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The aquaculture industry is hindered by various factors. One of the most noticeable factors is infection by parasites and pathogens. Argulus stands out as a prominent and economically significant ectoparasite in freshwater aquaculture. Argulus infestation causes severe immunomodulatory effects on its hosts by promoting argulosis, causing inflammation, extensive tissue damage, and death. Indian aquaculture sector faced a loss of 62.5 million USD due to Argulus infection. However, current control methods, such as pesticides, cause serious environmental damage. Herbal treatment methods are ineffective and have limitations. Hence, a more efficient and cost-effective control method is needed. In recent years, vaccine development has emerged as a promising avenue of research. Understanding the effect of the host-parasite relationship in the host immune system is essential to develop strategies for prevention, control, and management of argulosis. These interactions provide insights into the co-evolutionary dynamics between hosts and parasites. This review provides an overview of the current knowledge on the host-searching behaviour of Argulus, host-parasite interaction and control strategies. This review also highlights the need for further research and the development of sustainable control measures for Argulus infection.
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Acrylamide (ACR) is a water-soluble monomer with broad consumer applications, even in foods due to thermal processes. Acute exposure to ACR may lead to neurotoxic effects such as ataxia and skeletal muscle weakness in humans and experimental animals. Oxidative stress is the primary pathway in ACR toxicity; therefore, this study aimed to evaluate the possible protective effect of benzo[b]thiophene analogs as an antioxidant drug for ACR poisoning. For this purpose, adult zebrafish were chosen as the experimental model considering the 3Rs of research. Hydroxyl containing benzo[b]thiophene analogs, 1-(3-hydroxybenzo[b]thiophen-2-yl) ethanone (BP) and 1-(3-hydroxybenzo[b]thiophen-2-yl) propan-1-one hydrate (EP) were injected via intraperitoneal (i.p.) route at an effective dose of 5 mg/kg one hour before the exposure of ACR (0.75 mM) for three days. ACR fish showed aberrant socio-behavior with low exploration, tight circling, negative scototaxis, disrupted aggression, and tight shoaling. These results indicated depression comorbid and anxiety-like phenotype. BP and EP partially reduced the aberrant socio-behavior. BP and EP elevated the antioxidant defense and reduced the oxidative damage in the brain caused by ACR. Cellular and tissular alterations caused by ACR were visualized through histopathological study. BP and EP administration reduced and repaired the cellular changes via the antioxidant mechanism. BP and EP altered the axonal growth and regeneration gene and synaptic vesicle cycle gene expression necessary for neurotransmission. This combined gain-of-function of redox mechanism at molecular, cellular, and tissular levels explains the behavioral improvement at the organismal level of the organization.
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The prevalent use of Azorubine (E122) and the unintentional food additive, Bisphenol A (BPA), in ready-to-drink (RTD) beverages raises significant health concerns, especially for children. The combined impact on embryonic development must be explored despite individual safety assessments. Our investigation revealed that the combined exposure of E122 and BPA at beverage concentration significantly induces mortality and morphological deformities, including reduced growth, pericardial edema, and yolk sac edema. The co-exposure triggers oxidative stress, impairing antioxidant enzyme responses and resulting in lipid and cellular damage. Notably, apoptotic cells are observed in the neural tube and notochord of the co-exposed larvae. Critical genes related to the antioxidant response elements (nrf2, ho1, and nqo1), apoptosis activation (bcl2, bax, and p53), and pro/anti-inflammatory cytokines (nfkb, tnfa, il1b, tgfb, il10, and il12) displayed substantial changes, highlighting the molecular mechanisms. Behavior studies indicated hypo-locomotion with reduced thigmotaxis and touch response in co-exposed larvae, distinguishing it from individual exposures. These findings underscore the neurodevelopmental impacts of E122 and BPA at reported beverage concentrations, emphasizing the urgent need for comprehensive safety assessments, particularly for child consumption.
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Compuestos de Bencidrilo , Fenoles , Pez Cebra , Animales , Apoptosis/efectos de los fármacos , Compuestos de Bencidrilo/toxicidad , Bebidas , Embrión no Mamífero/efectos de los fármacos , Desarrollo Embrionario/efectos de los fármacos , Larva/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Fenoles/toxicidadRESUMEN
Exploration of Pleurotus ostreatus as a biological agent in the degradation of persistent plastics like polyethylene, polystyrene, polyvinyl chloride, and polyethylene terephthalate, revealing a promising avenue toward mitigating the environmental impacts of plastic pollution. Leveraging the intrinsic enzymatic capabilities of this fungus, mainly its production of laccase, presents a sustainable and eco-friendly approach to breaking down complex polymer chains into less harmful constituents. This review focused on enhancements in the strain's efficiency through genetic engineering, optimized culture conditions, and enzyme immobilization to underscore the potential for scalability and practical application of this bioremediation process. The utilization of laccase from P. ostreatus in plastic waste management demonstrates a vital step forward in pursuing sustainable environmental solutions. By using the potential of fungal bioremediation, researchers can move closer to a future in which the adverse effects of plastic pollution are significantly mitigated, benefiting the health of our planet and future generations.
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Biodegradación Ambiental , Lacasa , Microplásticos , Pleurotus , Lacasa/metabolismo , Lacasa/química , Pleurotus/enzimología , Microplásticos/química , Enzimas Inmovilizadas/metabolismo , Enzimas Inmovilizadas/químicaRESUMEN
The study "Systemic Lipopolysaccharide Exposure Exacerbates Choroidal Neovascularization in Mice" by Tsioti et al. explores the impact of systemic lipopolysaccharide (LPS) on choroidal neovascularization (CNV) progression. The findings reveal systemic LPS exposure significantly enhances fluorescein leakage, driven by increased pro-inflammatory monocyte-derived macrophages and microglia activation. The study underscores the importance of managing systemic inflammation to mitigate CNV progression, suggesting potential therapeutic strategies targeting CSF1R inhibition and Müller cell modulation. Future research should focus on elucidating the molecular pathways involved in LPS-induced CNV exacerbation and translating these findings into clinical interventions.
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Neoplasias de Cabeza y Cuello , Inhibidores de Puntos de Control Inmunológico , Recurrencia Local de Neoplasia , Carcinoma de Células Escamosas de Cabeza y Cuello , Humanos , Inhibidores de Puntos de Control Inmunológico/uso terapéutico , Carcinoma de Células Escamosas de Cabeza y Cuello/tratamiento farmacológico , Neoplasias de Cabeza y Cuello/tratamiento farmacológico , Neoplasias de Cabeza y Cuello/patología , Metástasis de la NeoplasiaAsunto(s)
Inestabilidad Genómica , Neoplasias Orofaríngeas , Humanos , Neoplasias Orofaríngeas/virología , Neoplasias Orofaríngeas/terapia , Neoplasias Orofaríngeas/genética , Infecciones por Papillomavirus/complicaciones , Infecciones por Papillomavirus/virología , Carcinoma de Células Escamosas/virología , Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/terapia , Masculino , Persona de Mediana Edad , Femenino , Integración Viral , Papillomaviridae/genéticaRESUMEN
The escalating focus on ageing-associated disease has generated substantial interest in the phenomenon of cognitive impairment linked to diabetes. Hyperglycemia exacerbates oxidative stress, contributes to ß-amyloid accumulation, disrupts mitochondrial function, and impairs cognitive function. Existing therapies have certain limitations, and apigenin (AG), a natural plant flavonoid, has piqued interest due to its antioxidant, anti-inflammatory, and anti-hyperglycemic properties. So, we anticipate that AG might be a preventive medicine for hyperglycemia-associated amnesia. To test our hypothesis, naïve zebrafish were trained to acquire memory and pretreated with AG. Streptozotocin (STZ) was administered to mimic hyperglycemia-induced memory dysfunction. Spatial memory was assessed by T-maze and object recognition through visual stimuli. Acetylcholinesterase (AChE) activity, antioxidant enzyme status, and neuroinflammatory genes were measured, and histopathology was performed in the brain to elucidate the neuroprotective mechanism. AG exhibits a prophylactic effect and improves spatial learning and discriminative memory of STZ-induced amnesia in zebrafish under hyperglycemic conditions. AG also reduces blood glucose levels, brain oxidative stress, and AChE activity, enhancing cholinergic neurotransmission. AG prevented neuronal damage by regulating brain antioxidant response elements (ARE), collectively contributing to neuroprotective properties. AG demonstrates a promising effect in alleviating memory dysfunction and mitigating pathological changes via activation of the Nrf2/ARE mechanism. These findings underscore the therapeutic potential of AG in addressing memory dysfunction and neurodegenerative changes associated with hyperglycemia.
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Amnesia , Apigenina , Hiperglucemia , Factor 2 Relacionado con NF-E2 , Fármacos Neuroprotectores , Estrés Oxidativo , Pez Cebra , Animales , Factor 2 Relacionado con NF-E2/metabolismo , Hiperglucemia/complicaciones , Hiperglucemia/tratamiento farmacológico , Hiperglucemia/metabolismo , Amnesia/tratamiento farmacológico , Amnesia/metabolismo , Estrés Oxidativo/efectos de los fármacos , Apigenina/farmacología , Apigenina/uso terapéutico , Fármacos Neuroprotectores/farmacología , Fármacos Neuroprotectores/uso terapéutico , Acetilcolinesterasa/metabolismo , Transducción de Señal/efectos de los fármacos , Encéfalo/efectos de los fármacos , Encéfalo/metabolismo , Encéfalo/patología , Antioxidantes/farmacología , Antioxidantes/uso terapéutico , Proteínas de Pez Cebra/metabolismo , Glucemia/metabolismo , Glucemia/efectos de los fármacos , Masculino , Estreptozocina , Aprendizaje por Laberinto/efectos de los fármacos , Memoria Espacial/efectos de los fármacos , Modelos Animales de EnfermedadRESUMEN
Epilepsy is a chronic neurological disease characterized by a persistent susceptibility to seizures. Pharmaco-resistant epilepsies, impacting around 30 % of patients, highlight the urgent need for improved treatments. Neuroinflammation, prevalent in epileptogenic brain regions, is a key player in epilepsy, prompting the search for new mechanistic therapies. Hence, in this study, we explored the anti-inflammatory potential of pyrazole benzenesulfonamide derivative (T1) against pentylenetetrazole (PTZ) induced epilepsy-like conditions in in-vivo zebrafish model. The results from the survival assay showed 79.97 ± 6.65 % at 150 µM of T1 compared to PTZ-group. The results from reactive oxygen species (ROS), apoptosis and histology analysis showed that T1 significantly reduces cellular damage due to oxidative stress in PTZ-exposed zebrafish. The gene expression analysis and neutral red assay results demonstrated a notable reduction in the inflammatory response in zebrafish pre-treated with T1. Subsequently, the open field test unveiled the anti-convulsant activity of T1, particularly at a concentration of 150 µM. Moreover, both RT-PCR and immunohistochemistry findings indicated a concentration-dependent potential of T1, which inhibited COX-2 in zebrafish exposed to PTZ. In summary, T1 protected zebrafish against PTZ-induced neuronal damage, and behavioural changes by mitigating the inflammatory response through the inhibition of COX-2.
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Epilepsia , Pentilenotetrazol , Animales , Humanos , Pez Cebra , Bencenosulfonamidas , Ciclooxigenasa 2/genética , Ciclooxigenasa 2/metabolismo , Epilepsia/inducido químicamente , Epilepsia/tratamiento farmacológico , Epilepsia/metabolismo , Pirazoles/farmacología , Pirazoles/uso terapéutico , Modelos Animales de EnfermedadRESUMEN
This study investigates the individual and combined toxic effects of Bisphenol A (BPA) and Cadmium (Cd) in zebrafish, recognizing the complex mixture of pollutants organisms encounter in their natural environment. Examining developmental, neurobehavioral, reproductive, and physiological aspects, the study reveals significant adverse effects, particularly in combined exposures. Zebrafish embryos exposed to BPA + Cd exhibit synergistically increased mortality, delayed hatching, and morphological abnormalities, emphasizing the heightened toxicity of the combination. Prolonged exposure until 10 days post-fertilization underscores enduring effects on embryonic development. BPA and Cd induce oxidative stress, as evidenced by increased production of reactive oxygen species and lipid peroxidation. This oxidative stress disrupts cellular functions, affecting lipid metabolism and immune response. Adult zebrafish exposed to BPA and Cd for 40 days display compromised neurobehavioral functions, altered antioxidant defenses, and increased oxidative stress, suggesting potential neurotoxicity. Additionally, disruptions in ovarian follicle maturation and skeletal abnormalities indicate reproductive and skeletal impacts. Histological analysis reveals significant liver damage, emphasizing the synergistic hepatotoxicity of BPA and Cd. Molecular assessments further demonstrate compromised cellular defense mechanisms, synaptic function, and elevated cellular stress and inflammation-related gene expression in response to combined exposures. Bioaccumulation analysis highlights differential tissue accumulation patterns. In conclusion, this study provides comprehensive insights into the multifaceted toxicological effects of BPA and Cd in zebrafish, raising concerns about potential adverse impacts on environmental ecosystems and human health.
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Cadmio , Fenoles , Pez Cebra , Humanos , Animales , Femenino , Cadmio/toxicidad , Cadmio/metabolismo , Pez Cebra/fisiología , Ecosistema , Compuestos de Bencidrilo/toxicidad , Compuestos de Bencidrilo/metabolismo , Estrés Oxidativo , HepatocitosRESUMEN
INTRODUCTION: Argulus spp. infestation is a significant challenge for aquaculture, currently, there are no approved medications available to efficiently manage this parasite. Consequently, mechanical removal of parasites using forceps and natural substances like herbs are being explored as alternative treatment methods. Pellitorine (PLE) is a naturally occurring compound found in several plant species. It is classified as an alkaloid and belongs to the class of compounds known as amides. MATERIALS AND METHODS: This study aimed to evaluate the effectiveness of PLE in preventing Argulus spp. infestations in goldfish (Carassius auratus) and to determine the optimal dosage of PLE for the detachment of Argulus spp. RESULTS: The findings of this study revealed that PLE enhanced the immune response of goldfish by promoting superoxide dismutase (SOD) and catalase (CAT) in Argulus-infected goldfish. Additionally, PLE induces reactive oxygen species (ROS) generation and cellular damage in the Argulus. PLE at a dosage of 5 mg/mL was able to detach 80% of the argulus from goldfish within 12 h. Therapeutic index was found to be 5.99, suggesting that PLE is the safest drug. CONCLUSIONS: Therefore, our findings suggest that PLE can be a suitable and effective treatment option for preventing Argulus infestations in goldfish. The results of this study can guide the use of PLE at an optimal dosage to control Argulus infestation in goldfish.
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Antioxidantes , Antiparasitarios , Arguloida , Ácidos Grasos Insaturados , Enfermedades de los Peces , Carpa Dorada , Animales , Carpa Dorada/parasitología , Arguloida/efectos de los fármacos , Enfermedades de los Peces/parasitología , Enfermedades de los Peces/tratamiento farmacológico , Antioxidantes/farmacología , Antiparasitarios/farmacología , Alcamidas Poliinsaturadas/farmacología , Especies Reactivas de Oxígeno/metabolismo , Catalasa/metabolismo , Superóxido Dismutasa/metabolismoRESUMEN
Shrimp, a globally consumed perishable food, faces rapid deterioration during storage and marketing, causing nutritional and economic losses. With a rising environmental consciousness regarding conventional plastic packaging, consumers seek sustainable options. Utilizing natural waste resources for packaging films strengthens the food industry. In this context, we aim to create chitosan-based active films by incorporating Terminalia catappa L. leaves extract (TCE) to enhance barrier properties and extend shrimp shelf life under refrigeration. Incorporation of TCE improves mechanical, microstructural, UV, and moisture barrier properties of the chitosan film due to cross-linking interactions, resulting in robust, foldable packaging film. Active TCE film exhibits high antioxidant property due to polyphenols. These films also exhibited low wettability and showed hydrophobicity than neat CH films which is essential for meat packaging. These biodegradable films offer an eco-friendly end-of-life option when buried in soil. TCE-loaded films effectively control spoilage organisms, prevent biochemical spoilage, and maintain shrimp freshness compared to neat CH films during refrigerated condition. The active TCE film retains sensory attributes better than neat chitosan, aligning with consumer preference. The developed edible and active film from waste sources might offer sustainable, alternative packaging material with a lower carbon footprint than petroleum-based sources.
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Quitosano , Terminalia , Embalaje de Alimentos/métodos , Quitosano/química , Carne , Alimentos MarinosRESUMEN
Polycystic Ovary Syndrome (PCOS) and osteoporosis, though seemingly unrelated, exhibit intricate connections influenced by genetic and epigenetic factors. PCOS, characterized by elevated androgen levels, insulin resistance, and increased body weight, has historically been considered protective against bone fragility disorders. However, emerging research suggests that chronic inflammation, prevalent in PCOS, can adversely affect bone health. Studies have demonstrated variable bone mineral density loss in PCOS, often associated with leptin resistance and hyperinsulinemia. Key genes such as INS, IGF1, CTNNB1, AKT1, and STAT3 play pivotal roles in the complex interplay between PCOS and osteoporosis, influencing insulin signaling, oxidative stress, and inflammatory pathways. Oxidative stress, a prominent element in PCOS, can lead to osteoporosis through hormonal imbalances, chronic inflammation, insulin resistance, and lifestyle factors. The insulin signaling pathway also significantly impacts both conditions by contributing to hormonal imbalances and bone health alterations. This intricate network of genetic and epigenetic factors underscores the need for a deeper understanding of their interrelationships. Thus, this review elucidates the multifaceted genetic, epigenetic, and inflammatory connections between PCOS and osteoporosis, highlighting their implications for bone health management in individuals with PCOS.
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Hiperandrogenismo , Resistencia a la Insulina , Osteoporosis , Síndrome del Ovario Poliquístico , Femenino , Humanos , Síndrome del Ovario Poliquístico/complicaciones , Síndrome del Ovario Poliquístico/genética , Síndrome del Ovario Poliquístico/metabolismo , Hiperandrogenismo/complicaciones , Insulina , Osteoporosis/genética , Inflamación/complicacionesRESUMEN
Obesity and diabetes constitute significant global health issues associated with one another. In contrast to diabetes, which is characterised by oxidative stress that enhances cellular damage and the following complications. Obesity dynamics involve chronic inflammation that promotes insulin resistance and metabolic disruptions. Anti-inflammatory and antioxidant agents, therefore, hold promise for synergistic effects, addressing inflammation and oxidative stress, key factors in managing obesity and diabetes. These agents can be utilized in novel drug delivery approaches. The complex interactions between deacetylepoxyazadiradione (DEA) and zebrafish larva subjected to metabolic impairment due to a high-fat diet (HFD) are examined in this study. The survival assay showed a significantly lower rate (79% survival rate) in the larvae exposed to HFD. Contrastingly, DEA treatment showed significant results with survival rates increasing dose-dependently (84%, 89%, and 94% at concentrations of 50 µM, 100 µM, and 150 µM, respectively). Further investigations revealed that DEA could reduce hyperlipidemic and hyperglycemic conditions in zebrafish larvae. Glucose levels significantly dropped in the DEA treatment, which was associated with a decline in larval weight, lipid accumulation, oxidative stress and apoptosis. Enzyme assays revealed higher antioxidant enzyme concentrations in DEA treated in-vivo larval models, which were associated with reduced expression of pro-inflammatory genes. In conclusion, the results demonstrate that DEA can alleviate oxidative stress and inflammation, effectively easing the diabesity-like state in zebrafish larvae. This offers potential avenues for developing DEA as a valuable drug candidate to manage the intricate diabesity condition.
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Antioxidantes , Diabetes Mellitus , Animales , Antioxidantes/farmacología , Pez Cebra/metabolismo , Adipoquinas/metabolismo , Larva/metabolismo , Obesidad/tratamiento farmacológico , Estrés Oxidativo , Inflamación/tratamiento farmacológico , Dieta Alta en Grasa , Diabetes Mellitus/tratamiento farmacológicoRESUMEN
Environmental pollution is inherently linked to several metabolic diseases and high mortality. The kidney is more susceptible to environmental pollutants compared to other organs as it is involved in concentrating and filtering most of these toxins. Few epidemiological studies revealed the intrinsic relationship between exposure to Endocrine Disrupting Chemicals (EDCs) and CKD development. Though EDCs have the potential to cause severe pathologies, the specific molecular mechanisms by which they accelerate the progression of CKD remain elusive. In particular, our understanding of how pollutants affect the progression of chronic kidney disease (CKD) through the gut-kidney axis is currently limited. EDCs modulate the composition and function of the gut microbial community and favor the colonization of harmful gut pathogens. This alteration leads to an overproduction of uremic toxin and membrane vesicles. These vesicles carry several inflammatory molecules that exacerbate inflammation and renal tissue damage and aggravate the progression of CKD. Several experimental studies have revealed potential pathways by which uremic toxin further aggravates CKD. These include the induction of membrane vesicle production in host cells, which can trigger inflammatory pathways and insulin resistance. Reciprocally, CKD can also modulate gut bacterial composition that might further aggravate CKD condition. Thus, EDCs pose a significant threat to kidney health and the global CKD burden. Understanding this complicated issue necessitates multidisciplinary initiatives such as strict environmental controls, public awareness, and the development of novel therapeutic strategies targeting EDCs.
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Disruptores Endocrinos , Insuficiencia Renal Crónica , Toxinas Biológicas , Humanos , Disruptores Endocrinos/toxicidad , Tóxinas Urémicas , Insuficiencia Renal Crónica/inducido químicamente , Riñón/metabolismo , InflamaciónRESUMEN
Microplastics (MP), tiny plastic particles, can be ingested by fish through their habitat or contaminated food sources. When combined with a high-fat diet (HFD), MP exposure may lead to increased MP accumulation in fish and negative impacts on their health. However, the underlying mechanisms of how MP and HFD interact to promote fat accumulation in fish remain poorly understood. In this study, we aimed to evaluate the combined effect of HFD and polyethylene MP (PE-MP) in the zebrafish model (Danio rerio) and decipher its molecular mechanisms. Adult zebrafish exposed to the combined HFD and PE-MP showed elevated lipid accumulation, total cholesterol, triglycerides, and abnormal swimming behavior compared to HFD-fed fish. Histological and gene expression analysis revealed severe hepatic inflammation and injury, resembling nonalcoholic fatty liver disease (NAFLD) in the HFD + PE-MP exposed zebrafish. Moreover, HFD and PE-MP exposure upregulated genes related to lipogenesis (SREBP1, FAS, and C/EBPα) and inflammation (tnfα, il1ß, and il-6) in the liver. These findings underscore the interactive effect of environmental pollutants and fish diet, emphasizing the importance of improving fish culture practices to safeguard fish health and human consumers from microplastic contamination through the food chain. This research sheds light on the complex interactions between microplastics and diet, providing valuable insights into the potential risks of microplastic pollution in aquatic ecosystems and the implications for human health. Understanding the underlying molecular mechanisms will contribute to international research efforts to mitigate the adverse effects of microplastics on both environmental and public health.
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Metabolismo de los Lípidos , Enfermedad del Hígado Graso no Alcohólico , Animales , Adulto , Humanos , Microplásticos/toxicidad , Microplásticos/metabolismo , Pez Cebra/metabolismo , Plásticos/metabolismo , Polietileno/toxicidad , Polietileno/metabolismo , Dieta Alta en Grasa/efectos adversos , Larva/metabolismo , Ecosistema , Hígado/metabolismo , Inflamación/patologíaRESUMEN
Bisphenol A (BPA) leaches from plastic products have become a major inevitable concern among the research society. Human exposure to BPA leads to deleterious effects on multiple organs by the induced hyper inflammatory and oxidative stress responses. Due to the compromised antioxidant mechanism, the brain environment was highly susceptible and required special concern to ameliorate the effects of BPA. Hence, this study investigates the potential of neem-derived semi natural deacetyl epoxyazadiradione (DEA) against the oxidative stress and inflammatory response induced by BPA exposure in N9 cells and zebrafish larvae. The results from the in vitro analyses showed a decrease in cell viability in the MTT assay and a decline in mitochondrial damage in BPA-exposed N9 cells. Further in vivo, results revealed that pre-treatment of DEA to zebrafish larvae has significantly reduced the level of superoxide anion and increased the production of antioxidant enzymes such as SOD, CAT, GST, GPx and GR. We also found a significant decrease in the production of nitric oxide (p < 0.0001) and iNOS gene expression at 150 µM concentration. Further, DEA pre-treatment improved the behaviour of zebrafish larvae by ameliorating the production of the AChE enzyme. In conclusion, DEA protected zebrafish larvae from BPA toxicity by ameliorating oxidative stress and inflammatory responses.
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Antioxidantes , Pez Cebra , Animales , Humanos , Pez Cebra/metabolismo , Antioxidantes/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Larva , Estrés Oxidativo , Compuestos de Bencidrilo/toxicidad , Compuestos de Bencidrilo/metabolismoRESUMEN
Diverse microbial communities colonize different habitats of the human body, including gut, oral cavity, nasal cavity and tissues. These microbial communities are known as human microbiome, plays a vital role in maintaining the health. However, changes in the composition and functions of human microbiome can result in chronic low-grade inflammation, which can damage the epithelial cells and allows pathogens and their toxic metabolites to translocate into other organs such as the liver, heart, and kidneys, causing metabolic inflammation. This dysbiosis of human microbiome has been directly linked to the onset of several non-communicable diseases. Recent metabolomics studies have revealed that pathogens produce several uraemic toxins. These metabolites can serve as inter-kingdom signals, entering the circulatory system and altering host metabolism, thereby aggravating a variety of diseases. Interestingly, Enterobacteriaceae, a critical member of Proteobacteria, has been commonly associated with several non-communicable diseases, and the abundance of this family has been positively correlated with uraemic toxin production. Hence, this review provides a comprehensive overview of Enterobacterial translocation and their metabolites role in non-communicable diseases. This understanding may lead to the identification of novel biomarkers for each metabolic disease as well as the development of novel therapeutic drugs.