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BACKGROUND: Although Basidiomycota produce pharmaceutically and ecologically relevant natural products, knowledge of how they coordinate their primary and secondary metabolism is virtually non-existent. Upon transition from vegetative mycelium to carpophore formation, mushrooms of the genus Psilocybe use L-tryptophan to supply the biosynthesis of the psychedelic tryptamine alkaloid psilocybin with the scaffold, leading to a strongly increased demand for this particular amino acid as this alkaloid may account for up to 2% of the dry mass. Using Psilocybe mexicana as our model and relying on genetic, transcriptomic, and biochemical methods, this study investigated if L-tryptophan biosynthesis and degradation in P. mexicana correlate with natural product formation. RESULTS: A comparative transcriptomic approach of gene expression in P. mexicana psilocybin non-producing vegetative mycelium versus producing carpophores identified the upregulation of L-tryptophan biosynthesis genes. The shikimate pathway genes trpE1, trpD, and trpB (encoding anthranilate synthase, anthranilate phosphoribosyltransferase, and L-tryptophan synthase, respectively) were upregulated in carpophores. In contrast, genes idoA and iasA, encoding indole-2,3-dioxygenase and indole-3-acetaldehyde synthase, i.e., gateway enzymes for L-tryptophan-consuming pathways, were massively downregulated. Subsequently, IasA was heterologously produced in Escherichia coli and biochemically characterized in vitro. This enzyme represents the first characterized microbial L-tryptophan-preferring acetaldehyde synthase. A comparison of transcriptomic data collected in this study with prior data of Psilocybe cubensis showed species-specific differences in how L-tryptophan metabolism genes are regulated, despite the close taxonomic relationship. CONCLUSIONS: The upregulated L-tryptophan biosynthesis genes and, oppositely, the concomitant downregulated genes encoding L-tryptophan-consuming enzymes reflect a well-adjusted cellular system to route this amino acid toward psilocybin production. Our study has pilot character beyond the genus Psilocybe and provides, for the first time, insight in the coordination of mushroom primary and secondary metabolism.
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Oral squamous cell carcinoma (OSCC) is considered a multifactorial disease and has been associated with microbial infections, although the association with Candida spp. is still controversial. This systematic review focused on clinical trials which evaluated the relation between oral Candida spp colonization and OSCC. PubMed; Scopus; Embase; Web of Science and Scientific Direct were assessed. Independent reviewers conducted the diagram steps. For data extraction the PRISMA protocol was followed. The quality analysis of case-control studies was performed based on the Newcastle-Ottawa scale. Meta-analysis was performed to evaluate the frequency of Candida spp and the levels of microbial acetaldehyde production (MAP) being odds ratio (OR) the effect-measure applied. Eight and six studies were included in the qualitative analysis and meta-analysis, respectively. It was noted that there was a significantly higher frequency of Candida species (p = 0.0003/OR = 9.50) in patients diagnosed with OSCC than healthy patients, especially Candida krusei (p = 0.0167/OR=4.62). Candida spp., from oral cancer patients demonstrated significantly greater biofilm, biofilm metabolic activity, phospholipase, proteinase activity and a higher production of MAP (p = 0.0111/OR = 2.67). Candida species may have a potential role in OSCC development. Further studies should be conducted to elucidate the mechanism of action of Candida spp and others risk factors in the development of OSCC.
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Studies presented in this chapter show that: (1) in the brain, ethanol is metabolized by catalase to acetaldehyde, which condenses with dopamine forming salsolinol; (2) acetaldehyde-derived salsolinol increases the release of dopamine mediating, via opioid receptors, the reinforcing effects of ethanol during the acquisition of ethanol consumption, while (3) brain acetaldehyde does not influence the maintenance of chronic ethanol intake, it is suggested that a learned cue-induced hyperglutamatergic system takes precedence over the dopaminergic system. However, (4) following a prolonged ethanol deprivation, the generation of acetaldehyde in the brain again plays a role, contributing to the increase in ethanol intake observed during ethanol re-access, called the alcohol deprivation effect (ADE), a model of relapse behavior; (5) naltrexone inhibits the high ethanol intake seen in the ADE condition, suggesting that acetaldehyde-derived salsolinol via opioid receptors also contributes to the relapse-like drinking behavior. The reader is referred to glutamate-mediated mechanisms that trigger the cue-associated alcohol-seeking and that also contribute to triggering relapse.
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Alcohol-induced pancreas damage remains as one of the main risk factors for pancreatitis development. This disorder is poorly understood, particularly the effect of acetaldehyde, the primary alcohol metabolite, in the endocrine pancreas. Hepatocyte growth factor (HGF) is a protective protein in many tissues, displaying antioxidant, antiapoptotic, and proliferative responses. In the present work, we were focused on characterizing the response induced by HGF and its protective mechanism in the RINm5F pancreatic cell line treated with ethanol and acetaldehyde. RINm5F cells were treated with ethanol or acetaldehyde for 12 h in the presence or not of HGF (50 ng/ml). Cells under HGF treatment decreased the content of reactive oxygen species and lipid peroxidation induced by both toxics, improving cell viability. This effect was correlated to an improvement in insulin expression impaired by ethanol and acetaldehyde. Using a specific inhibitor of Erk1/2 abrogated the effects elicited by the growth factor. In conclusion, the work provides mechanistic evidence of the HGF-induced-protective response to the alcohol-induced damage in the main cellular component of the endocrine pancreas.
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Acetaldeído , Etanol , Acetaldeído/toxicidade , Acetaldeído/metabolismo , Linhagem Celular , Etanol/toxicidade , Fator de Crescimento de Hepatócito , Pâncreas/metabolismo , Sistema de Sinalização das MAP QuinasesRESUMO
A close communication exists between the microorganisms that live in the intestine and the brain, the so-called microbiota-gut-brain axis. This interaction occurs at different levels, such as the induction by bacteria of an inflammatory state in the intestine that produces (i) stimulation of the vagus nerve that conducts information to the brain, and (ii) the release of proinflammatory cytokines - such as TNF-α- to circulation, which can then be transported to the brain and trigger neuroinflammation. Ethanol-induced neuroinflammation is produced, in part, by the impairment of the epithelial barrier function of the intestine, since acetaldehyde generated in the gut from ethanol oxidation produces a disassembly of the tight junctions (TJ), which allows diffusion of bacterial components into the blood; these events trigger a systemic inflammatory response that crosses the blood-brain barrier and induce neuroinflammation. Some short-chain fatty acids (SCFAs) such as butyrate, propionate, and acetate, are produced from indigestible polysaccharides (fibers) by certain bacteria in the microbiota. These SCFAs have shown a protective function of the TJ against intestinal injuries, preserving the intestinal barrier function. In this perspective article, we discuss the therapeutic possibility to increase the production of SCFAs in the intestine of patients with AUD, to protect the integrity of TJ and thus modulate the neuroinflammatory process that helps to the establishment of chronic alcohol intake. In this way, a new therapeutic alternative is proposed here through a simple dietary intervention in the patient, increasing their fiber consumption.
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Alcoolismo , Humanos , Doenças Neuroinflamatórias , Fibras na Dieta , Ácidos Graxos Voláteis/farmacologia , Etanol , Consumo de Bebidas AlcoólicasRESUMO
Early ontogeny of the rat (late gestation and postnatal first week) is a sensitive period to ethanol's positive reinforcing effects and its detrimental effects on respiratory plasticity. Recent studies show that acetaldehyde, the first ethanol metabolite, plays a key role in the modulation of ethanol motivational effects. Ethanol brain metabolization into acetaldehyde via the catalase system appears critical in modulating ethanol positive reinforcing consequences. Catalase system activity peak levels occur early in the ontogeny. Yet, the role of ethanol-derived acetaldehyde during the late gestational period on respiration response, ultrasonic vocalizations (USVs), and ethanol intake during the first week of the rat remains poorly explored. In the present study, pregnant rats were given a subcutaneous injection of an acetaldehyde-sequestering agent (D-penicillamine, 50 mg/kg) or saline (0.9% NaCl), 30 min prior to an intragastric administration of ethanol (2.0 g/kg) or water (vehicle) on gestational days 17-20. Respiration rates (breaths/min) and apneic episodes in a whole-body plethysmograph were registered on postnatal days (PDs) 2 and 4, while simultaneously pups received milk or ethanol infusions for 40-min in an artificial lactation test. Each intake test was followed by a 5-min long USVs emission record. On PD 8, immediately after pups completed a 15-min ethanol intake test, brain samples were collected and kept frozen for catalase activity determination. Results indicated that a moderate experience with ethanol during the late gestational period disrupted breathing plasticity, increased ethanol intake, as well brain catalase activity. Animals postnatally exposed to ethanol increased their ethanol intake and exerted differential affective reactions on USVs and apneic episodes depending on whether the experience with ethanol occur prenatal or postnatally. Under the present experimental conditions, we failed to observe, a clear role of acetaldehyde mediating ethanol's effects on respiratory plasticity or affective states, nevertheless gestational acetaldehyde was of crucial importance in determining subsequent ethanol intake affinity. As a whole, results emphasize the importance of considering the participation of acetaldehyde in fetal programming processes derived from a brief moderate ethanol experience early in development, which in turn, argues against "safe or harmless" ethanol levels of exposure.
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Aldehydes, particularly acetaldehyde, are carcinogenic molecules and their concentrations in foodstuffs should be controlled to avoid upper aerodigestive tract (UADT) and liver cancers. Highly reactive, acetaldehyde forms DNA and protein adducts, impairing physiological functions and leading to the development of pathological conditions. The consumption of aged beer, outside of the ethanol metabolism, exposes habitual drinkers to this carcinogen, whose concentrations can be over-increased due to post-brewing chemical and biochemical reactions. Storage-related changes are a challenge faced by the brewing industry, impacting volatile compound formation and triggering flavor instability. Aldehydes are among the volatile compounds formed during beer aging, recognized as off-flavor compounds. To track and understand aldehyde formation through multiple pathways during beer storage, consequent changes in flavor but particularly quality losses and harmful compound formation, this systematic review reunited data on volatile compound profiles through gas chromatography analyses from 2011 to 2021. Conditions to avoid flavor instability and successful methods for reducing beer staling, and consequent acetaldehyde accumulation, were raised by exploring the dynamic conversion between free and bound-state aldehydes. Future research should focus on implementing sensory analyses to investigate whether adding aldehyde-binding agents, e.g., cysteine and bisulfite, would contribute to consumer acceptance, restore beer flavor, and minimize acetaldehyde-related health damage.
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Acetaldeído , Aldeídos , Humanos , Idoso , Cerveja , Carcinógenos , CarcinogêneseRESUMO
Corky disorders in apples represent a significant problem for long-term storage where controlled atmosphere (CA) is mainly used. Ultra-low oxygen (ULO) is an alternative to CA, which consists of low partial pressure of O2 to maintain a low metabolism in the apple fruit, achieving an effective decrease in the ethylene production and physiological disorders. The aim of this research was to study the effectiveness of a short hypoxia period on the development of cork physiological disorders during the storage of apple. 'Fuji' apples were prestored under ULO (0.5 kPa O2) for two periods of time (15 and 30 days) and at two temperatures (0 or 5°C). Corky physiological disorders increased at 5°C prestorage temperature; however, ULO treatments for 15 or 30 days at 0 or 5°C achieved a significant reduction in corky disorders near to 1%, compared with control treatments. In addition, a considerable reduction in ethylene production for up to 30 days was observed in ULO-treated fruit at 0 and 5°C. ULO for 30 days at 0 and 5°C increased the internal production of ethanol and acetaldehyde, causing a lower sensory quality due to the presence of fermentative flavors in fruit stored at 5°C. ULO of 15 days of conditioning decreased the relative expression of ethylene biosynthesis genes MdACS1 and MdACO1, resulting in lower ethylene production.
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Acetaldehyde is an important chemical commodity and a building block for producing several other high-value products in the chemical industry. This has motivated the search for suitable, efficient, stable, and selective catalysts, as well as renewable raw materials such as ethanol. In this work, supported copper catalysts were prepared from CuZnAl layered double hydroxides (LDHs) with different copper contents (5, 10, and 20 wt %) for application in the ethanol dehydrogenation reaction (EDR). The samples were thoroughly characterized by a series of techniques, which allowed for analysis of all of the copper and zinc species involved in the different catalyst preparation steps and during the EDR. The results obtained by in situ quick extended X-ray absorption fine structure (EXAFS) measurements, combined with multivariate data analysis, showed that the copper content in the pristine LDH influenced the phase composition of the mixed oxide support, which consequently affected the dispersion of copper nanoparticles. The higher the copper content, the higher are the ZnAl2O4 and zinc tetrahedral prenuclei (TPN) contents, to the detriment of the ZnO content. All the samples showed high selectivity (>97%) and stability in the catalytic reactions at 300 and 350 °C, with no observed deactivation during 6 h on-stream. Although the samples with lower copper content presented higher copper dispersion and reactivity, the sample containing 20 wt % of copper outperformed the others, with greater conversion and higher activity toward acetaldehyde.
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Aldehydes are abundantly present in tobacco smoke and in urban air pollution and are endogenously generated as products of the lipid peroxidation process. These molecules can react with DNA bases forming mutagenic exocyclic adducts, which have been used as biomarkers of aldehyde exposure and as potential tools for the study of inflammation, metal storage diseases, neurodegenerative disorders, and cancer. High-performance liquid chromatography-tandem mass spectrometry (HPLC/MS/MS) provides a highly precise, specific and ultrasensitive method for the detection of exocyclic DNA adducts. Here we present and describe a validated micro-HPLC-Electro Spray Ionization (ESI)-MS/MS method for the quantification of 1,N2-propanodGuo, an adduct produced following the reaction between 2'-deoxyguanosine and acetaldehyde or crotonaldehyde.
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Adutos de DNA/metabolismo , Dano ao DNA , Pulmão/metabolismo , Espectrometria de Massas por Ionização por Electrospray , Espectrometria de Massas em Tandem , Animais , Cromatografia Líquida de Alta Pressão , Desoxiguanosina/metabolismo , RatosRESUMO
The anatomo-physiological disruptions inherent to different categories of the Fetal Alcohol Spectrum Disorder do not encompass all the negative consequences derived from intrauterine ethanol (EtOH) exposure. Preclinical, clinical and epidemiological studies show that prenatal EtOH exposure also results in early programming of alcohol affinity. This affinity has been addressed through the examination of how EtOH prenatally exposed organisms recognize and prefer the drug's chemosensory cues and their predisposition to exhibit heightened voluntary EtOH intake during infancy and adolescence. In altricial species these processes are determined by the interaction of at least three factors during stages equivalent to the 2nd and 3rd human gestational trimester: (i) fetal processing of the drug's olfactory and gustatory attributes present in the prenatal milieu; (ii) EtOH's recruitment of central reinforcing effects that also imply progressive sensitization to the drug's motivational properties; and (iii) an associative learning process involving the prior two factors. This Pavlovian learning phenomenon is dependent upon the recruitment of the opioid system and studies also indicate a significant role of EtOH's principal metabolite (acetaldehyde, ACD) which is rapidly generated in the brain via the catalase system. The central and rapid accumulation of this metabolite represents a major factor involved in the process of fetal alcohol programming. According to recent investigations, it appears that ACD exerts early positive reinforcing consequences and antianxiety effects (negative reinforcement). Finally, this review also acknowledges human clinical and epidemiological studies indicating that moderate and binge-like drinking episodes during gestation result in neonatal recognition of EtOH's chemosensory properties coupled with a preference towards these cues. As a whole, the studies under discussion emphasize the notion that even subteratogenic EtOH exposure during fetal life seizes early functional sensory and learning capabilities that pathologically shape subsequent physiological and behavioral reactivity towards the drug.
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Developmentally-lead (Pb)-exposed rats showed an enhanced vulnerability to the stimulating and motivational effects of ethanol (EtOH). This is accompanied by differential activity of the brain EtOH-metabolizing enzymes catalase (CAT) and mitochondrial aldehyde dehydrogenase (ALDH2). Based on the theory that brain acetaldehyde accumulation is associated with the reinforcing properties of EtOH, this study sought to determine brain CAT and ALDH2 expression in limbic areas of control and Pb-exposed animals after voluntary EtOH intake. Thirty-five-day-old rats perinatally exposed to 220â¯ppm Pb were offered with water or increasing EtOH solutions (2-10% v/v) during 28 days until postnatal day (PND) 63. Once intake was stable, the animals were administered: 1) saline (SAL; test days 21-24 or 21-28, as corresponds), or 2) a CAT inhibitor: 3-amine 1, 2, 4-triazole (AT; 250â¯mg/kg intraperitoneally [i.p.], 5â¯h before the last eight EtOH intake sessions -test days 21-24 and 25-28), or 3) a CAT booster: 3-nitropropionic acid (3NPA; 20â¯mg/kg subcutaneously [s.c.], 45â¯min before the last four EtOH intake sessions -test days 25-28). Two additional groups were centrally-administered cyanamide (CY, an ALDH2 inhibitor, 0.3â¯mg i.c.v. immediately before the last four EtOH sessions, test days 25-28) or its corresponding vehicle (VEH). Lead exposure increased EtOH intake, an effect potentiated in both groups by 3NPA or CY pretreatments and reduced by AT, albeit selectivity in the Pb group. Catalase abundance in limbic areas parallels these observations in the Pb group, showing higher CAT expression in all areas after EtOH consumption respect to the controls, an effect prevented by AT administration. In contrast, ALDH2 expression was reduced in the Pb animals after EtOH intake, with CY potentiating this effect in all brain areas under study. Based on these results and on previous evidences, we suggest that Pb exposure promotes acetaldehyde accumulation in limbic regions, providing some insights into the mechanism of action that underlies the vulnerability to the excessive EtOH consumption reported in these animals.
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Encéfalo/efeitos dos fármacos , Etanol/farmacologia , Intoxicação do Sistema Nervoso por Chumbo/metabolismo , Consumo de Bebidas Alcoólicas/metabolismo , Consumo de Bebidas Alcoólicas/psicologia , Aldeído-Desidrogenase Mitocondrial/antagonistas & inibidores , Aldeído-Desidrogenase Mitocondrial/metabolismo , Animais , Encéfalo/enzimologia , Encéfalo/metabolismo , Catalase/metabolismo , Cianamida/farmacologia , Feminino , Masculino , Nitrocompostos/farmacologia , Propionatos/farmacologia , Ratos , Ratos WistarRESUMO
The objective of this study was to review technological and toxicological factors related to presence of carbonyl compounds found in wines, including acetaldehyde, formaldehyde, acrolein, ethyl carbamate (EC) and furfural. Acetaldehyde and formaldehyde may be formed through the ethanol and methanol oxidation, respectively. Acrolein may arise as a thermal degradation product of glycerol, amino acids, carbohydrates and triglycerides or by metabolic activity of microorganisms. In addition, acrolein and furfural are formed during wood combustion; therefore, these aldehydes may be present in raw materials due to the environmental contamination. Furfural is also a product of the Maillard reaction formed from sugars and amino acids, while ethyl carbamate occurs through the reaction between urea and ethanol. These compounds may react with SO2 and phenolic compounds to form non-volatile adducts, which positively modulates color stability, astringency and aroma in wine. However, when ingested through wine, electrophilic carbonyl compounds may form adducts with nucleophilic targets, such as DNA, resulting in genotoxicity along the gastrointestinal tract. Furthermore, carbonyl compounds induce the increase of reactive oxygen species and can trigger apoptosis, in addition to hepatocellular adenoma and carcinoma as a consequence of chronic hepatotoxicity. Neurodegenerative diseases may be related to the exposure to carbonyl compounds. Therefore, strategies to reduce the levels of these compounds should be studied in order to get the most out of the beneficial functional properties of wine consumption.(AU)
O objetivo deste estudo foi revisar os fatores tecnológicos e toxicológicos relacionados à presença de compostos carbonílicos encontrados em vinhos, incluindo acetaldeído, formaldeído, acroleína, carbamato de etila (CE) e furfural. O acetaldeído e o formaldeído podem ser formados através da oxidação do etanol e do metanol, respectivamente. A acroleína pode surgir como um produto de degradação térmica de glicerol, aminoácidos, carboidratos e triglicerídeos ou pela atividade metabólica de microorganismos. Além disso, a acroleína e o furfural são formados durante a combustão da madeira. Portanto, esses aldeídos podem estar presentes nas matérias-primas devido à contaminação ambiental. O furfural é também um produto da reação de Maillard formado a partir de açúcares e aminoácidos, enquanto o carbamato de etila ocorre através da reação entre uréia e etanol. Estes compostos podem reagir com SO2 e compostos fenólicos para formar adutos não voláteis, que modulam positivamente a estabilidade da cor, adstringência e aroma no vinho. No entanto, quando ingeridos através do vinho, os compostos carbonílicos que são eletrofílicos podem formar adutos com alvos nucleofílicos, como o DNA, resultando em genotoxicidade ao longo do trato gastrintestinal. Além disso, os compostos carbonílicos também induzem o aumento de espécies reativas de oxigênio e podem desencadear a apoptose, além de adenoma e carcinoma hepatocelular como consequência da hepatotoxicidade crônica. Doenças neurodegenerativas podem estar relacionadas à exposição aos compostos carbonílicos. Com isso, estratégias para reduzir os níveis desses compostos devem ser estudadas para obter o máximo das propriedades funcionais benéficas do consumo de vinho.(AU)
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Acetaldeído/toxicidade , Formaldeído/toxicidade , Uretana/toxicidade , Furaldeído/toxicidade , Acroleína/toxicidade , Vinho/análiseRESUMO
Lead (Pb) is a developmental neurotoxicant. We have demonstrated that perinatally Pb-exposed rats consume more ethanol than their control counterparts, a response that seems to be mediated by catalase (CAT) and centrally-formed acetaldehyde, ethanol's first metabolite with attributed reinforcing effects in the brain. The present study sought to disrupt ethanol intake (2-10% ethanol v/v) in rats exposed to 220 ppm Pb or filtered water during gestation and lactation. Thus, to block brain CAT expression, a lentiviral vector coding for a shRNA against CAT (LV-antiCAT vector) was microinfused in the posterior ventral tegmental area (pVTA) either at the onset or towards the end of a chronic voluntary ethanol consumption test. At the end of the study, rats were euthanized and pVTA dissected to measure CAT expression by Western blot. The LV-antiCAT vector administration not only reversed, but also prevented the emergence of the elevated ethanol intake reported in the perinatally Pb-exposed animals, changes that were supported by a significant reduction in CAT expression in the pVTA. These results provide further evidence of the crucial role of this enzyme in the reinforcing properties of ethanol and in the impact of the perinatal Pb programming to challenging events later in life.
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Consumo de Bebidas Alcoólicas/prevenção & controle , Encéfalo/enzimologia , Catalase/biossíntese , Etanol/toxicidade , Chumbo/toxicidade , Efeitos Tardios da Exposição Pré-Natal/enzimologia , Consumo de Bebidas Alcoólicas/efeitos adversos , Animais , Encéfalo/efeitos dos fármacos , Catalase/antagonistas & inibidores , Catalase/genética , Etanol/administração & dosagem , Feminino , Regulação Enzimológica da Expressão Gênica , Chumbo/administração & dosagem , Masculino , Gravidez , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Efeitos Tardios da Exposição Pré-Natal/prevenção & controle , Ratos , Ratos WistarRESUMO
ABSTRACT: The objective of this study was to review technological and toxicological factors related to presence of carbonyl compounds found in wines, including acetaldehyde, formaldehyde, acrolein, ethyl carbamate (EC) and furfural. Acetaldehyde and formaldehyde may be formed through the ethanol and methanol oxidation, respectively. Acrolein may arise as a thermal degradation product of glycerol, amino acids, carbohydrates and triglycerides or by metabolic activity of microorganisms. In addition, acrolein and furfural are formed during wood combustion; therefore, these aldehydes may be present in raw materials due to the environmental contamination. Furfural is also a product of the Maillard reaction formed from sugars and amino acids, while ethyl carbamate occurs through the reaction between urea and ethanol. These compounds may react with SO2 and phenolic compounds to form non-volatile adducts, which positively modulates color stability, astringency and aroma in wine. However, when ingested through wine, electrophilic carbonyl compounds may form adducts with nucleophilic targets, such as DNA, resulting in genotoxicity along the gastrointestinal tract. Furthermore, carbonyl compounds induce the increase of reactive oxygen species and can trigger apoptosis, in addition to hepatocellular adenoma and carcinoma as a consequence of chronic hepatotoxicity. Neurodegenerative diseases may be related to the exposure to carbonyl compounds. Therefore, strategies to reduce the levels of these compounds should be studied in order to get the most out of the beneficial functional properties of wine consumption.
RESUMO: O objetivo deste estudo foi revisar os fatores tecnológicos e toxicológicos relacionados à presença de compostos carbonílicos encontrados em vinhos, incluindo acetaldeído, formaldeído, acroleína, carbamato de etila (CE) e furfural. O acetaldeído e o formaldeído podem ser formados através da oxidação do etanol e do metanol, respectivamente. A acroleína pode surgir como um produto de degradação térmica de glicerol, aminoácidos, carboidratos e triglicerídeos ou pela atividade metabólica de microorganismos. Além disso, a acroleína e o furfural são formados durante a combustão da madeira. Portanto, esses aldeídos podem estar presentes nas matérias-primas devido à contaminação ambiental. O furfural é também um produto da reação de Maillard formado a partir de açúcares e aminoácidos, enquanto o carbamato de etila ocorre através da reação entre uréia e etanol. Estes compostos podem reagir com SO2 e compostos fenólicos para formar adutos não voláteis, que modulam positivamente a estabilidade da cor, adstringência e aroma no vinho. No entanto, quando ingeridos através do vinho, os compostos carbonílicos que são eletrofílicos podem formar adutos com alvos nucleofílicos, como o DNA, resultando em genotoxicidade ao longo do trato gastrintestinal. Além disso, os compostos carbonílicos também induzem o aumento de espécies reativas de oxigênio e podem desencadear a apoptose, além de adenoma e carcinoma hepatocelular como consequência da hepatotoxicidade crônica. Doenças neurodegenerativas podem estar relacionadas à exposição aos compostos carbonílicos. Com isso, estratégias para reduzir os níveis desses compostos devem ser estudadas para obter o máximo das propriedades funcionais benéficas do consumo de vinho.
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Abstract Acetaldehyde, associated with consumption of alcoholic beverages, is known to be a carcinogen and to be related to the tongue dorsum. Objective The aim of this study was to investigate the relationship between acetaldehyde concentration in mouth air and bacterial characteristics on the tongue dorsum. Methodology Thirty-nine healthy volunteers participated in the study. Acetaldehyde concentrations in mouth air were evaluated by a high-sensitivity semiconductor gas sensor. A 16S rRNA gene sequencing technique was used to compare microbiomes between two groups, focusing on the six samples with the highest acetaldehyde concentrations (HG) and the six samples with lowest acetaldehyde concentrations (LG). Results Acetaldehyde concentration increased in correlation with the increase in bacterial count (p=0.048). The number of species observed in the oral microbiome of the HG was higher than that in the oral microbiome of the LG (p=0.011). The relative abundances of Gemella sanguinis, Veillonella parvula and Neisseria flavescens in the oral microbiome of the HG were higher than those in the oral microbiome of the LG (p<0.05). Conclusion Acetaldehyde concentration in mouth air was associated with bacterial count, diversity of microbiome, and relative abundance of G. sanguinis, V. parvula, and N. flavescens.
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Humanos , Masculino , Feminino , Adulto , Adulto Jovem , Língua/microbiologia , Microbiota , Acetaldeído/análise , Boca/cirurgia , Valores de Referência , Bactérias/isolamento & purificação , Bactérias/genética , Língua/metabolismo , Candida/isolamento & purificação , Consumo de Bebidas Alcoólicas/metabolismo , RNA Ribossômico 16S/análise , RNA Ribossômico 16S/metabolismo , Fumar/metabolismo , Estudos Transversais , Inquéritos e Questionários , Estatísticas não Paramétricas , Carga Bacteriana , Japão , Acetaldeído/metabolismo , Boca/metabolismoRESUMO
Dekkera bruxellensis is continuously changing its status in fermentation processes, ranging from a contaminant or spoiling yeast to a microorganism with potential to produce metabolites of biotechnological interest. In spite of that, several major aspects of its physiology are still poorly understood. As an acetogenic yeast, minimal oxygen concentrations are able to drive glucose assimilation to oxidative metabolism, in order to produce biomass and acetate, with consequent low yield in ethanol. In the present study, we used disulfiram to inhibit acetaldehyde dehydrogenase activity to evaluate the influence of cytosolic acetate on cell metabolism. D. bruxellensis was more tolerant to disulfiram than Saccharomyces cerevisiae and the use of different carbon sources revealed that the former yeast might be able to export acetate (or acetyl-CoA) from mitochondria to cytoplasm. Fermentation assays showed that acetaldehyde dehydrogenase inhibition re-oriented yeast central metabolism to increase ethanol production and decrease biomass formation. However, glucose uptake was reduced, which ultimately represents economical loss to the fermentation process. This might be the major challenge for future metabolic engineering enterprises on this yeast.
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Acetatos/metabolismo , Dekkera/metabolismo , Etanol/metabolismo , Fermentação , Acetatos/análise , Aldeído Oxirredutases/antagonistas & inibidores , Carbono/metabolismo , Meios de Cultura , Dekkera/efeitos dos fármacos , Dissulfiram/farmacologia , Glucose/metabolismo , Microbiologia Industrial , Saccharomyces cerevisiae/efeitos dos fármacos , Saccharomyces cerevisiae/metabolismoRESUMO
Acetone is an important solvent and widely used in the synthesis of drugs and polymers. Currently, acetone is mainly generated by the Cumene Process, which employs benzene and propylene as fossil raw materials. Phenol is a co-product of this synthesis. However, this ketone can be generated from ethanol (a renewable feedstock) in one-step. The aim of this work is to describe the influence of physical-chemical properties of three different catalysts on each step of this reaction. Furthermore, contribute to improve the description of the mechanism of this synthesis. The acetone synthesis from ethanol was studied employing Cu/ZnO/Al2O3, Ce0.75Zr0.25O2 and ZrO2. It was verified that the acidity of the catalysts needs fine-tuning in order to promote the oxygenate species adsorption and avoid the dehydration of ethanol. The higher the reducibility and the H2O dissociation activity of the catalysts are, the higher the selectivity to acetone is. In relation to the oxides, these properties are associated with the presence of O vacancies. The H2 generation, which occurs during the TPSR, indicates the redox character of this synthesis. The main steps of the acetone synthesis from ethanol are the generation of acetaldehyde, the oxidation of this aldehyde to acetate species (which reduces the catalyst), the H2O dissociation, the oxidation of the catalyst producing H2, and, finally, the ketonization reaction. These pieces of information will support the development of active catalysts for not only the acetone synthesis from ethanol, but also the isobutene and propylene syntheses in which this ketone is an intermediate. Graphical abstract Acetone from ethanol.
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This review article provides evidence of the impact of the environmental contaminant lead (Pb) on the pattern of the motivational effects of ethanol (EtOH). To find a mechanism that explains this interaction, the focus of this review article is on central EtOH metabolism and the participating enzymes, as key factors in the modulation of brain acetaldehyde (ACD) accumulation and resulting effect on EtOH intake. Catalase (CAT) seems a good candidate for the shared mechanism between Pb and EtOH due to both its antioxidant and its brain EtOH-metabolizing properties. CAT overactivation was reported to increase EtOH consumption, while CAT blockade reduced it, and both scenarios were modified by Pb exposure, probably as the result of elevated brain and blood CAT activity. Likewise, the motivational effects of EtOH were enhanced when brain ACD metabolism was prevented by ALDH2 inhibition, even in the Pb animals that evidenced reduced brain ALDH2 activity after chronic EtOH intake. Overall, these results suggest that brain EtOH metabolizing enzymes are modulated by Pb exposure with resultant central ACD accumulation and a prevalence of the reinforcing effects of the metabolite in brain against the aversive peripheral ACD accumulation. They also support the idea that early exposure to an environmental contaminant, even at low doses, predisposes at a later age to differential reactivity to challenging events, increasing, in this case, vulnerability to acquiring addictive behaviors, including excessive EtOH intake.