RESUMEN
Weed resistance to a range of herbicides has rapidly evolved, often with different mechanisms of action. The resulting uninhibited growth of weeds poses demonstrable threats to crop production and sustainable agriculture. Digitaria sanguinalis (L.) Scop., a troublesome weed in corn and other agricultural fields, has developed resistance to herbicides that inhibiting ALS (Acetolactate Synthase), such as nicosulfuron. Understanding the weed's resistance patterns and mechanisms is crucial. However, little is known of the non-target site resistance (NTSR) mechanisms of D. sanguinalis owing to a lack of relevant genome sequences and other materials. Therefore, in this study, a population of D.sanguinalis presenting multiple resistance was tested and found that its high level of resistance to ALS-inhibiting herbicides was not associated with target-related alterations.Administration of P450 inhibitors reversed the resistance to ALS-inhibiting herbicides. Following the application of ALS-inhibiting herbicides, the activities of NADPH-P450 reductase and p-nitroanisole O-demethylase (PNOD) were notably greater in the resistant population of D. sanguinalis than those in the susceptible population. The results suggested P450 enzyme familyplays a major role in the metabolic resistance mechanism, that increased P450 enzyme activity promote cross-resistance in D. sanguinalis to ALS-inhibiting herbicides. RNA-seq analysis showed that five genes from the P450 family (CYP709B2, CYP714C2, CYP71A1, CYP76C2, and CYP81E8) were upregulated in resistant D. sanguinalis. In conclusion, the upregulation of several P450 genes is responsible for establishing resistance to ALS-inhibiting herbicides in D. sanguinalis.
Asunto(s)
Acetolactato Sintasa , Sistema Enzimático del Citocromo P-450 , Digitaria , Resistencia a los Herbicidas , Herbicidas , Herbicidas/farmacología , Herbicidas/toxicidad , Acetolactato Sintasa/metabolismo , Acetolactato Sintasa/genética , Acetolactato Sintasa/antagonistas & inhibidores , Resistencia a los Herbicidas/genética , Sistema Enzimático del Citocromo P-450/metabolismo , Sistema Enzimático del Citocromo P-450/genética , Digitaria/efectos de los fármacos , Compuestos de Sulfonilurea/farmacología , Malezas/efectos de los fármacos , Malezas/metabolismo , Proteínas de Plantas/genética , Proteínas de Plantas/metabolismo , PiridinasRESUMEN
Herbicide exposure can pose a considerable threat to non-target aquatic animals. We aimed to study changes in the liver proteome of a model cyprinid fish species, zebrafish Danio rerio, to provide a molecular basis for the adverse effects of environmentally relevant concentrations of glyphosate (100 µg/L), its breakdown product aminomethylphosphonic acid (AMPA; 100 µg/L), and a mixture of both (50 + 50 µg/L) in the presence of humic acid (20 mg/L), which simulated a component of natural organic matter in the aquatic environment. Proteomic analysis was performed by means of high-performance liquid chromatography-tandem mass spectrometry employing a label-free quantification approach. The results present molecular evidence of the stress responses and disturbance of primary metabolic processes such as immune response, dysregulation in DNA repair, necroptosis and apoptosis signaling pathways, oxidative phosphorylation, cholesterol, lipoprotein, and carbohydrate metabolism. We registered the synergistic effect of the glyphosate and AMPA co-exposure, which was expressed in a substantial increase in the number of dysregulated proteins compared to the solo treatments. Humic acid alleviated the effects of glyphosate and its mixture with AMPA and aggravated the impact of AMPA exposure. RuvB-like 2, a protein taking part in DNA repair, and EIF2S1, involved in the regulation of stress-induced gene expression, were downregulated in the liver of zebrafish from all treatments.
Asunto(s)
Glicina , Glifosato , Herbicidas , Sustancias Húmicas , Hígado , Proteoma , Pez Cebra , Animales , Pez Cebra/metabolismo , Glicina/análogos & derivados , Glicina/toxicidad , Hígado/efectos de los fármacos , Hígado/metabolismo , Proteoma/metabolismo , Proteoma/efectos de los fármacos , Herbicidas/toxicidad , Organofosfonatos/toxicidad , Contaminantes Químicos del Agua/toxicidadRESUMEN
Lindane (LDN) is a well-known herbicidal drug that exerts deleterious impacts on vital body organs including the liver. Catechin (CTN) is a plant-based flavonoid that demonstrates various pharmacological abilities. This trial was executed to evaluate the ameliorative efficacy of CTN to combat LDN instigated hepatotoxicity in male albino rats (Rattus norvegicus). Thirty-two rats were categorized into four groups including control, LDN (30 mg/kg), LDN (30 mg/kg) + CTN (40 mg/kg) and CTN (40 mg/kg) alone treated group. It was observed that LDN dysregulated the expressions of PI3K/PIP3/Akt and Nrf-2/Keap-1 pathway. Moreover, the activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), hemeoxygenase-1 (HO-1) and glutathione reductase (GSR) were subsided after LDN intoxication. Besides, the levels of reactive oxygen species (ROS), malondialdehyde (MDA), ALT (Alanine aminotransferase), AST (Aspartate transaminase), Gamma-glutamyl transferase (GGT) and ALP (Alkaline phosphatase) were increased whereas reduced the levels of albumin and total proteins in response to LDN exposure. Additionally, LDN administration escalated the levels of Interleukin-6 (IL-6), Nuclear factor kappa-B (NF-κB), Interleukin-1ß (IL-1ß), tumor necrosis factor-α (TNF-α), and the activity of cyclooxygenase-2 (COX-2). Furthermore, the gene expressions of Bcl-2-associated X protein (Bax) and Cysteinyl aspartate-acid proteases-3 (Caspase-3) were enhanced whereas the expression of B-cell lymphoma-2 (Bcl-2) was lowered following the LDN treatment. LDN instigated various histological impairments in hepatic tissues. Nonetheless, concurrent administration of CTN remarkably ameliorated liver impairments via regulating aforementioned disruptions owing to its antioxidant, anti-apoptotic and histo-protective potentials.
Asunto(s)
Catequina , Hexaclorociclohexano , Hígado , Factor 2 Relacionado con NF-E2 , FN-kappa B , Fosfatidilinositol 3-Quinasas , Proteínas Proto-Oncogénicas c-akt , Animales , Masculino , Ratas , Hígado/efectos de los fármacos , Hígado/metabolismo , Factor 2 Relacionado con NF-E2/metabolismo , FN-kappa B/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Fosfatidilinositol 3-Quinasas/metabolismo , Catequina/farmacología , Hexaclorociclohexano/toxicidad , Proteína 1 Asociada A ECH Tipo Kelch/metabolismo , Enfermedad Hepática Inducida por Sustancias y Drogas/metabolismo , Enfermedad Hepática Inducida por Sustancias y Drogas/prevención & control , Transducción de Señal/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Herbicidas/toxicidadRESUMEN
Herbicides are the main class of pesticides applied in crops and are capable of polluting the surrounding freshwater system; thus, understanding their impact on non-target species, whose mechanism of action is not described, helps to elucidate the real risks of these pollutants to the environment. 2,4-dichlorophenoxyacetic acid (2,4-D) is frequently detected in water and, due to its persistence, poses a risk to wildlife. In this way, the present work aimed to describe the implication of exposure to concentrations of 2,4-D already reported in aquatic environments in several physiological mechanisms of C. riparius at molecular and biochemical levels. To achieve this, bioassays were conducted with fourth instar larvae exposed to three concentrations of 2,4-D (0.1, 1.0, and 7.5 µg L-1). Larvae were collected after 24 and 96 h of exposure, and the expression of 42 genes, related to six subcellular mechanisms, was assessed by Real-Time PCR (RT-PCR). Besides, the activity of the enzymes catalase (CAT), glutathione S-transferase (GST), and acetylcholinesterase (AChE) was determined. The main metabolic route altered after exposure to 2,4-D was the endocrine system (mainly related to 20-hydroxyecdysone and juvenile hormone), confirming its endocrine disruptor potential. Four of the eleven stress response genes studied were down-regulated, and later exposure modulated DNA-repair genes suggesting genotoxic capacity. Moreover, only one gene from each detoxification phase was modulated at short exposure to 1.0 µg L-1. The molecular responses were not dose-dependent, and some early responses were not preserved after 96 h, indicating a transient response to the herbicide. Exposure to 2,4-D did not alter the activity of CAT, GST, and AChE enzymes. The responses described in this study reveal new mechanistic pathways of toxicity for 2,4-D in non-target organisms and highlight potential ecological consequences for chironomids in aquatic systems at the edges of agricultural fields.
Asunto(s)
Ácido 2,4-Diclorofenoxiacético , Chironomidae , Glutatión Transferasa , Herbicidas , Ácido 2,4-Diclorofenoxiacético/toxicidad , Animales , Chironomidae/efectos de los fármacos , Chironomidae/genética , Herbicidas/toxicidad , Glutatión Transferasa/metabolismo , Glutatión Transferasa/genética , Acetilcolinesterasa/metabolismo , Acetilcolinesterasa/genética , Larva/efectos de los fármacos , Larva/genética , Larva/metabolismo , Contaminantes Químicos del Agua/toxicidad , Catalasa/metabolismo , Catalasa/genética , Expresión Génica/efectos de los fármacosRESUMEN
Although graphene oxide (GO) has extensive recognized application prospects in slow-release fertilizer, plant pest control, and plant growth regulation, the incorporation of GO into nano herbicides is still in its early stages of development. This study selected a pair of sweet corn sister lines, nicosulfuron (NIF)-resistant HK301 and NIF-sensitive HK320, and sprayed them both with 80 mg kg-1 of GO-NIF, with clean water as a control, to study the effect of GO-NIF on sweet corn seedling growth, photosynthesis, chlorophyll fluorescence, and antioxidant system enzyme activity. Compared to spraying water and GO alone, spraying GO-NIF was able to effectively reduce the toxic effect of NIF on sweet corn seedlings. Compared with NIF treatment, 10 days after of spraying GO-NIF, the net photosynthetic rate (A), stomatal conductance (Gs), transpiration rate (E), photosystem II photochemical maximum quantum yield (Fv/Fm), photochemical quenching coefficient (qP), and photosynthetic electron transfer rate (ETR) of GO-NIF treatment were significantly increased by 328.31%, 132.44%, 574.39%, 73.53%, 152.41%, and 140.72%, respectively, compared to HK320. Compared to the imbalance of redox reactions continuously induced by NIF in HK320, GO-NIF effectively alleviated the observed oxidative pressure. Furthermore, compared to NIF treatment alone, GO-NIF treatment effectively increased the activities of superoxide dismutase (SOD), guaiacol peroxidase (POD), catalase (CAT), and ascorbate peroxidase (APX) in both lines, indicating GO induced resistance to the damage caused by NIF to sweet corn seedlings. This study will provides an empirical basis for understanding the detoxification promoting effect of GO in NIF and analyzing the mechanism of GO induced allogeneic detoxification in cells.
Asunto(s)
Antioxidantes , Clorofila , Grafito , Herbicidas , Fotosíntesis , Compuestos de Sulfonilurea , Zea mays , Fotosíntesis/efectos de los fármacos , Clorofila/metabolismo , Zea mays/efectos de los fármacos , Zea mays/metabolismo , Zea mays/crecimiento & desarrollo , Compuestos de Sulfonilurea/farmacología , Compuestos de Sulfonilurea/toxicidad , Antioxidantes/metabolismo , Grafito/toxicidad , Herbicidas/toxicidad , Herbicidas/farmacología , Piridinas/farmacología , Fluorescencia , Superóxido Dismutasa/metabolismo , Plantones/efectos de los fármacos , Plantones/crecimiento & desarrollo , Plantones/metabolismoRESUMEN
Microalgae are unicellular, photosynthetic organisms in aquatic environments and are sensitive to water quality and contaminants. While green algae and diatoms are widely used for toxicity assessments, there is a relatively limited amount of toxicity data available for freshwater dinoflagellates. Here, we evaluated the sub-lethal effects of the metals Cu, Cr, Ni, and Zn and the herbicides atrazine and S-metolachlor on the freshwater dinoflagellate Palatinus apiculatus. Based on the 72-h median effective concentration (EC50), P. apiculatus showed sensitive responses to metals in the order of Cu (0.052 mg L-1), Cr (0.085 mg L-1), Zn (0.098 mg L-1), and Ni (0.13 mg L-1). Among the tested herbicides, P. apiculatus was more sensitive to atrazine (0.0048 mg L-1) than S-metolachlor (0.062 mg L-1). In addition, we observed morphological alterations and significant increases in reactive oxygen species (ROS) production in cells exposed to 0.05 mg L-1 of Cu and 0.005 mg L-1 of atrazine. These indicated that metals and pesticides induced oxidative stress in cellular metabolic processes and consequently caused severe physiological damage to the cells. Our results provide baseline data on the toxic effects of typical environmental contaminants on freshwater dinoflagellate, suggesting that P. apiculatus could be used as a bioindicator in freshwater toxicity assessments. PRACTITIONER POINTS: The sub-lethal effects of metals and pesticides on the freshwater dinoflagellate Palatinus apiculatus were evaluated. Palatinus sensitively responded to metals and pesticides; of test chemicals, atrazine (0.0048 mg L-1 of EC50) was the most sensitive. Metals and pesticides induced oxidative stress and consequently caused severe physiological damage to the Palatinus cells. The freshwater dinoflagellate Palatinus can be used as a bioindicator in freshwater toxicity assessments.
Asunto(s)
Dinoflagelados , Contaminantes Químicos del Agua , Dinoflagelados/efectos de los fármacos , Contaminantes Químicos del Agua/toxicidad , Agua Dulce , Metales/toxicidad , Plaguicidas/toxicidad , Herbicidas/toxicidad , Especies Reactivas de Oxígeno/metabolismo , Atrazina/toxicidadRESUMEN
BACKGROUND: Atrazine (ATR), a commonly used herbicide, is linked to dopaminergic neurotoxicity, which may cause symptoms resembling Parkinson's disease (PD). This study aims to reveal the molecular regulatory networks responsible for ATR exposure and its effects on dopaminergic neurotoxicity based on an integration strategy. METHODS: Our approach involved network toxicology, construction of protein-protein interaction (PPI) networks, gene ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, as well as molecular docking techniques. Subsequently, we validated the predicted results in PC12 cells in vitro. RESULTS: An integrated analysis strategy indicating that 5 hub targets, including mitogen-activated protein kinase 3 (Mapk3), catalase (Cat), heme oxygenase 1 (Hmox1), tumor protein p53 (Tp53), and prostaglandin-endoperoxide synthase 2 (Ptgs2), may play a crucial role in ATR-induced dopaminergic injury. Molecular docking indicated that the 5 hub targets exhibited certain binding activity with ATR. Cell counting kit-8 (CCK8) results illustrated a dose-response relationship in PC12 cells. Real-time quantitative polymerase chain reaction (RT-qPCR) displayed notable changes in the expression of hub targets mRNA levels, with the exception of Mapk3. Western blotting results suggested that ATR treatment in PC12 cells resulted in an upregulation of the Cat, Hmox1, and p-Mapk3 protein expression levels while causing a downregulation in Tp53, Ptgs2, and Mapk3. CONCLUSION: Our findings indicated that 5 hub targets identified could play a vital role in ATR-induced dopaminergic neurotoxicity in PC12 cells. These results provide preliminary support for further investigation into the molecular mechanism of ATR-induced toxicity.
Asunto(s)
Atrazina , Neuronas Dopaminérgicas , Herbicidas , Simulación del Acoplamiento Molecular , Atrazina/toxicidad , Animales , Células PC12 , Ratas , Herbicidas/toxicidad , Neuronas Dopaminérgicas/efectos de los fármacos , Mapas de Interacción de Proteínas , Dopamina/metabolismoRESUMEN
BACKGROUND: The commercial utilization of genetically modified soybeans has yielded substantial economic advantages. Nevertheless, the genetic drift towards wild soybeans is one of the main ecological risks that needs to be addressed. Previous experiments demonstrated the absence of fitness cost or florescence overlap in hybrid offspring resulting from the crossbreeding of transgenic soybean GTS40-3-2 and Zhengzhou wild soybeans. In this study, hybrid progeny was systematically crossed with wild soybeans to establish a backcross progeny system. This system was employed to evaluate the ecological risk associated with the backcross progeny of transgenic and wild soybeans. RESULTS: The findings indicated that the offspring from the backcross exhibited glyphosate tolerance. Furthermore, the expression of foreign proteins in the backcross offspring was notably lower than in the transgenic soybean, and there was no significant difference when compared to the hybrid progeny. Parameters such as germination rate, aboveground biomass, pods per plant, full seeds per plant, and 100-grain weight exhibited no significant differences between the negative and positive lines of the backcross progenies, and no fitness cost was identified in comparison to wild soybeans. These results underscore the potential for foreign genes to propagate within other wild soybeans, which requires continuous attention. CONCLUSIONS: The widespread adoption of genetically modified soybeans has undeniably led to substantial economic gains. However, the research findings emphasize the critical importance of addressing the ecological risks posed by genetic drift towards wild soybeans. The backcross progeny system established in this study indicates that the potential for foreign gene dissemination to wild soybean populations warrants continued attention and mitigation strategies.
Asunto(s)
3-Fosfoshikimato 1-Carboxiviniltransferasa , Glycine max , Glicina , Glifosato , Resistencia a los Herbicidas , Plantas Modificadas Genéticamente , Glycine max/genética , Glycine max/efectos de los fármacos , Glycine max/crecimiento & desarrollo , Plantas Modificadas Genéticamente/genética , Glicina/análogos & derivados , Glicina/farmacología , Resistencia a los Herbicidas/genética , 3-Fosfoshikimato 1-Carboxiviniltransferasa/genética , Aptitud Genética , Herbicidas/farmacología , Herbicidas/toxicidadRESUMEN
Glyphosate, the world's most widely used herbicide, has a low toxicity rating despite substantial evidence of adverse health effects. Furthermore, glyphosate-based formulations (GBFs) contain several other chemicals, some of which are known to be harmful. Additionally, chronic, and acute exposure to GBFs among rural workers may lead to health impairments, such as neurodegenerative diseases and cancer. P53 is known as a tumor suppressor protein, acting as a key regulator of the cellular response to stress and DNA damage. Therefore, mutations in the TP53 gene, which encodes p53, are common genetic alterations found in various types of cancer. Therefore, this study aimed to evaluate the cytotoxicity and genotoxicity of GBF in two glioblastoma cell lines: U87MG (TP53-proficient) and U251MG (TP53-mutant). Additionally, the study aimed to identify the main proteins involved in the response to GBF exposure using Systems Biology in a network containing p53 and another network without p53. The MTT assay was used to study the toxicity of GBF in the cell lines, the clonogenic assay was used to investigate cell survival, and the Comet Assay was used for genotoxicity evaluation. For data analysis, bioinformatics tools such as String 12.0 and Stitch 5.0 were applied, serving as a basis for designing binary networks in the Cytoscape 3.10.1 program. From the in vitro test analyses, it was observed a decrease in cell viability at doses starting from 10â¯ppm. Comet Assay at concentrations of 10â¯ppm and 30â¯ppm for the U251MG and U87MG cell lines, respectively observed DNA damage. The network generated with systems biology showed that the presence of p53 is important for the regulation of biological processes involved in genetic stability and neurotoxicity, processes that did not appear in the TP53-mutant network.
Asunto(s)
Supervivencia Celular , Daño del ADN , Glioblastoma , Glicina , Glifosato , Herbicidas , Proteína p53 Supresora de Tumor , Humanos , Glicina/análogos & derivados , Glicina/toxicidad , Herbicidas/toxicidad , Proteína p53 Supresora de Tumor/genética , Proteína p53 Supresora de Tumor/metabolismo , Glioblastoma/genética , Glioblastoma/patología , Línea Celular Tumoral , Daño del ADN/efectos de los fármacos , Supervivencia Celular/efectos de los fármacos , Ensayo Cometa , Mutación , Relación Dosis-Respuesta a DrogaRESUMEN
Lewy body disease (LBD), one of the most common neurodegenerative diseases (NDDs), is characterized by excessive accumulation of α-synuclein (α-syn) in neurons. In recent years, environmental factors such as exposure to herbicides and pesticides have been attributed to the development of this condition. While majority of the studies on neurotoxic effects of paraquat (PQ) have focused on α-syn-mediated neuronal damage in the early stages of α-syn accumulation in neurons, efforts to explore the key target for α-syn degradation are limited. Recent research has suggested that histone deacetylase 6 (HDAC6) might possibly regulate amyloid clearance, and that the metabolism of compounds in neurons is also directly affected by axonal transport in neurons. Dynein predominantly mediates reverse transportation of metabolites and uptake of signal molecules and other compounds at the end of axons, which is conducive to the reuse of cell components. However, the role of interaction of dynein with HDAC6 in metabolites transport is still unclear. Therefore, this study aimed to investigate the role of HDAC6 in α-syn accumulation/clearance in neurons and the associated possible influencing factors. The results revealed that HDAC6 could transport ubiquitinated α-syn, bind to dynein, form an aggresome, and relocate to the center of the microtubule tissue, ultimately reducing abnormal accumulation of α-syn. However, PQ treatment resulted in HDAC6 upregulation, causing abnormal aggregation of α-syn. Taken together, these findings indicated that PQ exposure caused abnormal accumulation of α-syn and decreased effective degradation of α-syn by HDAC6-mediated aggresome-autophagy-lysosome pathway.
Asunto(s)
Dineínas , Histona Desacetilasa 6 , Paraquat , alfa-Sinucleína , Histona Desacetilasa 6/metabolismo , Paraquat/toxicidad , alfa-Sinucleína/metabolismo , Animales , Dineínas/metabolismo , Herbicidas/toxicidad , Neuronas/efectos de los fármacos , Neuronas/metabolismo , Neuronas/patología , Transporte Axonal/efectos de los fármacos , RatonesRESUMEN
The potential connection between exposure to glyphosate and glyphosate-based herbicides (GBHs) and breast cancer risk is a topic of research that is rapidly gaining the public's attention due to the conflicting reports surrounding glyphosate's potential carcinogenicity. In this review, we synthesize the current published biomedical literature works that have explored associations of glyphosate, its metabolite, aminomethylphosphonic acid (AMPA), and GBHs with breast cancer risk in humans and human cell-based models. Using PubMed as our search engine, we identified a total of 14 articles that were included in this review. In the four human studies, urinary glyphosate and/or AMPA were associated with breast cancer risk, endocrine disruption, oxidative stress biomarkers, and changes in DNA methylation patterns. Among most of the 10 human cell-based studies, glyphosate exhibited endocrine disruption, induced altered gene expression, increased DNA damage, and altered cell viability, while GBHs were more cytotoxic than glyphosate alone. In summary, numerous studies have shown glyphosate, AMPA, and GBHs to have potential carcinogenic, cytotoxic, or endocrine-disruptive properties. However, more human studies need to be conducted in order for more definitive and supported conclusions to be made on their potential effects on breast cancer risk.
Asunto(s)
Neoplasias de la Mama , Glicina , Glifosato , Herbicidas , Humanos , Glicina/análogos & derivados , Glicina/toxicidad , Herbicidas/toxicidad , Neoplasias de la Mama/inducido químicamente , Femenino , Organofosfonatos/toxicidadRESUMEN
The regulation solutions and mechanisms of reducing pesticide phytotoxicity to nontarget plants are not well-defined and detailed. Here, we have proposed a new detoxification strategy to control the toxic effects of herbicide imazethapyr (IM) induced in wheat seedlings from the perspective of the plasma membrane (PM) H+-ATPase. We found that the changes in PM H+-ATPase activity have a regulatory effect on the phytotoxic effects induced by IM in plants. Treatment with PM H+-ATPase activators restored the reduced auxin content and photosynthetic efficiency caused by IM, thereby promoting plant growth. Application of a PM H+-ATPase inhibitor further reduced phosphorus content and significantly increased 2,4-dihydroxy-7-methoxy-2H,1,4-benzoxazin-3(4H)one (DIMBOA) and jasmonic acid levels. These effects indicate that auxin and DIMBOA may regulate plant growth trends and detoxification effects mediated by PM H+-ATPase. This work opens a new strategy for regulating herbicide toxicity to nontarget plants from the PM H+-ATPase.
Asunto(s)
Herbicidas , Ácidos Nicotínicos , Proteínas de Plantas , ATPasas de Translocación de Protón , Triticum , Triticum/crecimiento & desarrollo , Triticum/efectos de los fármacos , Triticum/metabolismo , Triticum/enzimología , Herbicidas/toxicidad , ATPasas de Translocación de Protón/metabolismo , Proteínas de Plantas/metabolismo , Proteínas de Plantas/genética , Ácidos Nicotínicos/toxicidad , Ácidos Nicotínicos/farmacología , Ácidos Indolacéticos/metabolismo , Plantones/efectos de los fármacos , Plantones/crecimiento & desarrollo , Plantones/metabolismo , Oxilipinas/farmacología , Ciclopentanos/farmacologíaRESUMEN
Phytotoxic compounds isolated and identified from different plants have the ability to use as plant-based herbicides. Phytotoxic chemicals may be essential to weed management and environmental protection in order to reduce the indiscriminate use of synthetic pesticides. It has been reported that Elaeocarpus floribundus plant possesses phytotoxic compounds. The leaf extracts of this species demonstrated significant growth inhibition against the tested plants (dicot plant lettuce and plant monocot timothy) and inhibition was dose- and species-dependent pattern. Two phytotoxic compounds were separated using different purifications methods and identified as compounds 1 and 2. All phytotoxic compounds displayed potent growth limitation against the tested species (cress). The compound concentrations needed for the inhibition of 50% growth (IC50 value) of tested species ranged from 1.06 to 8.53 µM (micromolar). Findings of this research suggest that these compounds might be responsible for the phytotoxicity of Elaeocarpus floribundus plant. The results of this study may be helpful for the development of natural herbicide to control weeds.
Asunto(s)
Herbicidas , Extractos Vegetales , Malezas , Herbicidas/farmacología , Herbicidas/toxicidad , Malezas/efectos de los fármacos , Malezas/crecimiento & desarrollo , Extractos Vegetales/farmacología , Extractos Vegetales/química , Extractos Vegetales/toxicidad , Control de Malezas/métodos , Hojas de la Planta/efectos de los fármacos , Hojas de la Planta/químicaRESUMEN
The unsustainable use of manmade chemicals poses significant threats to biodiversity and human health. Emerging evidence highlights the potential of certain chemicals to cause transgenerational impacts on metabolic health. Here, we investigate male transmitted epigenetic transgenerational effects of the anti-androgenic herbicide linuron in the pancreas of Xenopus tropicalis frogs, and their association with metabolic phenotypes. Reduced representation bisulfite sequencing (RRBS) was used to assess genome-wide DNA methylation patterns in the pancreas of adult male F2 generation ancestrally exposed to environmentally relevant linuron levels (44 ± 4.7 µg/L). We identified 1117 differentially methylated regions (DMRs) distributed across the X. tropicalis genome, revealing potential regulatory mechanisms underlying metabolic disturbances. DMRs were identified in genes crucial for pancreatic function, including calcium signalling (clstn2, cacna1d and cadps2), genes associated with type 2 diabetes (tcf7l2 and adcy5) and a biomarker for pancreatic ductal adenocarcinoma (plec). Correlation analysis revealed associations between DNA methylation levels in these genes and metabolic phenotypes, indicating epigenetic regulation of glucose metabolism. Moreover, differential methylation in genes related to histone modifications suggests alterations in the epigenetic machinery. These findings underscore the long-term consequences of environmental contamination on pancreatic function and raise concerns about the health risks associated with transgenerational effects of pesticides.
Asunto(s)
Metilación de ADN , Epigénesis Genética , Páncreas , Fenotipo , Xenopus , Animales , Metilación de ADN/efectos de los fármacos , Masculino , Páncreas/efectos de los fármacos , Páncreas/metabolismo , Epigénesis Genética/efectos de los fármacos , Linurona/toxicidad , Herbicidas/toxicidad , Plaguicidas/toxicidadRESUMEN
In recent years, there has been a need for environmentally friendly compounds for weed management in agriculture. This study is aimed to assess the phytotoxic constituents of oils obtained from oleoresins of seven Copaifera species (known as copaiba oils). Copaiba oils were separated from the resins by hydro-distillation, and the distillates were analyzed using gas chromatography-mass spectrometry (GC-MS) to characterize their chemical compositions. Multivariate analyses and molecular networking of GC-MS data were conducted to discern patterns in the chemical composition and phytotoxic activity of the oils, with the aim of identifying key compounds associated with phytotoxic activity. Seed germination bioassay revealed strong or complete germination inhibition against the monocot, Agrostis stolonifera but not the dicot Lactuca sativa. GC-MS analysis showed variations in composition among Copaifera species with some common compounds identified across multiple species. Caryophyllene oxide and junenol were associated with the observed phytotoxic effects. Automated flash chromatography was used to isolate the major compounds of the oils. Isolated compounds exhibited differing levels of phytotoxicity compared to the oils, suggesting the importance of interactions or synergism among oil components. These findings highlight the potential of copaiba oils as natural herbicidal agents and underscore the importance of considering species-specific responses in weed management strategies.
Asunto(s)
Fabaceae , Cromatografía de Gases y Espectrometría de Masas , Germinación , Aceites Volátiles , Semillas , Fabaceae/química , Aceites Volátiles/química , Aceites Volátiles/toxicidad , Aceites Volátiles/farmacología , Semillas/química , Semillas/efectos de los fármacos , Semillas/crecimiento & desarrollo , Germinación/efectos de los fármacos , Aceites de Plantas/química , Aceites de Plantas/toxicidad , Aceites de Plantas/farmacología , Lactuca/efectos de los fármacos , Lactuca/crecimiento & desarrollo , Herbicidas/farmacología , Herbicidas/química , Herbicidas/toxicidadRESUMEN
Detection of autofluorescence parameters is a useful approach to gain insight into the physiological state of plants and algae, but the effect of reabsorption hinders unambiguous interpretation ofin vivodata. The exceptional morphological features ofNitellopsis obtusamade it possible to measure autofluorescence spectra along single internodal cells and estimate relative changes in autofluorescence intensity in selected spectral regions at room temperatures, avoiding the problems associated with thick or optically dense samples. The response of algal cells to controlled white light and DCMU herbicide was analyzed by monitoring changes in peak FL intensity at 680 nm and in F680/F750 ratio. Determining the association between the selected spectral FL parameters revealed an exponential relationship, which provides a quantitative description of photoinduced changes. The ability to discern the effect of DCMU not only in the autofluorescence spectra of dark-adapted cells, but also in the case of light-adapted cells, and even after certain doses of excess light, suggests that the proposed autofluorescence analysis ofN. obtusamay be useful for detecting external stressors in the field.
Asunto(s)
Luz , Estrés Fisiológico/fisiología , Espectrometría de Fluorescencia/métodos , Fluorescencia , Herbicidas/toxicidadRESUMEN
Terbuthylazine (TBA) is a common triazine herbicide used in agricultural production, which causes toxic damage in multiple tissues. Hesperidin (HSP) is a flavonoid derivative that has anti-inflammatory, antioxidant and cytoprotective effects, but its role in reducing toxic damage caused by pesticides is still unclear. In this study, we aimed to investigate the toxic effect of TBA exposure on chicken hepatocytes and the therapeutic effect of HSP on the TBA-induced hepatotoxicity. Our results demonstrated that HSP could alleviate TBA exposure-induced endoplasmic reticulum (ER) stress. Interestingly, TBA significantly disrupted the integrity of mitochondria-associated endoplasmic reticulum membrane (MAM), while HSP treatment showed the opposite tendency. In addition, TBA could significantly trigger ferroptosis in liver, and HSP treatment reversed ferroptosis under TBA exposure. These results suggested that HSP could inhibit ER stress and alleviate ferroptosis under TBA exposure via maintaining MAM integrity, which provided a novel strategy to take precautions against TBA toxicity.
Asunto(s)
Pollos , Retículo Endoplásmico , Ferroptosis , Hepatocitos , Hesperidina , Animales , Hepatocitos/efectos de los fármacos , Hepatocitos/metabolismo , Ferroptosis/efectos de los fármacos , Hesperidina/farmacología , Retículo Endoplásmico/efectos de los fármacos , Retículo Endoplásmico/metabolismo , Estrés del Retículo Endoplásmico/efectos de los fármacos , Mitocondrias/efectos de los fármacos , Mitocondrias/metabolismo , Herbicidas/toxicidadRESUMEN
Glyphosate, a prevalent herbicide, has raised concerns due to its potential ecological impact, especially on aquatic ecosystems. While it is crucial for managing agricultural productivity, its inadvertent effects on non-target aquatic species like the red swamp crayfish, Procambarus clarkii, are not fully understood. In the present study, the neurotoxicity, oxidative stress, and immune suppression of glyphosate on P. clarkii were investigated. Sublethal glyphosate exposure (5, 10 and 20 mg/L) for 96 h was found to significantly decrease AChE activity in both brain and hepatopancreas, correlating with reduced foraging efficiency and increased turnover time. Oxidative stress was evident through increased lipid peroxidation (LPO) and malondialdehyde (MDA) levels and altered antioxidant enzyme activities such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). In addition, the total antioxidative capacity (T-AOC) was inhibited at 10 and 20 mg/L of glyphosate exposure. Immune assays revealed a decrease in total hemocyte counts (THC) and suppression of key immune enzyme activities and transcriptional expressions at higher concentrations, suggesting compromised immune defenses. The findings demonstrate that glyphosate can induce considerable neurotoxic and immunotoxic effects in P. clarkii, disrupting essential physiological functions and behavior.
Asunto(s)
Astacoidea , Glicina , Glifosato , Herbicidas , Estrés Oxidativo , Contaminantes Químicos del Agua , Animales , Astacoidea/efectos de los fármacos , Astacoidea/inmunología , Glicina/análogos & derivados , Glicina/toxicidad , Estrés Oxidativo/efectos de los fármacos , Contaminantes Químicos del Agua/toxicidad , Herbicidas/toxicidad , Peroxidación de Lípido/efectos de los fármacos , Superóxido Dismutasa/metabolismo , Catalasa/metabolismo , Encéfalo/efectos de los fármacos , Encéfalo/metabolismo , Hepatopáncreas/efectos de los fármacos , Antioxidantes/metabolismo , Malondialdehído/metabolismo , Acetilcolinesterasa/metabolismoRESUMEN
Prometryn is commonly used in agricultural and non-agricultural settings. However, possible harm to aquatic organisms remains a persistent concern. Prometryn was also the only one of the 26 triazine herbicides detected in this study. Numerous studies have assessed the harmful effects of prometryn in teleost fish and shrimp. There is a lack of information regarding the ecological and human health risks, as well as the toxic mechanisms affecting crayfish. In this study, human health risk assessment (THQ) and ecological risk assessment (RQ) were conducted on P. clarkii in the rice-crayfish co-culture (IRCC) farming model. The 96 h of exposure to 0.286 mg/L and 1.43 mg/L prometryn was conducted to investigate the potential effects and molecular mechanisms of hepatopancreatic resistance to prometryn in P. clarkii. The original sample analysis revealed that the THQ calculated from the prometryn levels in the muscle and hepatopancreas was below 0.1, suggesting no threat to human health. However, the calculated RQ values were >0.1, indicating a risk to P. clarkii. Histological analysis and biochemical index detection of the experimental samples revealed that the hepatopancreatic injury and oxidative damage in P. clarkii were caused by prometryn. Moreover, transcriptome analysis identified 2512 differentially expressed genes (DEGs) after 96 h of prometryn exposure. Prometryn exposure caused significant changes in metabolic pathways, including oxoacid metabolic processes and cytochrome P450-associated drug metabolism. Further hub gene analysis via PPI indicated that exposure to prometryn may inhibit lipid synthesis, storage, and amino acid transport and affect glucose metabolic pathways and hormone synthesis. Additionally, we hypothesized that prometryn-triggered cell death could be linked to the PI3K-Akt signaling cascade. This study's findings have significant meaning for the efficient and logical application of herbicides in IRCC, ultimately aiding in advancing a highly productive agricultural system.
Asunto(s)
Astacoidea , Herbicidas , Prometrina , Contaminantes Químicos del Agua , Astacoidea/efectos de los fármacos , Animales , Contaminantes Químicos del Agua/toxicidad , Herbicidas/toxicidad , Medición de Riesgo , Prometrina/toxicidadRESUMEN
Atrazine is one of the most used herbicides in the world, although it is banned in several countries. Pollution of terrestrial and aquatic ecosystems represents a threat to non-target organisms, with various damages already reported in different species. However, there is controversy in studies on atrazine. The question of whether atrazine increases animal mortality is not yet clearly resolved. In this context, this study aimed to carry out a meta-analytic review, focusing on studies on environmental concentrations of the herbicide atrazine to evaluate its lethal effects on various animal species. We identified and analyzed 107 datasets through a selection process that used the Scopus, PubMed, and Web of Science (WoS) databases. A significant increase in the mortality rate of animals exposed to environmental concentrations of atrazine was observed. Nematodes, amphibians, molluscs, insects, and fish showed increased mortality after exposure to atrazine. Animals in the larval and juvenile stages showed greater susceptibility when exposed to different concentrations of atrazine. Furthermore, both commercial and pure formulations resulted in high mortality rates for exposed animals. Atrazine and other pesticides had a synergistic effect, increasing the risk of mortality in animals. There are still many gaps to be filled, and this study can serve as a basis for future regulations involving atrazine.