney (urea, creatinine) function was evaluated using serum biochemical markers. Microchemical and histological analysis revealed the presence of particles, though no structural alterations, in TiO2 -exposed groups. NBT test showed an increase in the percentage of reactive cells and antioxidant enzyme consumption in lung samples in the 45 µm and 5 nm TiO2 -exposed groups. Only the 5 nm particles caused a decrease in SOD and CAT activity in the liver. No changes in renal oxidative metabolism were observed in either of the TiO2 -exposed groups. Determination of serum biochemical markers and analysis of oxidative metabolism are not early bioindicators of tissue damage caused by TiO2 MPs and NPs.

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Performing repetitions to failure (RF) is a strategy that might acutely reduce neuromuscular performance, as well as increase the rating of perceived exertion (RPE) and the internal training load (ITL) during and after a resistance training (RT) session. Thus, this study aimed to analyze the acute effects of RF or repetitions not to failure (RNF) on countermovement jump (CMJ) performance and the ITL in trained male adults. Eleven men performed two experimental protocols in randomized order (RF vs. RNF). Under the RF condition, participants performed three sets of the leg extension exercise using 100% of the 10RM load and rest intervals of 180-s between sets. Under the RNF condition, participants were submitted to six sets of five repetitions with the same intensity and an 80-s rest interval between sets in the same exercise. The CMJ test was analyzed before and following (15-s and 30-min, respectively) each experimental session. The ITL was evaluated by multiplying the RPE and the total session time, 30-min after the protocol. No main effect or interaction time vs. condition was found for CMJ performance (p > 0.05). In contrast, the ITL showed higher values under the RF condition (p = 0.003). Therefore, even though RF-induced a greater ITL, our results suggest that adopting this strategy in one single-joint exercise for the lower limbs does not seem sufficient to reduce CMJ height.

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Abstract Aims: This study aimed to verify whether vigorous exercise is capable of generating mental fatigue. Methods: To do so, 16 young adult male (29.4 ± 5.2 years old) cyclists (5.4 ± 4.6 years of training) underwent three visits: 1) control session (rest); 2) session with cognitive demand (20 minutes of AX-CPT); 3) session with vigorous exercise (10km time trial). Mental fatigue was assessed using the visual analog scale of fatigue in the pre-and post-session moments. A two-way ANOVA of repeated measures followed by the Bonferroni posthoc was used to verify the effect of the condition (control, cognitive demand, and exercise) and time (pre and post) interaction. The paired "t" test was used to compare the delta of mental fatigue (post - pre) of the sessions. The partial eta squared was used to determine the effect size of the variance. The significance adopted was p < 0.05. Results: A condition x time interaction was observed (F (2.30) = 5.349, p = 0.010, partial η2 = 0.263). When comparing the deltas, a mean difference was found between the control and vigorous exercise (p = 0.033) conditions and cognitive demand and vigorous exercise (p = 0.017) conditions. Control and cognitive demand sessions showed no difference (p = 0.801). Conclusion: The findings suggest that intense physical exercise seems to cause mental fatigue after practice.

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The aim of this study was to compare the acute effect of resistance exercise (RE) with and without blood flow restriction (BFR) on heart rate (HR), double product (DP), oxygen saturation (SpO2 ) and rating of perceived exertion (RPE). Twenty-four men (21·79 ± 3·21 years) performed three experimental protocols in a random order (crossover): (i) high-intensity RE at 80% of 1RM (HI), (ii) low-intensity RE at 20% of 1RM (LI) and (iii) low-intensity RE at 20% of 1RM combined with partial blood flow restriction (LI+BFR). HR, blood pressure, SpO2 and RPE were assessed. The data were analysed using repeated measures analysis of variance and the Wilcoxon test for RPE. The results indicated that all protocols significantly increased HR, both immediately postexercise and during the subsequent 60 min (P<0·05), and postexercise DP (P<0·05), but there were no differences between protocols. The protocols of LI and LI+BFR reduced postexercise SpO2 (P = 0·033, P = 0·007), and the LI+BFR protocol presented a perception of greater exertion in the lower limbs compared with HI (P = 0·022). We conclude that RE performed at low intensity combined with BFR seems to reduce the SpO2 after exercise and increase HR and DP while maintaining a perception of greater exertion on the lower limbs.

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Fundamento: O treinamento aeróbio intervalado produz maior benefício na função cardiovascular comparado ao treinamento aeróbio contínuo. Objetivo: O presente estudo teve como objetivo analisar os efeitos de ambas as modalidades nas respostas hemodinâmicas de ratos sadios. Métodos: Ratos machos foram distribuídos aleatoriamente em três grupos: exercício contínuo (EC, n = 10); exercício intervalado (EI, n = 10); e controle (C, n = 10). A sessão do grupo EC consistiu em 30 min à intensidade de 50% da velocidade máxima (Vel Máx). O grupo EI realizou 30 min, incluindo três períodos de 4 min a 60% da Vel Máx intercalados com 4 min de recuperação a 40% da Vel Máx. Frequência Cardíaca (FC), Pressão Arterial (PA) e Duplo Produto (DP) foram medidos antes, durante e após o exercício. Resultados: Os grupos EC e EI apresentaram aumento da PA sistólica e DP durante o exercício em comparação ao repouso. Após o término do exercício, o grupo EC mostrou menor resposta da PA sistólica e do DP em relação ao repouso, enquanto o grupo EI apresentou menor PA sistólica e PA média. No entanto, somente no grupo EI a FC e o DP apresentaram menor resposta na recuperação. Conclusão: Uma sessão de exercício intervalado em ratos sadios induziu respostas hemodinâmicas similares durante o exercício às obtidas em exercício contínuo. Na recuperação, o exercício intervalado promoveu maiores reduções no esforço cardíaco do que em sessões contínuas de exercício. .

Background: Aerobic interval exercise training has greater benefits on cardiovascular function as compared with aerobic continuous exercise training. Objective: The present study aimed at analyzing the effects of both exercise modalities on acute and subacute hemodynamic responses of healthy rats. Methods: Thirty male rats were randomly assigned into three groups as follows: continuous exercise (CE, n = 10); interval exercise (IE, n = 10); and control (C, n = 10). Both IE and CE groups performed a 30-minute exercise session. The IE group session consisted of three successive 4-minute periods at 60% of maximal velocity (Max Vel), with 4-minute recovery intervals at 40% of Max Vel. The CE group ran continuously at 50% of Max Vel. Heart rate (HR), blood pressure(BP), and rate pressure product (RPP) were measured before, during and after the exercise session. Results: The CE and IE groups showed an increase in systolic BP and RPP during exercise as compared with the baseline values. After the end of exercise, the CE group showed a lower response of systolic BP and RPP as compared with the baseline values, while the IE group showed lower systolic BP and mean BP values. However, only the IE group had a lower response of HR and RPP during recovery. Conclusion: In healthy rats, one interval exercise session, as compared with continuous exercise, induced similar hemodynamic responses during exercise. However, during recovery, the interval exercise caused greater reductions in cardiac workload than the continuous exercise. .

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A radioterapia em região de cabeça e pescoço provoca inúmeras sequelas ao paciente irradiado, afetando o sistema estomatognático e com repercussões sistêmicas importantes. As sequelas da radiação ionizante podem ser extensas e, algumas vezes, permanentes, em especial nas glândulas salivares e no tecido ósseo. É relevante que o cirurgião dentista tenha conhecimento das reações adversas e das formas adequadas de prevenção e tratamento para amenizar o desconforto e melhorar a condição de vida do paciente irradiado. Portanto, a conscientização e motivação deste paciente, com a promoção de saúde oral através da adequação do meio bucal e orientações sobre ações preventivas, são essenciais para se obter o melhor prognóstico.

Head and neck radiotherapy causes countless sequelae in irradiated patients, affecting the stomatognathic system, with significant systemic implications. Sequelae of exposure to ionizing radiation may be extensive and sometimes permanent, particularly in the salivary glands and bone tissue. It is of utmost importance that the surgeon dentist be aware of adverse reactions and appropriate forms of treatment to alleviate discomfort and improve the quality of life of the irradiated patient. Therefore, awareness and motivation of the patient, with promotion of oral health through the adaptation of the oral environment and guidance on preventive measures are essential to get a better prognosis.

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The present study investigated with the distribution of mercury chloride in muscle, liver and gills of Hoplias malabaricus contaminated through intraperitoneal injection (6 µg in 0.1mL of PBS) for a period of 24, 48, 72 and 96h. The liver, gill and muscle were analyzed for mercury content in an ICP/AES (Varian Liberty II) with vapor generating accessory (VGA 77). The muscle and liver tissues presented the same contamination pattern increasing concentrations in 24 h of exposure with a decrease in Hg concentration with 72 h and a new increase in Hg concentrations with 96 h of exposure. The Hg concentrations in contaminated organisms were always higher than the control although only for liver samples the difference was statistically significant. Liver samples always presented higher Hg contents when compared with gill and muscle samples.

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Oxidative stress plays a major role in the pathogenesis of particle-dependent lung injury. Ambient particle levels from vehicles have not been previously shown to cause oxidative stress to the lungs. The present study was conducted to a) determine whether short-term exposure to ambient levels of particulate air pollution from vehicles elicits inflammatory responses and lipid peroxidation in rat lungs, and b) determine if intermittent short-term exposures (every 4 days) induce some degree of tolerance. Three-month-old male Wistar rats were exposed to ambient particulate matter (PM) from vehicles (N = 30) for 6 or 20 continuous hours, or for intermittent (5 h) periods during 20 h for 4 consecutive days or to filtered air (PM <10 mum; N = 30). Rats continuously breathing polluted air for 20 h (P-20) showed a significant increase in the total number of leukocytes in bronchoalveolar lavage compared to control (C-20: 2.61 x 105 ± 0.51;P-20: 5.01 x 105 ± 0.81; P < 0.05) and in lipid peroxidation ([MDA] nmol/mg protein: C-20: 0.148 ± 0.01; P-20: 0.226 ± 0.02; P < 0.05). Shorter exposure (6 h) and intermittent 5-h exposures over a period of 4 days did not cause significant changes in leukocytes. Lipid damage resulting from 20-h exposure to particulate air pollution did not cause a significant increase in lung water content. These data suggest oxidative stress as one of the mechanisms responsible for the acute adverse respiratory effects of particles, and suggest that short-term inhalation of ambient particulate air pollution from street with high automobile traffic represents a biological hazard.

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