Phenylalanine treatment induces tomato resistance to Tuta absoluta via increased accumulation of benzenoid/phenylpropanoid volatiles serving as defense signals.

Tuta absoluta ("leafminer"), is a major pest of tomato crops worldwide. Controlling this insect is difficult due to its efficient infestation, rapid proliferation, and resilience to changing weather conditions. Furthermore, chemical pesticides have only a short-term effect due to rapid development of T. absoluta strains. Here, we show that a variety of tomato cultivars, treated with external phenylalanine solutions exhibit high resistance to T. absoluta, under both greenhouse and open field conditions, at different locations. A large-scale metabolomic study revealed that tomato leaves absorb and metabolize externally given Phe efficiently, resulting in a change in their volatile profile, and repellence of T. absoluta moths. The change in the volatile profile is due to an increase in three phenylalanine-derived benzenoid phenylpropanoid volatiles (BPVs), benzaldehyde, phenylacetaldehyde, and 2-phenylethanol. This treatment had no effect on terpenes and green leaf volatiles, known to contribute to the fight against insects. Phe-treated plants also increased the resistance of neighboring non-treated plants. RNAseq analysis of the neighboring non-treated plants revealed an exclusive upregulation of genes, with enrichment of genes related to the plant immune response system. Exposure of tomato plants to either benzaldehyde, phenylacetaldehyde, or 2-phenylethanol, resulted in induction of genes related to the plant immune system that were also induced due to neighboring Phe-treated plants. We suggest a novel role of phenylalanine-derived BPVs as mediators of plant-insect interactions, acting as inducers of the plant defense mechanisms.

Effects of Bulleyaconitine A on Extracellular Matrix Secretion and Expression of Related Proteins in Acetaldehyde-Activated Hepatic Stellate Cells.

Activated hepatic stellate cells differentiate into myofibroblasts, which synthesize and secrete extracellular matrix (ECM) leading to liver fibrosis. It was previously demonstrated that bulleyaconitine A (BLA), an alkaloid from Aconitum bulleyanum, inhibits proliferation and promotes apoptosis of human hepatic Lieming Xu-2 (LX-2) cells. In this study, we analyzed the effect of BLA on the production of ECM and related proteins by LX-2 cells activated with acetaldehyde (AA). The cells were randomized into the control group, AA group (cells activated with 400 µM AA), and BLA+AA group (cells cultured in the presence of 400 µM AA and 18.75 µg/ml BLA). In the BLA+AA group, the contents of collagens I and III and the expression of α-smooth muscle actin and transforming growth factor-ß1 (TGF-ß1) were statistically significantly higher than in the control, but lower than in the AA group. Expression of MMP-1 in the BLA+AA group was also significantly higher than in the AA group, but lower than in the control. Expression of TIMP-1 in the BLA+AA group was significantly higher than in the control, but lower than in the AA group. Thus, BLA suppressed activation and proliferation of LX-2 cells by inhibiting TGF-ß1 signaling pathway and decreasing the content of collagens I and III by reducing the MMP-1/TIMP-1 ratio.

Molluscicidal effect mechanism study on metaldehyde to Pomacea canaliculate at low temperature.

BACKGROUND: Metaldehyde is a molluscicide commonly used to control Pomacea canaliculate. Its efficacy is significantly impacted by water temperature, although the underlying mechanisms have not been fully explored. RESULTS: In this study, we systematically investigated the temperature effect and molecular mechanisms of metaldehyde on P. canaliculata. The molluscicidal effect at various temperatures indicated that metaldehyde's molluscicidal activity significantly decreases with a drop in temperature. The LC50 value was only 458.8176 mg/L at 10 °C, while it surged to a high of 0.8249 mg/L at 25 °C. The impact of low temperature (10 °C) on metaldehyde's molluscicidal activity was analyzed via transcriptomics. The results revealed that the effect of low temperature primarily influences immunity, lipid synthesis, and oxidative stress. The expression of stress and immune-related genes, such as MANF, HSP70, Cldf7, HSP60, and PclaieFc, significantly increased. Furthermore, we studied the function of five target genes using RNA interference (RNAi) and discovered that Cldf7 and HSP70 could notably affect metaldehyde's molluscicidal effect. The mortality of P. canaliculata increased by 36.17% (72 h) after Cldf7 interference and by 48.90% (72 h) after HSP70 interference. CONCLUSION: Our findings demonstrate that low temperature can induce the extensive expression of the Cldf7 and HSP70 genes, resulting in a substantial reduction in metaldehyde's molluscicidal activity. © 2024 Society of Chemical Industry.

ALDH1A3-acetaldehyde metabolism potentiates transcriptional heterogeneity in melanoma.

Cancer cellular heterogeneity and therapy resistance arise substantially from metabolic and transcriptional adaptations, but how these are interconnected is poorly understood. Here, we show that, in melanoma, the cancer stem cell marker aldehyde dehydrogenase 1A3 (ALDH1A3) forms an enzymatic partnership with acetyl-coenzyme A (CoA) synthetase 2 (ACSS2) in the nucleus to couple high glucose metabolic flux with acetyl-histone H3 modification of neural crest (NC) lineage and glucose metabolism genes. Importantly, we show that acetaldehyde is a metabolite source for acetyl-histone H3 modification in an ALDH1A3-dependent manner, providing a physiologic function for this highly volatile and toxic metabolite. In a zebrafish melanoma residual disease model, an ALDH1-high subpopulation emerges following BRAF inhibitor treatment, and targeting these with an ALDH1 suicide inhibitor, nifuroxazide, delays or prevents BRAF inhibitor drug-resistant relapse. Our work reveals that the ALDH1A3-ACSS2 couple directly coordinates nuclear acetaldehyde-acetyl-CoA metabolism with specific chromatin-based gene regulation and represents a potential therapeutic vulnerability in melanoma.

Participación de receptores J pulmonares en reflejo cardiorespiratorio provocado por acetaldehido en ratas / Pulmonary J receptors in the cardiorespiratory response induced by acetaldehyde in rats

Anteriormente demostramos que la administración endovenosa de acetaldehido (AcH) y etanol, provoca en la rata una triple respuesta refleja caracterizada por bradicardia, hipotensión y apnea, cuya vía eferente es vagal. La activación central del vago, como un mecanismo de iniciación de esta respuesta refleja se descartó mediante la inyección intracarotídea (hacia el SNC) de (AcH), la que produce hipertensión sin bradicardia. La administración de AcH en el ventrículo izquierdo no produce reflejo, y sin embargo su administración en ventrículo derecho produce una respuesta refleja mayor y con una latencia significativamente menor que por vía endovenosa. Esto sugiere la estimulación de receptores sensitivos ubicados en la circulación pulmonar. De éstos, sólo la estimulación de los receptores J pulmonares puede producir una respuesta refleja con bradicardia, hipotensión y apnea, y dada su ubicación entre el alvéolo y capilar pulmonar, son accesibles por la circulación pulmonar y por vía respiratoria. Con el objeto de precisar la participación de estos receptores en la respuesta refleja se administró AcH mediante nebulización a ratas anestesiadas y traqueotomizadas. El AcH administrado por vía respiratoria produjo la misma respuesta refleja, caracterizada por bradicardia (-52.8ñ21.73%). hipotensión (-36,9ñ12.10%) y apnea (4/7), pero con una latencia significativamente menor (p=0.0001) que por la vía endovenosa. La frecuencia respiratoria, volumen corriente y ventilación minuto no se modificaron significativamente. La vagotomía cervical bilateral bloqueó totalmente la bradicardia y la apnea, observándose una hipotensión de menor magnitud (p=0.0001) y con una latencia mayor (p=0.0001). La nebulización de solución Ringer Locke, a 10§C y a 37§C, produjo solamente hipotensión que no se modificó con vagotomía. Los resultados sugieren que la respuesta inducida por AcH, es mediada por un aumento reflejo en el tonovagal y que los neurorreceptores involucrados en la iniciación de este reflejo se ubican a nivel pulmonar y corresponderían a los receptores J pulmonares

Inhibitory action of in vitro ethanol and acetaldehyde exposure on LHRH and phorbol ester stimulated testerone secretion by rat testicular interstitial cells

Ha sido demostrado que el etanol y el acetaldehido inhiben la esteroidogenesis testicular. No obstante el (los) mecanismo(s) de trasnducción de señal envuelto en su acción no fue aún elucidado. Hemos examinado el posible envolvimiento de la proteína quinasa sensible a fosfolípidos y dependiente de calcio (proteína quinasa C, PK-C) en el mecanismo intracelular de acción de etanol y de acetaldehido, estimulando la producción de testosterona en células intersticiales de testículo de rata con LHRH y éster de forbolPDBu, los cuales activan la PK-C a nivel de receptor (LHRH) y pos-receptor (PDBu). El etanol(2000 mg por ciento) inhibió la producción de testosterona estimulada con 10**-7 M LHRH y 200 nM PDBu en 81 + 4,7 por ciento y 60 + 20.4 por ciento respectivamente. El acetaldehido (20 mg por ciento) redujo la cantidad de testosterona producida por 10**-7 M LHRH y 200 nM PDBu en 59,4 + 1,2 por ciento, respectivamente. El nivel basal de testosterona no fue modificado por el etanol pero si fue reducido por el acetaldehido. No obstante, la prueba funcional de la viabilidad celular a través de la preincubación de las células con las referidas dosis de etanol y acetaldehido no disminuyó la capacidad de respuesta a una subsecuente estimulación con LHRH, demostrando que la viabilidad celular no fue afectada por la incubación con esas substancias. Los resultados aquí presentados sugieren que la exposición directa al etanol y acetaldehido redujo la habilidad de las células intersticiales del testículo de rata de responder a la estimulación de la vía mediada por la PK-C