RESUMO
Tryptophan metabolites, such as 5-hydroxytryptophan (5-HTP), serotonin, and melatonin, hold significant promise as supplements for managing various mood-related disorders, including depression and insomnia. However, their chemical production via chemical synthesis and phytochemical extraction presents drawbacks, such as the generation of toxic byproducts and low yields. In this study, we explore an alternative approach utilizing S. cerevisiae STG S101 for biosynthesis. Through a series of eleven experiments employing different combinations of tryptophan supplementation, Tween 20, and HEPES buffer, we investigated the production of these indolamines. The tryptophan metabolites were analyzed using liquid chromatography with tandem mass spectrometry (LC-MS/MS). Notably, setups replacing peptone in the YPD media with tryptophan (Run 3) and incorporating tryptophan along with 25 mM HEPES buffer (Run 4) demonstrated successful biosynthesis of 5-HTP and serotonin. The highest 5-HTP and serotonin concentrations were 58.9 ± 16.0 mg L-1 and 0.0650 ± 0.00211 mg L-1, respectively. Melatonin concentrations were undetected in all the setups. These findings underscore the potential of using probiotic yeast strains as a safer and conceivably more cost-effective alternative for indolamine synthesis. The utilization of probiotic strains presents a promising avenue, potentially offering scalability, sustainability, reduced environmental impact, and feasibility for large-scale production.
Assuntos
5-Hidroxitriptofano , Vias Biossintéticas , Saccharomyces cerevisiae , Serotonina , Triptofano , Triptofano/metabolismo , Saccharomyces cerevisiae/metabolismo , Serotonina/metabolismo , Serotonina/biossíntese , 5-Hidroxitriptofano/metabolismo , Melatonina/metabolismo , Melatonina/biossíntese , Espectrometria de Massas em Tandem , Cromatografia Líquida/métodosRESUMO
The growing recognition of the association between maternal chronic kidney disease (CKD) and fetal programming highlights the increased vulnerability of hypertension in offspring. Potential mechanisms involve oxidative stress, dysbiosis in gut microbiota, and activation of the renin-angiotensin system (RAS). Our prior investigation showed that the administration of adenine to pregnant rats resulted in the development of CKD, ultimately causing hypertension in their adult offspring. Citrulline, known for enhancing nitric oxide (NO) production and possessing antioxidant and antihypertensive properties, was explored for its potential to reverse high blood pressure (BP) in offspring born to CKD dams. Male rat offspring, both from normal and adenine-induced CKD models, were randomly assigned to four groups (8 animals each): (1) control, (2) CKD, (3) citrulline-treated control rats, and (4) citrulline-treated CKD rats. Citrulline supplementation successfully reversed elevated BP in male progeny born to uremic mothers. The protective effects of perinatal citrulline supplementation were linked to an enhanced NO pathway, decreased expression of renal (pro)renin receptor, and changes in gut microbiota composition. Citrulline supplementation led to a reduction in the abundance of Monoglobus and Streptococcus genera and an increase in Agothobacterium Butyriciproducens. Citrulline's ability to influence taxa associated with hypertension may be linked to its protective effects against maternal CKD-induced offspring hypertension. In conclusion, perinatal citrulline treatment increased NO availability and mitigated elevated BP in rat offspring from uremic mother rats.
Assuntos
Doenças do Sistema Nervoso Autônomo , Hipertensão , Pré-Eclâmpsia , Efeitos Tardios da Exposição Pré-Natal , Insuficiência Renal Crônica , Gravidez , Humanos , Feminino , Ratos , Animais , Masculino , Citrulina/farmacologia , Citrulina/uso terapêutico , Ratos Sprague-Dawley , Hipertensão/etiologia , Insuficiência Renal Crônica/etiologia , Insuficiência Renal Crônica/complicações , Adenina/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamenteRESUMO
In the evolving field of electrocatalysis, thermal treatment of nano-electrocatalysts has become an essential strategy for performance enhancement. This review systematically investigates the impact of various thermal treatments on the catalytic potential of nano-electrocatalysts. The focus encompasses an in-depth analysis of the changes induced in structural, morphological, and compositional properties, as well as alterations in electro-active surface area, surface chemistry, and crystal defects. By providing a comprehensive comparison of commonly used thermal techniques, such as annealing, calcination, sintering, pyrolysis, hydrothermal, and solvothermal methods, this review serves as a scientific guide for selecting the right thermal technique and favorable temperature to tailor the nano-electrocatalysts for optimal electrocatalysis. The resultant modifications in catalytic activity are explored across key electrochemical reactions such as electrochemical (bio)sensing, catalytic degradation, oxygen reduction reaction, hydrogen evolution reaction, overall water splitting, fuel cells, and carbon dioxide reduction reaction. Through a detailed examination of the underlying mechanisms and synergistic effects, this review contributes to a fundamental understanding of the role of thermal treatments in enhancing electrocatalytic properties. The insights provided offer a roadmap for future research aimed at optimizing the electrocatalytic performance of nanomaterials, fostering the development of next-generation sensors and energy conversion technologies.
RESUMO
Chronic kidney disease (CKD) affects 10% of the global population, including pregnant women. Adverse maternal conditions determine the developmental programming of many diseases later in life. We previously demonstrated that adult rat offspring born to dams with CKD developed hypertension and renal hypertrophy. Trimethylamine-N-oxide (TMAO), a uremic toxin derived from the gut microbiota, has been linked to hypertension. This study assesses the effects of TMAO inhibition by iodomethylcholine (IMC) treatment on offspring hypertension programmed by maternal CKD. Female rats were fed either a control or a 0.5% adenine diet before conception, with or without IMC treatment during pregnancy and lactation. Maternal IMC treatment averted maternal CKD-primed offspring hypertension and renal hypertrophy in 12-week-old offspring. Offspring hypertension is associated with increases in the plasma TMAO concentration and oxidative stress and shifts in gut microbiota. The beneficial effects of IMC are related to a reduction in TMAO; increases in genera Acetatifactor, Bifidobacterium, and Eubacterium; and decreases in genera Phocacecola and Bacteroides. Our findings afford insights into the targeting of the gut microbiota to deplete TMAO production, with therapeutic potential for the prevention of offspring hypertension programmed by maternal CKD, although these results still need further clinical translation.
Assuntos
Hipertensão , Insuficiência Renal Crônica , Feminino , Ratos , Humanos , Animais , Gravidez , Insuficiência Renal Crônica/tratamento farmacológico , Metilaminas , Hipertensão/prevenção & controle , Hipertrofia , Óxidos/uso terapêuticoRESUMO
Emerging evidence supports that hypertension can be programmed or reprogrammed by maternal nutrition. Maternal exposures during pregnancy, such as maternal nutrition or antibiotic use, could alter the offspring's gut microbiota. Short-chain fatty acids (SCFAs) are the major gut microbiota-derived metabolites. Acetate, the most dominant SCFA, has shown its antihypertensive effect. Limited information exists regarding whether maternal acetate supplementation can prevent maternal minocycline-induced hypertension in adult offspring. We exposed pregnant Sprague Dawley rats to normal diet (ND), minocycline (MI, 50 mg/kg/day), magnesium acetate (AC, 200 mmol/L in drinking water), and MI + AC from gestation to lactation period. At 12 weeks of age, four groups (n = 8/group) of male progeny were sacrificed. Maternal acetate supplementation protected adult offspring against minocycline-induced hypertension. Minocycline administration reduced plasma acetic acid level, which maternal acetate supplementation prevented. Additionally, acetate supplementation increased the protein level of SCFA receptor G protein-coupled receptor 41 in the offspring kidneys. Further, minocycline administration and acetate supplementation significantly altered gut microbiota composition. Maternal acetate supplementation protected minocycline-induced hypertension accompanying by the increases in genera Roseburia, Bifidobacterium, and Coprococcus. In sum, our results cast new light on targeting gut microbial metabolites as early interventions to prevent the development of hypertension, which could help alleviate the global burden of hypertension.
Assuntos
Hipertensão , Efeitos Tardios da Exposição Pré-Natal , Acetatos/farmacologia , Animais , Pressão Sanguínea , Suplementos Nutricionais , Feminino , Humanos , Hipertensão/induzido quimicamente , Hipertensão/tratamento farmacológico , Hipertensão/metabolismo , Lactação , Masculino , Exposição Materna/efeitos adversos , Minociclina/farmacologia , Gravidez , Efeitos Tardios da Exposição Pré-Natal/prevenção & controle , Ratos , Ratos Sprague-DawleyRESUMO
Platelet-rich plasma (PRP) is widely utilized in the treatment of sports injuries. However, potential systemic effects after localized PRP injection are unclear at present. In this prospective randomized study, 24 Taiwanese male athletes with tendinopathy were randomized into a PRP group (n = 13) or a saline group (n = 11). The concentrations of serum and urine biomarkers were quantified by enzyme-linked immunosorbent assay assessment as well as gas chromatographic and mass spectrometric analysis, respectively. The results showed no significant differences in serum levels of growth hormone, insulin-like growth factor-1, insulin-like growth factor-binding protein 3, vascular endothelial growth factor, platelet-derived growth factor-BB, or serum substance P(SP) between the two groups before intervention, nor at 1, 2, or 7 days after intervention. However, a significant decrease in the serum SP level 1 and 7 days after PRP injection was observed. Regarding urinary concentrations of metabolites of anabolic androgenic steroids (AAS), no between-group differences before intervention, nor at 1, 2, or 7 days after intervention, were observed. Our study failed to observe significant surge of serum anabolic molecules and urinary excretion of anabolic AAS metabolites after PRP injection.
Assuntos
Plasma Rico em Plaquetas , Biomarcadores , Humanos , Masculino , Estudos Prospectivos , Tendinopatia , Fator A de Crescimento do Endotélio VascularRESUMO
Maternal chronic kidney disease (CKD) during pregnancy causes adverse fetal programming. Nitric oxide (NO) deficiency, gut microbiota dysbiosis, and dysregulated renin-angiotensin system (RAS) during pregnancy are linked to the development of hypertension in adult offspring. We examined whether maternal adenine-induced CKD can program hypertension and kidney disease in adult male offspring. We also aimed to identify potential mechanisms, including alterations of gut microbiota composition, increased trimethylamine-N-oxide (TMAO), reduced NO bioavailability, and dysregulation of the RAS. To construct a maternal CKD model, female Sprague-Dawley rats received regular chow (control group) or chow supplemented with 0.5% adenine (CKD group) for 3 weeks before pregnancy. Mother rats were sacrificed on gestational day 21 to analyze placentas and fetuses. Male offspring (n = 8/group) were sacrificed at 12 weeks of age. Adenine-fed rats developed renal dysfunction, glomerular and tubulointerstitial damage, hypertension, placental abnormalities, and reduced fetal weights. Additionally, maternal adenine-induced CKD caused hypertension and renal hypertrophy in adult male offspring. These adverse pregnancy and offspring outcomes are associated with alterations of gut microbiota composition, increased uremic toxin asymmetric and symmetric dimethylarginine (ADMA and SDMA), increased microbiota-derived uremic toxin TMAO, reduced microbiota-derived metabolite acetate and butyrate levels, and dysregulation of the intrarenal RAS. Our results indicated that adenine-induced maternal CKD could be an appropriate model for studying uremia-related adverse pregnancy and offspring outcomes. Targeting NO pathway, microbiota metabolite TMAO, and the RAS might be potential therapeutic strategies to improve maternal CKD-induced adverse pregnancy and offspring outcomes.
Assuntos
Hipertensão/metabolismo , Óxido Nítrico/genética , Efeitos Tardios da Exposição Pré-Natal/metabolismo , Insuficiência Renal Crônica/metabolismo , Adenina/efeitos adversos , Adenina/metabolismo , Animais , Modelos Animais de Doenças , Disbiose/genética , Disbiose/microbiologia , Feminino , Desenvolvimento Fetal/efeitos dos fármacos , Microbioma Gastrointestinal/genética , Hipertensão/etiologia , Hipertensão/microbiologia , Hipertensão/patologia , Herança Materna/genética , Óxido Nítrico/metabolismo , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Efeitos Tardios da Exposição Pré-Natal/microbiologia , Efeitos Tardios da Exposição Pré-Natal/patologia , Ratos , Insuficiência Renal Crônica/etiologia , Insuficiência Renal Crônica/microbiologia , Insuficiência Renal Crônica/patologia , Sistema Renina-Angiotensina/genéticaRESUMO
Cardiovascular disease (CVD) begins early in children with chronic kidney disease (CKD). Reduced nitric oxide (NO) bioavailability has been associated with increased CVD in CKD patients. Children tend to have more exposure to acrylamide, one of the most common toxins in food. We aimed to determine whether urinary levels of acrylamide metabolites N-acetyl-S-(2-carbamoylethyl)-cysteine (AAMA) and N-acetyl-S-(2-carbamoyl-2-hydroxyethyl)-cysteine (GAMA) are associated with CV risk markers in children with CKD. Data on 112 children and adolescents ages three to 18 years old with CKD stage G1-G4 are reported. We observed that 24 h ambulatory blood pressure monitoring (ABPM) abnormalities were greater, and left ventricular (LV) mass and ambulatory arterial stiffness index (AASI) were higher in children with CKD stage G2-G4 versus G1. Patients with CKD stage G2-G4 had a lower urinary acrylamide level, but a higher AAMA-to-GAMA ratio than those with CKD stage G1. Urinary acrylamide level was negatively associated with high systolic blood pressure (SBP) and diastolic BP (DBP) load on 24 h ABPM. Lower urinary levels of acrylamide, AAMA, and GAMA were correlated with LV mass. Additionally, GAMA are superior to AAMA related to NO-related parameters, namely citrulline and symmetric dimethylarginine (SDMA). This study suggests that determinations of urinary acrylamide level and its metabolites in the early stages of pediatric CKD may identify patients at risk of CVD. Further studies should clarify mechanisms underlying acrylamide exposure to define the treatment for protection against CVD.
Assuntos
Acrilamida/metabolismo , Doenças Cardiovasculares/epidemiologia , Metaboloma , Insuficiência Renal Crônica/metabolismo , Acrilamida/urina , Adolescente , Doenças Cardiovasculares/sangue , Doenças Cardiovasculares/urina , Criança , Pré-Escolar , Feminino , Humanos , Masculino , Óxido Nítrico/sangue , Análise de Regressão , Insuficiência Renal Crônica/sangue , Insuficiência Renal Crônica/urina , Fatores de RiscoRESUMO
Gut microbiota-dependent metabolites, in particular trimethylamine (TMA), are linked to hypertension. Maternal 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure or consumption of food high in fructose (HFR) can induce hypertension in adult offspring. We examined whether 3,3-maternal dimethyl-1-butanol (DMB, an inhibitor of TMA formation) therapy can protect adult offspring against hypertension arising from combined HFR and TCDD exposure. Pregnant Sprague-Dawley rats received regular chow or chow supplemented with fructose (60% diet by weight) throughout pregnancy and lactation. Additionally, the pregnant dams received TCDD (200 ng/kg BW orally) or a corn oil vehicle on days 14 and 21 of gestation, and days 7 and 14 after birth. Some mother rats received 1% DMB in their drinking water throughout pregnancy and lactation. Six groups of male offspring were studied (n = 8 for each group): regular chow (CV), high-fructose diet (HFR), regular diet+TCDD exposure (CT), HFR+TCDD exposure (HRT), high-fructose diet+DMB treatment (HRD), and HFR+TCDD+DMB treatment (HRTD). Our data showed that TCDD exacerbates HFR-induced elevation of blood pressure in male adult offspring, which was prevented by maternal DMB administration. We observed that different maternal insults induced distinct enterotypes in adult offspring. The beneficial effects of DMB are related to alterations of gut microbiota, the increase in nitric oxide (NO) bioavailability, the balance of the renin-angiotensin system, and antagonization of aryl hydrocarbon receptor (AHR) signaling. Our findings cast new light on the role of early intervention targeting of the gut microbiota-dependent metabolite TMA, which may allow us to prevent the development of hypertension programmed by maternal excessive fructose intake and environmental dioxin exposure.
Assuntos
Dieta da Carga de Carboidratos/efeitos adversos , Microbioma Gastrointestinal , Hipertensão , Exposição Materna/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal , Animais , Dioxinas/efeitos adversos , Feminino , Frutose/efeitos adversos , Masculino , Metilaminas/farmacologia , Gravidez , Substâncias Protetoras/farmacologia , Ratos , Ratos Sprague-DawleyRESUMO
Despite cardiovascular disease (CVD) being the leading cause of morbidity and mortality in chronic kidney disease (CKD), less attention has been paid to subclinical CVD in children and adolescents with early CKD stages. Gut microbiota and their metabolite, trimethylamine N-oxide (TMAO), have been linked to CVD. Ambulatory blood-pressure monitoring (ABPM) and arterial-stiffness assessment allow for early detection of subclinical CVD. We therefore investigated whether gut microbial composition and TMAO metabolic pathway are correlated with blood-pressure (BP) load and vascular abnormalities in children with early-stage CKD. We enrolled 86 children with G1â»G3 CKD stages. Approximately two-thirds of CKD children had BP abnormalities on ABPM. Children with CKD stage G2â»G3 had a higher uric acid level (6.6 vs. 4.8 mg/dL, p < 0.05) and pulse-wave velocity (4.1 vs. 3.8 m/s, p < 0.05), but lower TMAO urinary level (209 vs. 344 ng/mg creatinine, p < 0.05) than those with stage G1. Urinary TMAO level was correlated with the abundances of genera Bifidobacterium (r = 0.307, p = 0.004) and Lactobacillus (r = 0.428, p < 0.001). CKD children with abnormal ABPM profile had a lower abundance of the Prevotella genus than those with normal ABPM (p < 0.05). Our results highlight the link between gut microbiota, microbial metabolite TMAO, BP load, and arterial-stiffness indices in children with early-stage CKD. Early assessments of these surrogate markers should aid in decreasing cardiovascular risk in childhood CKD.
Assuntos
Pressão Sanguínea , Microbioma Gastrointestinal , Metilaminas/urina , Insuficiência Renal Crônica/microbiologia , Adolescente , Criança , Pré-Escolar , Feminino , Humanos , Masculino , Insuficiência Renal Crônica/fisiopatologia , Insuficiência Renal Crônica/urinaRESUMO
BACKGROUND/PURPOSE: This study aims to investigate what kinds of food products were contaminated by phthalates, mainly di-(2-ethylhexyl)phthalate (DEHP) and/or di-isononyl phthalate (DINP), during the 2011 phthalates incident in Taiwan, and whether the DEHP and/or DINP concentrations of some affected foods decreased after this incident. METHODS: During May-October, 2011, 2731 food items were sent by individual citizens or companies to a government-accredited laboratory for the analyses of six main phthalate chemicals, including DEHP, DINP, di-isodecyl phthalate, di(n-octyl)phthalate, di-n-butyl phthalate, and butyl benzyl phthalate. A concentration of ≥1 ppm for any of the six phthalate chemicals in the foods studied was defined as positive. RESULTS: The overall positive rate was 16.2%. The positive rate of possibly affected foods was similar between sanctioned and non-sanctioned foods categorized as "Others" by the government (16.0% vs. 16.4%). There were 33 food items, most of which belonged to the Others category, sent twice by companies on different dates. Of these, the positive rates of affected foods significantly decreased from 39.4% for DEHP and 72.7% for DINP at the first analyses to 3.0% for DEHP and 9.1% for DINP at the second, respectively (p < 0.0001). CONCLUSION: Besides the government-sanctioned foods, foods from the Others category were still affected by phthalate contamination. Thus, vigilant scrutiny of food safety in modern life is necessary.
Assuntos
Contaminação de Alimentos/estatística & dados numéricos , Ácidos Ftálicos/intoxicação , Contaminação de Alimentos/análise , Humanos , Estudos Retrospectivos , Taiwan/epidemiologiaRESUMO
Roasting is necessary for bringing out the aroma and flavor of coffee beans, making coffee one of the most consumed beverages. However, this process also generates a series of toxic compounds, including acrylamide and furanic compounds (5-hydroxymethylfurfural, furan, 2-methylfuran, 3-methylfuran, 2,3-dimethylfuran, and 2,5-dimethylfuran). Furthermore, not much is known about the formation of these compounds in emerging coffee formulations containing alcohol and sugars. Therefore, this study investigated the effect of roasting time and degree on levels of acrylamide and furanic compounds in arabica coffee using fast and slow roasting methods. The fast and slow roasting methods took 5.62 min and 9.65 min, respectively, and reached a maximum of 210 °C to achieve a light roast. For the very dark roast, the coffee beans were roasted for 10.5 min and the maximum temperature reached 245 °C. Our findings showed that the levels of acrylamide (375 ± 2.52 µg kg-1) and 5-HMF (194 ± 11.7 mg kg-1) in the slow-roasted coffee were 35.0 % and 17.4 % lower than in fast-roasted coffee. Furthermore, light roast coffee had significantly lower concentrations of acrylamide and 5-HMF than very dark roast, with values of 93.7 ± 7.51 µg kg-1 and 21.3 ± 10.3 mg kg-1, respectively. However, the levels of furan and alkylfurans increased with increasing roasting time and degree. In this study, we also examined the concentrations of these pollutants in new coffee formulations consisting of alcohol-, sugar-, and honey-infused coffee beans. Formulations with honey and sugar resulted in higher concentrations of 5-HMF, but no clear trend was observed for acrylamide. On the other hand, formulations with honey had higher concentrations of furan and alkylfurans. These results indicate that optimizing roasting time and temperature might not achieve the simultaneous reduction of all the pollutants. Additionally, sugar- and honey-infused coffee beans are bound to have higher furanic compounds, posing a higher health risk.
Assuntos
Acrilamida , Café , Furaldeído , Furanos , Temperatura Alta , Acrilamida/análise , Furanos/análise , Café/química , Furaldeído/análise , Furaldeído/análogos & derivados , Culinária/métodos , Coffea/química , Sementes/química , Manipulação de Alimentos/métodos , Fatores de Tempo , Aditivos Alimentares/análiseRESUMO
Cardiovascular diseases (CVDs) represent a significant challenge in global health, demanding advancements in diagnostic modalities. This review delineates the progressive and restrictive facets of nanomaterial-based biosensors in the context of detecting N-terminal pro-B-type natriuretic peptide (NT-proBNP), an indispensable biomarker for CVD prognosis. It scrutinizes the escalation in diagnostic sensitivity and specificity attributable to the incorporation of novel nanomaterials such as graphene derivatives, quantum dots, and metallic nanoparticles, and how these enhancements contribute to reducing detection thresholds and augmenting diagnostic fidelity in heart failure (HF). Despite these technological strides, the review articulates pivotal challenges impeding the clinical translation of these biosensors, including the attainment of clinical-grade sensitivity, the substantial costs associated with synthesizing and functionalizing nanomaterials, and their pragmatic deployment across varied healthcare settings. The necessity for intensified research into the synthesis and functionalization of nanomaterials, strategies to economize production, and amelioration of biosensor durability and ease of use is accentuated. Regulatory hurdles in clinical integration are also contemplated. In summation, the review accentuates the transformative potential of nanomaterial-based biosensors in HF diagnostics and emphasizes critical avenues of research requisite to surmount current impediments and harness the full spectrum of these avant-garde diagnostic instruments.
RESUMO
Resveratrol, acting as a prebiotic, and propionate, functioning as a postbiotic, hold promise for preventing hypertension in chronic kidney disease (CKD). Previously, we employed propionate to enhance the bioavailability of resveratrol through esterification, resulting in the production of a resveratrol propionate ester (RPE) mixture. In this study, we purified 3-O-propanoylresveratrol (RPE2) and 3,4'-di-O-propanoylresveratrol (RPE4) and investigated their protective effects in a juvenile rat adenine-induced CKD model. To this end, male Sprague Dawley rats aged three weeks (n = 40) were divided into five groups: control; CKD (rats fed adenine); CKRSV (CKD rats treated with 50 mg/L resveratrol); CDRPE2 (CKD rats treated with 25 mg/L RPE2); and CKRPE4 (CKD rats treated with 25 mg/L RPE 4). RPE2 and PRE4 similarly exhibited blood pressure-lowering effects comparable to those of resveratrol, along with increased nitric oxide (NO) availability. Furthermore, RPE2 and RPE4 positively influenced plasma short-chain fatty acid (SCFA) levels and induced distinct alterations in the gut microbial composition of adenine-fed juvenile rats. The supplementation of RPE2 and RPE4, by restoring NO, elevating SCFAs, and modulating the gut microbiota, holds potential for ameliorating CKD-induced hypertension.
Assuntos
Adenina , Anti-Hipertensivos , Pressão Sanguínea , Suplementos Nutricionais , Microbioma Gastrointestinal , Hipertensão , Ratos Sprague-Dawley , Insuficiência Renal Crônica , Resveratrol , Animais , Microbioma Gastrointestinal/efeitos dos fármacos , Resveratrol/farmacologia , Masculino , Adenina/farmacologia , Anti-Hipertensivos/farmacologia , Pressão Sanguínea/efeitos dos fármacos , Ratos , Hipertensão/tratamento farmacológico , Propionatos , Óxido Nítrico/metabolismo , Ácidos Graxos Voláteis/metabolismo , Modelos Animais de Doenças , DietaRESUMO
Cardiovascular diseases (CVDs) stand as a predominant global health concern, introducing vast socioeconomic challenges. In addressing this pressing dilemma, enhanced diagnostic modalities have become paramount, positioning electrochemical biosensing as an instrumental innovation. This comprehensive review navigates the multifaceted terrain of CVDs, elucidating their defining characteristics, clinical manifestations, therapeutic avenues, and intrinsic risk factors. Notable emphasis is placed on pivotal diagnostic tools, spotlighting cardiac biomarkers distinguished by their unmatched clinical precision in terms of relevance, sensitivity, and specificity. Highlighting the broader repercussions of CVDs, there emerges an accentuated need for refined diagnostic strategies. Such an exploration segues into a profound analysis of electrochemical biosensing, encapsulating its foundational principles, diverse classifications, and integral components, notably recognition molecules and transducers. Contemporary advancements in biosensing technologies are brought to the fore, emphasizing pioneering electrode architectures, cutting-edge signal amplification processes, and the synergistic integration of biosensors with microfluidic platforms. At the core of this discourse is the demonstrated proficiency of biosensors in detecting cardiovascular anomalies, underpinned by empirical case studies, systematic evaluations, and clinical insights. As the narrative unfolds, it addresses an array of inherent challenges, spanning intricate technicalities, real-world applicability constraints, and regulatory considerations, finally, by casting an anticipatory gaze upon the future of electrochemical biosensing, heralding a new era of diagnostic tools primed to revolutionize cardiovascular healthcare.
Assuntos
Biomarcadores , Técnicas Biossensoriais , Doenças Cardiovasculares , Técnicas Eletroquímicas , Humanos , Doenças Cardiovasculares/diagnóstico , Biomarcadores/análise , Biomarcadores/sangueRESUMO
Mercury's neurotoxic effects have prompted the development of advanced control and remediation methods to meet stringent measures for industries with high-mercury feedstocks. Industries with significant Hg emissions, including artisanal and small-scale gold mining (ASGM)-789.2 Mg year-1, coal combustion-564.1 Mg year-1, waste combustion-316.1 Mg year-1, cement production-224.5 Mg year-1, and non-ferrous metals smelting-204.1 Mg year-1, use oxidants and adsorbents capture Hg from waste streams. Oxidizing agents such as O3, Cl2, HCl, CaBr2, CaCl2, and NH4Cl oxidize Hg0 to Hg2+ for easier adsorption. To functionalize adsorbents, carbonaceous ones use S, SO2, and Na2S, metal-based adsorbents use dimercaprol, and polymer-based adsorbents are grafted with acrylonitrile and hydroxylamine hydrochloride. Adsorption capacities span 0.2-85.6 mg g-1 for carbonaceous, 0.5-14.8 mg g-1 for metal-based, and 168.1-1216 mg g-1 for polymer-based adsorbents. Assessing Hg contamination in soils and sediments uses bioindicators and stable isotopes. Remediation approaches include heat treatment, chemical stabilization and immobilization, and phytoremediation techniques when contamination exceeds thresholds. Achieving a substantially Hg-free ecosystem remains a formidable challenge, chiefly due to the ASGM industry, policy gaps, and Hg persistence. Nevertheless, improvements in adsorbent technologies hold potential.
RESUMO
The emissions of polybrominated dibenzo-pdioxins,dibenzofurans (PBDD/Fs), and polybrominated diphenyl ethers (PBDEs) from trial combustion of 10 wt % dried industrial wastewater-treatment sludge (IWTS) and 90 wt % woodchip in an industrial boiler were investigated and compared to that from woodchip combustion. The PBDD/F toxic equivalent (TEQ) andPBDE emissions increased from 0.121 pg TEQ Nm−3 and 2260 pgNm−3, respectively, of the woodchip combustion to 0.211 pg TEQNm−3 and 4200 pg Nm−3, respectively, of the trial combustion.PBDD/F and PBDE congener profiles of inputs and outputs of the same type of combustion were similar; they also show similarity between woodchip and trial combustions, revealing that the destruction pathway was little affected by the introduction of the IWTS. The fates of PBDD/Fs and PBDEs show that the indigenous pollutants in the feed were effectively depleted (>93.5%). The dominant releasing route of PBDD/F and PBDE shifted from the stack flue gas of woodchip combustion to the ashes of trial combustion. This study demonstrates that co-combustion not only handles the fast growing sludge stream but also yields a saving of 26.3% in the fuel cost and treatment fees of sludge and ashes.
Assuntos
Dioxinas/química , Monitoramento Ambiental , Éteres Difenil Halogenados/química , Esgotos , Águas Residuárias , Madeira/química , Poluentes Atmosféricos/análise , Gases/análise , ResíduosRESUMO
Reactive oxygen and nitrogen species (RONS), including 3-nitro-l-tyrosine, play a dual role in human health, inducing oxidative damage and regulating cellular functions. Early and accurate detection of such molecules, such as L-tyrosine in urine, can serve as critical biomarkers for various cancers. In this study, we aimed to enhance the electrochemical detection of these molecules through the synthesis of La2Sn2O7/f-HNT nanocomposites via a simple hydrothermal method. Detailed structural and morphological characterizations confirmed successful synthesis, consistent with our expected outcomes. The synthesized nanocomposites were utilized as nanocatalysts in electrochemical sensors, showing a notable limit of the detection of 0.012 µM for the real-time detection of 3-nitro-l-tyrosine. These findings underscore the potential of nanomaterial-based sensors in advancing early disease detection with high sensitivity, furthering our understanding of cellular oxidative processes.
Assuntos
Técnicas Eletroquímicas , Nanocompostos , Humanos , Técnicas Eletroquímicas/métodos , Tirosina , Espécies Reativas de Oxigênio , EletrodosRESUMO
Resveratrol (REV) is a plant polyphenol with a plethora of beneficial properties. We previously enhanced the efficacy of REV via esterification of REV with butyrate to form resveratrol butyrate ester (RBE). Compared with REV, RBE exhibits higher bioavailability and better antioxidant effects. Hypertension can originate in early life because of maternal toxic chemical exposure. This study aims to examine the effectiveness of RBE in the protection of offspring hypertension induced by maternal di-2-ethylhexylphthalate (DEHP) exposure and to explore the underlying mechanisms. DEHP (10 mg/kg/day) was used as oral gavage to pregnant rats during gestation and lactation. The control group received the vehicle. Three groups of DEHP-exposed dams received REV (6.67 mg/kg/day), or low-dose (3.33 mg/kg/day) or high-dose (6.67 mg/kg/day) RBE in drinking water during gestation and lactation. Perinatal DEHP exposure resulted in hypertension and bodyweight gain in adult male offspring, which was prevented by high-dose RBE. REV supplementation attenuated DEHP exposure-induced increases in blood pressure but not bodyweight. High-dose RBE decreased renal oxidative damage, increased plasma butyrate concentrations, and altered short chain fatty acid receptor (SCFA) expression. Low-dose RBE treatment reduced downstream mediators of the acryl hydrocarbon receptor (AHR) signaling pathway. Moreover, DEHP exposure, REV and RBE treatment differentially shaped the offspring's gut microbiota. In particular, high-dose RBE increased the abundance of the genus Duncaniella. The beneficial effects of RBE treatment were related to reducing oxidative damage, increasing plasma butyrate concentrations, downregulating SCFA receptor expression, antagonizing AHR signaling, and altering the gut microbiota. This study provides the first evidence of RBE as a novel plant polyphenol bioproduct targeting the oxidative stress and gut microbiota to protect against maternal DEHP exposure-primed offspring hypertension.
Assuntos
Dietilexilftalato , Hipertensão , Efeitos Tardios da Exposição Pré-Natal , Resveratrol , Animais , Feminino , Gravidez , Ratos , Butiratos , Suplementos Nutricionais , Dietilexilftalato/toxicidade , Ésteres , Ácidos Graxos Voláteis , Hipertensão/induzido quimicamente , Hipertensão/prevenção & controle , Exposição Materna/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/metabolismo , Resveratrol/farmacologiaRESUMO
Antrodia cinnamomea (AC), a medicinal mushroom, has multiple beneficial actions, such as acting as a prebiotic. The incidence of chronic kidney disease (CKD) in children has steadily increased year by year, and CKD is related to gut microbiota dysbiosis. Herein, we investigated the renoprotection of solid-state cultivated AC in adenine-induced CKD juvenile rats. CKD was induced in 3-week-old male rats by feeding with adenine (0.5%) for three weeks. Treated groups received oral administration of AC extracts at either a low (10 mg/kg/day) or high dose (100 mg/kg/day) for six weeks. At nine weeks of age, the rats were sacrificed. Renal outcomes, blood pressure, and gut microbiome composition were examined. Our results revealed that AC treatment, either low- or high-dose, improved kidney function, proteinuria, and hypertension in CKD rats. Low-dose AC treatment increased plasma concentrations of short-chain fatty acids (SCFAs). Additionally, we observed that AC acts like a prebiotic by enriching beneficial bacteria in the gut, such as Akkermansia and Turicibacter. Moreover, the beneficial action of AC against CKD-related hypertension might also be linked to the inhibition of the renin-angiotensin system. This study brings new insights into the potential application of AC as a prebiotic dietary supplement in the prevention and treatment of pediatric CKD.