Uncoupling as initiating event in mitochondrial dysfunction after diuron exposure.

Diuron, a herbicide derived from urea, has been shown to induce urinary bladder urothelial tumors in rodents, leading the U.S. Environmental Protection Agency (USEPA) to designate it as a 'known/likely' human carcinogen. In our laboratory, a series of studies investigating the carcinogenic mode of action (MoA) of Diuron have consistently revealed its cytotoxic effects on the urinary bladder urothelium. Prolonged exposure to relatively high doses of Diuron results in urothelial necrosis, regenerative hyperplasia, and eventually, the development of tumors. The hypothesis posited is that Diuron and its metabolites exert toxicity by causing damage to mitochondria, a phenomenon referred to as mitotoxicity. Our research focuses on evaluating how Diuron and its metabolites affect mitochondria isolated from both the urothelium and the liver, the primary organ for Diuron biotransformation. In this context, we present and discuss data pertaining to mitochondria isolated from the liver of Wistar rats exposed to Diuron or its metabolites 3-(3,4-diclorofenil)-1-metilureia (DCPMU) or 3,4-dichloroaniline (DCA) at concentrations ranging from 0.5 to 500 µM in vitro. The findings indicate that, at concentrations of 100 and 500 µM, the tested chemicals induce uncoupling of oxidative phosphorylation, as evidenced by the dissipation of mitochondrial membrane potential and basal oxygen consumption. Notably, at 500 µM, DCA causes mitochondrial swelling, a morphofunctional indicator of severe organelle damage. These outcomes underscore the classification of Diuron and its metabolites, DCA and DCPMU, as mitotoxic to liver cells, given the pronounced mitochondrial dysfunction they induce.

Diuron, DCA, and DCPMU uncouple the electron transport chain in to hepatic mitochondria.Diuron, DCA, and DCPMU are mitotoxic agents.The metabolite DCA is the most toxic to hepatic mitochondria and can induce mitochondrial swelling.

Effect of Heated Saline Solution on Pain Intensity, Wound Bed Temperature, and Comfort during Chronic Wound Dressing Changes: Crossover Randomized Clinical Trial.

OBJECTIVE: To evaluate the use of heated saline solution during wound cleaning on the intensity of pain related to the procedure, the temperature of the wound bed, and the comfort of patients with chronic wounds. Further, to investigate patient preference in relation to the temperature of the solution used for cleaning. METHODS: Crossover, single-blind, clinical trial with 32 people with chronic wounds. Providers cleaned the wounds with room temperature and heated saline solution. Participants were randomized into group 1 A/B (heated solution first, room temperature second) or group 2 B/A (room temperature solution first, heated solution second), with a 10-minute washout period. Investigators evaluated pain intensity, wound bed temperature, and patient-reported comfort and preference. RESULTS: The heated solution was preferred (P = .04) and more often referred to as comfortable (P = .04) by the participants. There was no difference in pain intensity before and after cleaning with room temperature (2.03; P = .155) and heated saline (2.25; P = .44). The heated solution increased the temperature of the wound bed by 0.5 °C. CONCLUSIONS: Although heating saline solution could be an important comfort measure during dressing changes, quantitatively, the temperature of the solution did not significantly change the temperature of the wound bed nor the intensity of pain patients experienced.

Diuron and its metabolites induce mitochondrial dysfunction-mediated cytotoxicity in urothelial cells.

In the environment, or during mammalian metabolism, the diuron herbicide (3-(3,4-dichlorophenyl)-1,1-dimethylurea) is transformed mainly into 3-(3,4-dichlorophenyl)-1-methylurea (DCPMU) and 3,4-dichloroaniline (DCA). Previous research suggests that such substances are toxic to the urothelium of Wistar rats where, under specific exposure conditions, they may induce urothelial cell degeneration, necrosis, hyperplasia, and eventually tumors. However, the intimate mechanisms of action associated with such chemical toxicity are not fully understood. In this context, the purpose of the current in vitro study was to analyze the underlying mechanisms involved in the urothelial toxicity of those chemicals, addressing cell death and the possible role of mitochondrial dysfunction. Thus, human 1T1 urothelial cells were exposed to six different concentrations of diuron, DCA, and DCPMU, ranging from 0.5 to 500 µM. The results showed that tested chemicals induced oxidative stress and mitochondrial damage, cell cycle instability, and cell death, which were more expressive at the higher concentrations of the metabolites. These data corroborate previous studies from this laboratory and, collectively, suggest mitochondrial dysfunction as an initiating event triggering urothelial cell degeneration and death.

Molecular signatures associated with diuron exposure on rat urothelial mitochondria.

Diuron, 3-(3,4-dichlorophenyl)-1,1-dimethylurea, is a worldwide used herbicide whose biotransformation gives rise to the metabolites, 3-(3,4-dichlorophenyl)-1-methylurea (DCPMU) and 3,4-dichloroaniline (DCA). Previous studies indicate that diuron and/or its metabolites are toxic to the bladder urothelium of the Wistar rats where, under certain conditions of exposure, they may induce successively urothelial cell degeneration, necrosis, hyperplasia and eventually tumors. The hypothesis was raised that the molecular initiating event (MIE) of this Adverse Outcome Pathway is the mitochondrial toxicity of those compounds. Therefore, this study aimed to investigate in vitro the metabolic alterations resulting from urothelial mitochondria isolated from male Wistar rats exposure to diuron, DCPMU and DCA at 10 and 100 µM. A non-targeted metabolomic analysis using mass spectrometry showed discriminative clustering among groups and alterations in the intensity abundance of membrane-associated molecules phosphatidylcholine, phosphatidylinositol and phosphatidylserine, in addition to methylhexanoyl-CoA and, particularly for diuron 100 µM, dehydro-L-gulonate, all of them involved in critical mitochondrial metabolism. Collectively, these data indicate the mitochondrial dysfunction as an MIE that triggers cellular damage and death observed in previous studies.

Rupture of Brumadinho dam (Minas Gerais, Brazil): embryotoxicity in zebrafish induced by metal mixture-contaminated water.

Rupture of dam B-1 at the Córrego do Feijão mine in Brumadinho, state of Minas Gerais, Brazil (25/Jan/2019) contaminated the Paraopeba River with mine waste. To identify the adverse effects of this event on public and environmental health, we conducted the Fish Embryo Acute Toxicity (FET) test (OECD No. 236). During the tests, zebrafish embryos were exposed for 144 hours to solutions containing realistic concentrations of dissolved iron and aluminum and total manganese at the following analysis points upstream or downstream of the dam: 10 km, upstream; 19.7 km, downstream, at the point where water for consumption is collected; 24.5 km, downstream, in the city of Mário Franco; and 59 km, downstream, on the border between the towns of Juatuba and Betim. Metal concentrations were taken from September 2019 report No. 53 released by IGAM. Mortality was high at all exposure points and reached 93% at the Juatuba/Betim point. We also detected lethal, sublethal and teratogenic effects, such as non-hatching, non-inflation of the swim bladder, pericardial edema and scoliosis, affecting up to 25% of embryos at the other analysis points. The results highlight the need for continuous monitoring of the water quality of the Paraopeba River.

Sex Differences in Coping Strategies Based on Chronic Pain Intensity Among Older Adults.

The aim of the current study was to investigate chronic pain coping strategies of older adults and the differences between sexes according to the intensity of pain. A cross-sectional study was performed in specialty clinics in midwestern Brazil. Participants comprised 276 older adults with chronic pain. The Brief Pain Inventory and Chronic Pain Coping Inventory-Brazilian version were used to assess self-reported pain intensity and pain coping strategies. Mann-Whitney U, Kruskal-Wallis, and Dunn tests were used for intergroup comparisons. The task persistence and coping self-statements subscales were the most used coping strategies. The strategies of exercise/stretching and task persistence were used differently between males and females. Males showed significant differences in asking for assistance, task persistence, and guarding subscales when pain intensity was taken into account, whereas females showed differences in the guarding and resting subscales. Adaptive coping was the most used coping strategy; however, some non-adaptive subscales were significant in both sexes when compared with levels of chronic pain intensity. [Journal of Gerontological Nursing, 47(10), 30-36.].

Do trifluralin and tebuthiuron impair isolated rat liver mitochondria?

Emerging contaminants, such as the herbicides trifluralin and tebuthiuron, comprise a class of compounds for which toxicological data are lacking, especially data regarding their harmful effects and biomarkers of exposure. Their potential damage to the environment and non-target organisms makes understanding their toxic mechanisms an urgent matter. Mitochondria, which exert an energy production function, play a vital role in maintaining many cellular activities and therefore are reliable predictors of substance toxicity. This study evaluates whether the herbicides trifluralin and tebuthiuron (at concentrations ranging from 1 to 100 µM) affect isolated rat liver mitochondria. The herbicides were analyzed according to their ability to interact with the mitochondrial membrane and induce swelling, lipoperoxidation, ROS formation, and NAD(P)H oxidation; dissipate the membrane potential; dysregulate calcium homeostasis; and alter ATP and GSH/GSSG levels. Tebuthiuron does not disrupt the mitochondrial biochemistry at any of the tested concentrations. In contrast, trifluralin can disturb the mitochondrial respiration, especially at the highest concentration, but it cannot induce oxidative stress. These results suggest that the aforementioned effects can occur as toxic mechanisms of trifluralin in non-target organisms, as well.

Niacin prevents mitochondrial oxidative stress caused by sub-chronic exposure to methylmercury.

Humans and animals can be exposed to different chemical forms of mercury (Hg) in the environment. For example, methylmercury (MeHg)-contaminated fish is part of the basic diet of the riparian population in the Brazilian Amazon Basin, which leads to high total blood and plasma Hg levels in people living therein. Hg induces toxic effects mainly through oxidative stress. Different compounds have been used to prevent the damage caused by MeHg-induced reactive oxygen species (ROS). This study aims to investigate the in vivo effects of sub-chronic exposure to low MeHg levels on the mitochondrial oxidative status and to evaluate the niacin protective effect against MeHg-induced oxidative stress. For this purpose, Male Wistar rats were divided into four groups: control group, treated with drinking water on a daily basis; group exposed to MeHg at a dose of 100 µg/kg/day; group that received niacin at a dose of 50 mg/kg/day in drinking water, with drinking water being administered by gavage; group that received niacin at a dose of 50 mg/kg/day in drinking water as well as MeHg at a dose of 100 µg/kg/day. After 12 weeks, the rats, which weighed 500-550 g, were sacrificed, and their liver mitochondria were isolated by standard differential centrifugation. Sub-chronic exposure to MeHg (100 µg/kg/day for 12 weeks) led to mitochondrial swelling (p < 0.05) and induced ROS overproduction as determined by increased DFCH oxidation (p < 0.05), increased gluthatione oxidation (p < 0.05), and reduced protein thiol content (p < 0.05). In contrast, niacin supplementation inhibited oxidative stress, which counteracted and minimized the toxic MeHg effects on mitochondria.

Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell death.

Polybrominated diphenyl ethers (PBDE) are ubiquitous environmental pollutants. Exposure to these chemicals has been associated with developmental neurotoxicity, endocrine dysfunctions, reproductive disorders, and hepatotoxicity. The widespread use of PBDE as flame retardants has culminated in daily exposure of humans and wildlife to these contaminants and resulted in their banned use. Thus assessment of the potential effects of each PBDE congener on living organisms has become cause for concern. The aim of this study was to (1) examine the effects of decabromodiphenyl ether (BDE)-209 on different functions of HepG2 cells and (2) investigate whether this congener is involved in mitochondrial toxicity. The use of multiple methods was employed to (i) study the influence of BDE-209 on mitochondrial permeability transition (MPT) process in mitochondria isolated from rat liver and (ii) determine the consequential cellular damage. Our results showed that BDE-209 induced matrix swelling related to MPT with 10 µM and ATP depletion with 0.1 µM. In addition, 0.5 µM BDE-209 reduced HepG2 cell viability, produced collapse of membrane potential, but increased levels of reactive oxygen species (ROS) after 48 h incubation. After 24 h with 5 µM treatment elevated levels of ROS, DNA fragmentation and cytochrome c release, accompanied by caspase 9 and caspase 3 activation was noted. Taken together, these results suggest that short-duration exposure (24 or 48 h) to 0.5 µM or 5 µM BDE-209 concentrations diminished HepG2 cell viability due to apoptosis associated with mitochondrial dysfunction.

Toxicity of brominated flame retardants, BDE-47 and BDE-99 stems from impaired mitochondrial bioenergetics.

Polybrominated diphenyl ethers (PBDEs) are used as flame retardants, and they have been detected in human blood, adipose tissue and breast milk, a consequence of their physicochemical and bioaccumulative properties, as well as their high environmental persistence. Many studies report liver toxicity related to exposure to PBDEs. In the present study, we investigated the toxicity of BDE-47 and BDE-99 at concentrations ranging from 0.1 to 50 µM in isolated rat liver mitochondria. We evaluated how incubation of a mitochondrial suspension with the PBDEs affected the mitochondrial inner membrane, membrane potential, oxygen consumption, calcium release, mitochondrial swelling, and ATP levels to find out whether the tested compound interfered with the bioenergetics of this organelle. Both PBDEs were toxic to mitochondria: BDE-47 and BDE-99 concentrations equal to or higher than 25 and 50 µM, respectively, modified all the parameters used to assess mitochondrial bioenergetics, which culminated in ATP depletion. These effects stemmed from the ability of both PBDEs to cause Membrane Permeability Transition (MPT) in mitochondria, which impaired mitochondrial bioenergetics. In particular, BDE-47, which has fewer bromine atoms in the molecule, can easily overcome biological membranes what would be responsible for the major negative effects exerted by this congener when compared with BDE-99.

[Pain intensity among institutionalized elderly: a comparison between numerical scales and verbal descriptors]. / Intensidade da dor em idosos institucionalizados: comparação entre as escalas numérica e de descritores verbais.

OBJECTIVE: Correlating two unidimensional scales for measurement of self-reported pain intensity for elderly and identifying a preference for one of the scales. METHOD: A study conducted with 101 elderly people living in Nursing Home who reported any pain and reached ( 13 the scores on the Mini-Mental State Examination. A Numeric Rating Scale - (NRS) of 11 points and a Verbal Descriptor Scale (VDS) of five points were compared in three evaluations: overall, at rest and during movement. RESULTS: Women were more representative (61.4%) and the average age was 77.0±9.1 years. NRS was completed by 94.8% of the elderly while VDS by 100%. The association between the mean scores of NRS with the categories of VDS was significant, indicating convergent validity and a similar metric between the scales. CONCLUSION: Pain measurements among institutionalized elderly can be made by NRS and VDS; however, the preferred scale for the elderly was the VDS, regardless of gender.

BDE-154 induces mitochondrial permeability transition and impairs mitochondrial bioenergetics.

Brominated flame retardants are used in various consumer goods to make these materials difficult to burn. Polybrominated diphenyl ethers (PBDE), which are representative of this class of retardants, consist of two benzene rings linked by an oxygen atom, and contain between 1 and 10 bromine atoms in their chemical structure, with the possibility of up to 209 different congeners. Among these congeners, BDE-154 (hexa-BDE) is persistent in the environment and easy to detect in the biota, but no apparent information regarding the mechanism underlying action and toxicity is available. Mitochondria, as the main energy-producing organelles, play an important role in the maintenance of various cellular functions. Therefore, mitochondria were used in the present study as an experimental model to determine the effects of BDE-154 congener at concentrations ranging from 0.1 µM to 50 µM. Our results demonstrated that BDE-154 interacts with the mitochondrial membrane, preferably by inserting into the hydrophobic core of the mitochondrial membrane, which partially inhibits respiration, dissipates Δψ, and permeabilizes the inner mitochondrial membrane to deplete ATP. These effects are more pronounced at concentrations equal to or higher than 10 µM. Results also showed that BDE-154 did not induce reactive oxygen species (ROS) accumulation within the mitochondria, indicating the absence of oxidative stress. Therefore, BDE-154 impairs mitochondrial bioenergetics and permeabilizes the mitochondrial membrane, potentially leading to cell death but not via mechanisms involving oxidative stress.

Embryotoxicity Induced by Triclopyr in Zebrafish (Danio rerio) Early Life Stage.

Triclopyr, an auxin-like herbicide that is widely employed for managing weeds in food crops and pastures, has been identified in various environmental settings, particularly aquatic ecosystems. Limited understanding of the environmental fate of this herbicide, its potential repercussions for both the environment and human health, and its insufficient monitoring in diverse environmental compartments has caused it to be recognized as an emerging contaminant of concern. In this study, we have investigated how triclopyr affects zebrafish, considering a new alternative methodology. We focused on the endpoints of developmental toxicity, neurotoxicity, and behavior of zebrafish embryos and larvae. We determined that triclopyr has a 96 h median lethal concentration of 87.46 mg/L (341.01 µM). When we exposed zebrafish embryos to sublethal triclopyr concentrations (0.5, 1, 5, 10, and 50 µM) for up to 144 h, we found that 50 µM triclopyr delayed zebrafish egg hatchability. Yolk sac malabsorption was significant at 0.5, 1, 5, and 10 µM triclopyr. In zebrafish larvae, uninflated swim bladder was significant only at 50 µM triclopyr. Furthermore, zebrafish larvae had altered swimming activity after exposure to 10 µM triclopyr for 144 h. In summary, these comprehensive results indicate that even low triclopyr concentrations can elicit adverse effects during early zebrafish development.

Effects of diuron and two of its metabolites in biochemical markers and behavior of zebrafish larvae.

Diuron (3-(3,4-dichlorophenyl)-1,1-dimethylurea) is an herbicide used in many crops, including sugar cane cultivation. It is commonly found in aquatic ecosystem and is of high concern due to its ability to persist in the environment. Diuron metabolites include DCA (3,4-dichloroaniline) and DCPMU (3-(3,4-dichlorophenyl-1-methylurea). The objective of this study was to evaluate the effects of diuron and two of its metabolites in zebrafish (Danio rerio) developing embryos, from biochemical to individual level. Activities of the enzymes acetylcholinesterase (AChE), catalase (CAT), glutathione-S-transferase (GST), and lactate dehydrogenase (LDH) and the levels of lipid peroxidation (LPO), swimming activity, and body length were investigated after an exposure of 120 h, and the heart rate was determined after 48 h of exposure. The range of concentrations tested was 0.003-3.000 mg/L diuron, 0.020-1.500 mg/L DCA, and 0.020-2.100 mg/L DCPMU. Results showed that AChE activity was inhibited by diuron (3.000 mg/L) and DCPMU (0.326, 0.828 mg/L). However, the swimming activity of fish larvae exposed to diuron or its metabolites was not affected. The CAT was induced by DCPMU, and GST was induced by diuron. This suggests that CAT is acting to cope with oxidative stress induced by DCPMU and GST might have a role in the detoxification of diuron. In addition, larvae exposed to DCA (0.633 and 1.500 mg/L) had a reduction in their length, and larvae exposed to diuron (0.754 and 3.000 mg/L) and DCA (0.267, 0.633, and 1.500 mg/L) presented bradycardia, suggesting cardiotoxicity. Overall, results indicate that diuron, DCA, or DCPMU induces adverse effects during the early phases of zebrafish development, such as the impairment of neurotransmission and cardiovascular function and alterations in antioxidant enzymes and growth. Diuron appeared as more toxic than its metabolites since the lowest LOEC (0.012 mg/L) and higher integrated biomarker response (IBR) values were obtained with exposure to this herbicide. Furthermore, as it is fast degraded into DCA and DCPMU, which also affected the zebrafish developing embryos at environmentally relevant concentrations, its use might be of concern in ecosystems that receive agriculture runoff due to their potential adverse effects to aquatic biota.

[The bioethical principlism model applied in pain management]. / O modelo bioético principialista aplicado no manejo da dor.

An integrative literature review was developed with the purpose to analyze the scientific production regarding the relationships between pain and the principles of bioethics (autonomy, beneficence, nonmaleficence and justice). Controlled descriptors were used in three international data sources (LILACS, SciELO, MEDLINE), in April of 2012, totaling 14 publications categorized by pain and autonomy, pain and beneficence, pain and nonmaleficence, pain and justice. The adequate relief of pain is a human right and a moral issue directly related with the bioethical principlism standard model (beneficence, non-maleficence, autonomy and justice). However, many professionals overlook the pain of their patients, ignoring their ethical role when facing suffering. It was concluded that principlism has been neglected in the care of patients in pain, showing the need for new practices to change this setting.

Pain management in indigenous and tribal peoples: a scoping review protocol.

INTRODUCTION: Effective and culturally safe pain management can facilitate analgesia and improve the quality of life. Individualised, multimodal and multidisciplinary approaches are highly recommended. There exist gaps in the knowledge on pain management, in terms of the assessment and/or treatment, in indigenous peoples and the currently available information is scattered in the literature. A scoping review will provide an overview or evidence map on the variety of approaches used in different cultures, in different parts of the world. METHODS AND ANALYSIS: The search strategy comprises three stages. The first stage identified the MeSH terms and keywords in PubMed. The second stage will consist of a search of MEDLINE, EMBASE, LILACS, CINAHL, Web of Science, APA PsycNet and Scopus, followed by a search in Google and Google Scholar, GreyGuide, ProQuest Dissertations and Theses, Theses Canada Portal (Library and Archives Canada), TROVE (National Library of Australia), Aboriginal and Torres Strait Islander Health Bibliography, and Cybertesis. The papers will be screened, selected and extracted independently by two researchers. Descriptive data analysis will be performed, and the results will be presented using a narrative summary, graphs, tables and figures. ETHICS AND DISSEMINATION: This review does not require ethical approval, as data from the literature available in databases will be collected and analysed. The protocol was registered at the Open Science Framework. The data on pain assessment and treatment in indigenous peoples will be presented through a narrative summary, figures, charts and tables. Results will be submitted to an open-access journal for publication and will be disseminated through scientific events, scientific meetings, public events and conversation circles with indigenous peoples.

Correction to "Synthesis of Lysoglycerophosphocholines from Crude Soybean Lecithins as Sustainable and Non-toxic Antifouling Agents against the Golden Mussel Limnoperna fortunei".

[This corrects the article DOI: 10.1021/acsomega.2c05645.].

Toxicity of Beauty Salon Effluents Contaminated with Hair Dye on Aquatic Organisms.

Cosmetic residues have been found in water resources, especially trace elements of precursors, couplers, and pigments of hair dyes, which are indiscriminately disposed of in the sewage system. These contaminants are persistent, bioactive, and bioaccumulative, and may pose risks to living beings. Thus, the present study assessed the ecotoxicity of two types of effluents generated in beauty salons after the hair dyeing process. The toxicity of effluent derived from capillary washing with water, shampoo, and conditioner (complete effluent-CE) and effluent not associated with these products (dye effluent-DE) was evaluated by tests carried out with the aquatic organisms Artemia salina, Daphnia similis, and Danio rerio. The bioindicators were exposed to pure samples and different dilutions of both effluents. The results showed toxicity in D. similis (CE50 of 3.43% and 0.54% for CE and DE, respectively); A. salina (LC50 8.327% and 3.874% for CE and DE, respectively); and D. rerio (LC50 of 4.25-4.59% and 7.33-8.18% for CE and DE, respectively). Given these results, we can infer that hair dyes, even at low concentrations, have a high toxic potential for aquatic biota, as they induced deleterious effects in all tested bioindicators.

[The occurrence of headaches and their effect upon nursing undergraduate students]. / Ocorrência e prejuízos da cefaleia em estudantes universitárias de enfermagem.

This study was performed with the objectives of identifying the occurrence of headache as the major cause of pain and characterizing the effect headaches have on the everyday activities of nursing undergraduate students. This cross-sectional study was performed at the College of Nursing of the Federal University of Goiás, Goiânia, Brazil, from May to June 2008. Participants included 203 students (mean age 21 years; s.d.=1.8), 48.5% from economic class A. Headaches were the major cause of pain for 34.5% of students; described as being of strong intensity; referred to as throbbing (74.3%), stabbing (62.9%), and causing nausea and/or vomiting (55.7%); with episodes occurring in the afternoon (52.9%), and lasting for several hours a day (51.4%). Factors related to the onset of pain were: studying (17.1%) and stress (11.4 %). The activities most affected were: their capacity to concentrate (84.3%) and their mood (84.3%) (p<0.05). Headaches are less common in the population compared to other country studies, and they affect the students' everyday activities.

Toxic Effects Induced by Diuron and Its Metabolites in Caenorhabditis elegans.

The toxicity of diuron herbicide and its metabolites has been extensively investigated; however, their precise toxic mechanisms have yet to be fully appreciated. In this context, we evaluated the toxic mechanism of diuron, 3,4-dichloroaniline (DCA) and 3-(3,4-dichlorophenyl)-1-methylurea (DCPMU), using Caenorhabditis elegans (C. elegans) in the L1 larval stage. For this purpose, worms were acutely exposed to the test chemicals with a preliminary concentration range of 0.5 to 500 µM and first analyzed for lethality (%). Next, the highest concentration (500 µM) was considered for survival (%), reactive oxygen and nitrogen species (RONS), glutathione (GSH) and ATP levels, autophagy index, behavior, and dopaminergic neurodegeneration parameters. Interestingly, increased lethality (%) was found for all chemicals at the higher concentrations tested (100 and 500 µM), with significant differences at 500 µM DCA (p < 0.05). A decrease in the median survival was observed mainly for DCA. Although no changes were observed in RONS production, GSH levels were significantly increased upon diuron and DCA treatment, likely reflecting an attempt to restore the redox status. Moreover, diuron and its metabolites impaired ATP levels, suggesting an alteration in mitochondrial function. The latter may trigger autophagy as an adaptive survival mechanism, but this was not observed in C. elegans. Dopaminergic neurotoxicity was observed upon treatment with all the tested chemicals, but only diuron induced alterations in the worms' locomotor behavior. Combined, these results indicate that exposure to high concentrations of diuron and its metabolites elicit distinct adverse outcomes in C. elegans, and DCA in particular, plays an important role in the overall toxicity observed in this experimental model.