RESUMEN
The research examined the impact of an ethanolic extract from the leaves of Kratom (Mitragyna speciosa (Korth.) Havil.) on the growth, antioxidant capacity, immune-related gene expression, and resistance to disease caused by Edwardsiella tarda in Nile tilapia (Oreochromis niloticus). The findings revealed that the extract had the important phytochemical content in the extract included total phenolics content, total flavonoids content, vitamin C, and total antioxidant capacity and 5.42 % of the crude extract was mitragynine. The extract demonstrated antioxidant activity, as evidenced by its IC50 values against ABTS and DPPH radicals and its ferric reducing power in vitro. Moreover, the MIC-IC50 value of 0.625 mg/mL indicated that the growth of the bacteria was reduced by approximately 50 %, and the MBC was 2.50 mg/mL against E. tarda. Furthermore, the orally administered Kratom leaf extract to fingerling tilapia for 8 weeks exhibited a noticeable increase in oxidative stress, as demonstrated by the increase in MDA production in the 10 and 25 g/kg groups. It also exhibited an increase in acetylcholinesterase (AChE) activity in muscle tissue at the 50 g/kg group. However, when administered at a feeding rate of 5-10 g/kg feed, the extract showed an increase in the expression of immune-related genes (IL1, IL6, IL8, NF-kB, IFNγ, TNFα, Mx, CC-chemokine, CD4, TCRß, MHC-IIß, IgM, IgT, IgD) and enhanced resistance to E. tarda infection in fish. Conversely, administering the extract at 25-50 g/kg feed resulted in contrasting effects, suppressing and reducing the observed parameters. Nevertheless, feeding the extract at all concentrations for 8 weeks did not produce any changes in the histology or systemic functioning of the liver and intestines, as indicated by blood biochemistry. These findings suggest that the ethanolic leaf extract from Kratom has the potential to be used as a substitute for antibiotics in the management of bacterial infections in Nile tilapia culture, with a recommended dosage of 5-10 g/kg feed/day for a maximum of 8 weeks.
Asunto(s)
Antibacterianos , Antioxidantes , Cíclidos , Edwardsiella tarda , Infecciones por Enterobacteriaceae , Enfermedades de los Peces , Mitragyna , Extractos Vegetales , Hojas de la Planta , Animales , Enfermedades de los Peces/inmunología , Extractos Vegetales/farmacología , Extractos Vegetales/química , Extractos Vegetales/administración & dosificación , Cíclidos/inmunología , Cíclidos/crecimiento & desarrollo , Edwardsiella tarda/efectos de los fármacos , Edwardsiella tarda/fisiología , Infecciones por Enterobacteriaceae/veterinaria , Infecciones por Enterobacteriaceae/inmunología , Antioxidantes/farmacología , Hojas de la Planta/química , Antibacterianos/farmacología , Mitragyna/química , Resistencia a la Enfermedad/efectos de los fármacos , Dieta/veterinaria , Alimentación Animal/análisis , Suplementos Dietéticos/análisisRESUMEN
Environmental pollution by micro- and nanosized plastic particles is a potential threat to aquatic animals. Polystyrene is one of the most common plastic particles in aquatic environments. Previous studies found that polystyrene nanoparticles (PNs) can penetrate the integument and accumulate in the organs of fish embryos. However, the potential impacts of PNs on fish embryos are not fully understood. To investigate this issue, zebrafish embryos were exposed to different concentrations (10, 25, and 50 mg/L) of PNs (25 nm) for 96 h (4-100 h post-fertilization), and various endpoints were examined, including developmental morphology (body length, sizes of the eyes, otic vesicles, otoliths, pericardial cavity, and yolk sac), locomotion (touch-evoked escape response and spinal motor neurons), and lateral-line function (hair cell number and hair bundle number). Exposure to 50 mg/L of PNs resulted in significant adverse effects across all endpoints studied, indicating that embryonic development was severely disrupted, and both locomotion and sensory function were impaired. However, at 25 mg/L of PNs, only locomotion and sensory function were significantly affected. The effects were insignificant in all examined endpoints at 10 mg/L of PNs. Transcript levels of several marker genes for neuronal function and eye development were suppressed after treatment. Exposure to fluorescent PNs showed that they accumulated in various organs including, the eyes, gills, blood vessels, gallbladder, gut, and lateral line neuromasts. Overall, this study suggests that short-term exposure to a high concentration of PNs can threaten fish survival by impairing embryonic development, locomotion performance, and mechanical sensory function.
Asunto(s)
Sistema de la Línea Lateral , Nanopartículas , Contaminantes Químicos del Agua , Animales , Pez Cebra , Poliestirenos/toxicidad , Nanopartículas/toxicidad , Sensación , Embrión no Mamífero , Contaminantes Químicos del Agua/metabolismoRESUMEN
The presence of nanoplastics in aquatic environments is a global problem. Accumulating evidence shows that nanoplastics can accumulate in fish and influence internal organs. However, it is still unknown if nanoplastics can impair skin cells (keratinocytes and ionocytes), which play critical roles in maintaining body fluid homeostasis. In the present study, zebrafish embryos were exposed to polystyrene nanoplastics (PS-NPs; 25 nm in size, at 0, 10, 25, and 50 mg/L) for 96 h to test the effects of PS-NPs on skin functions. After exposure to 50 mg/L, the survival rate, ion (Na+, K+, and Ca2+) contents, and acid/ammonia excretion by skin cells of embryos significantly declined. The apical structure of skin keratinocytes was damaged at 10, 25, and 50 mg/L. The number and mitochondrial activity of ionocytes were reduced at 25 and 50 mg/L. Reactive oxygen species (ROS) levels indicated by CellROX staining showed that both ionocytes and keratinocytes were under oxidative stress. PS-NPs reduced the mRNA expression of antioxidant genes (sod1, sod2, cat, and gpx1a), and promoted apoptosis-related genes (casp3a). Taken together, this study suggests that PS-NPs might suppress antioxidative reactions and induce oxidative stress, leading to mitochondrial damage and cell death of ionocytes, eventually impairing skin functions including ion uptake, pH regulation, and ammonia excretion.