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1.
Braz. j. med. biol. res ; 54(8): e10841, 2021. graf
Article in English | LILACS | ID: biblio-1249329

ABSTRACT

The present study was conducted to investigate the underlying mechanisms and effective components of Polygonum hydropiper in ethanol-induced acute gastric mucosal lesions. The ethanol extract was purified on an AB-8 macroporous resin column and eluted with 60% ethanol and was then injected into the HPLC system for quantitative analysis. Sprague-Dawley rats were orally pretreated with P. hydropiper extract (PHLE; 50, 100, and 200 mg/kg) for 5 days and then absolute ethanol was administered to induce gastric mucosal damage. One hour after ethanol ingestion, the rats were euthanized and stomach samples were collected for biochemical analysis. Antioxidant enzymes and anti-inflammatory cytokines were quantified. Western blotting was used to detect the expression levels of proteins. Cell proliferation was assayed by CCK-8 assays. The proportion of total flavonoids in the final extract of P. hydropiper was 50.05%, which contained three major bioactive flavonoid constituents, including rutin, quercitrin, and quercetin. PHLE significantly increased cell viability and effectively protected human gastric epithelial cells-1 against alcohol-induced damage in vitro. PHLE pretreatment attenuated gastric mucosal injuries in a dose-dependent manner in rats, and increased the activity of superoxide dismutase, glutathione peroxidase, and glutathione, and decreased the levels of malondialdehyde in gastric tissue. Pretreatment with PHLE also reduced the generation of the pro-inflammatory cytokines tumor necrosis factor-α and interleukin-1β in gastric tissue by downregulating the expression of nuclear factor-kappa B. PHLE exerted protective effects against gastric injury through antioxidant and anti-inflammatory pathways. Flavonoids might be the main effective components of P. hydropiper against gastric mucosal injury.


Subject(s)
Animals , Rats , Polygonum , Antioxidants/pharmacology , Plant Extracts/pharmacology , Rats, Sprague-Dawley , Ethanol/toxicity , Gastric Mucosa , Anti-Inflammatory Agents/pharmacology
2.
Article in English | WPRIM | ID: wpr-922259

ABSTRACT

: To investigate the protective effect of (FD) against ethanol-induced gastric ulcer and its mechanism. : Human gastric epithelial GES-1 cells were divided into normal control group, model control group, FD 95% alcohol extract group, FD 50% alcohol extract group and FD decoction extract group. Gastric ulcer was induced by treatment with 1% ethanol in GES-1 cells. The cell proliferation was detected with MTT method in each group. Sixty SD rats were randomly divided into normal control group, model control group, ranitidine group and low-dose, medium-dose, high-dose FD 95% alcohol extract groups (150, 300, 600 mg/kg). The corresponding drugs were administrated by gavage for The gastric ulcer model was induced by intragastric administration of anhydrous ethanol. The gastric ulcer area and ulcer inhibition rate of rats were measured in each group; the degree of gastricmucosal damage was observed by scanning electron microscopy; the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β in serum and the content of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), catalase (CAT) in gastric tissues were detected by ELISA method. : 95% alcohol extract of FD had the strongest protective effect on proliferation of GES-1 cells. In animal experiments, compared with the normal control group, a large area of ulcers appeared on the gastric mucosa in the model control group, while the ulcer areas of the FD groups and ranitidine group were significantly smaller than that of the model control group (all <0.05). Compared with the model control group, FD groups and ranitidine group significantly reduced the levels of TNF-α, IL-1β, IL-6 in serum and the MDA content in the gastric tissues, and increased the activity of SOD, CAT and GSH in gastric tissues (all <0.05). : The 95% alcohol extract of FD can reduce the levels of TNF-α, IL-1β and IL-6 in serum and the content of MDA in gastric tissues, and increase the activity of SOD, CAT and GSH in gastric tissues to achieve the protective effect against gastric ulcer.


Subject(s)
Animals , Ethanol/toxicity , Gastric Mucosa , Malondialdehyde , Rats , Rats, Sprague-Dawley , Stomach Ulcer/prevention & control , Superoxide Dismutase
3.
Article in Chinese | WPRIM | ID: wpr-879096

ABSTRACT

Prunella vulgaris(PV) is an edible and traditional medicinal herb which has a wide range application in fighting inflammation and oxidative stress, and protecting liver. Now it has been used to treat various types of liver diseases and has significant clinical efficacy. This study aims to investigate the effects of PV on ethanol-induced oxidative stress injury in rats and its metabolic mechanism. The rats were divided into control group, model group, PV group, and VC group. The liver protection of PV was identified by measuring pharmacological indexes such as antioxidant and anti-inflammatory activity. The metabolic mechanism of long-term ethanol exposure and the metabolic regulation mechanism of PV treatment were studied by LS-MS metabonomics. The pharmacological investigation indicated that ethanol could significantly decrease the contents of SOD, GSH-Px, CAT and other antioxidant enzymes in liver and increase the content of MDA. At the same time, PV could significantly reduce the contents of inflammatory factors(TNF-α, IL-6 and IL-1β) and liver function markers(ALT, AST, ALP) in serum. What's more, long-term ethanol exposure could significantly cause liver injury, while PV could protect liver. Metabolomics based on multiple statistical analyses showed that long-term ethanol exposure could cause significant metabolic disorder, and fatty acids, phospholipids, carnitines and sterols were the main biomarkers. Meanwhile, pathway analysis and enrichment analysis showed that the β oxidation of branched fatty acids was the main influencing pathway. Also, PV could improve metabolic disorder of liver injury induced by ethanol, and amino acids, fatty acids, and phospholi-pids were the main biomarkers in PV treatment. Metabolic pathway analysis showed that PV mainly regulated metabolic disorder of ethanol-induced liver injury through phenylalanine, tyrosine and tryptophan biosynthetic pathways. This study could provide a new perspective on the hepatoprotective effect of natural medicines, such as PV.


Subject(s)
Animals , Antioxidants/metabolism , Ethanol/toxicity , Liver/metabolism , Metabolomics , Oxidative Stress , Prunella , Rats
5.
Braz. J. Pharm. Sci. (Online) ; 55: e18107, 2019. tab, graf
Article in English | LILACS | ID: biblio-1039037

ABSTRACT

This study evaluated the acute and sub-chronic toxicities of ethanol leaf extract of Dryopteris filix-mas. Acute toxicity and phytochemical tests on ethanol leaf extract were determined. In sub-chronic toxicity test, animals were treated with 62.5, 125, 250 and 500 mg/kg of extract every day for 90 days. Blood samples were collected via retro-orbital puncture for baseline studies and at 31, 61 and 91st days for determination of hematological, kidney and liver function parameters. Liver and kidneys were harvested for histopathology analyses on 91st day. Also, a 28 day recovery study was carried out to determine reversibility in toxicological effects. Phytochemical screening revealed the presence of tannins, phenols, flavonoids, saponins, steroids, alkaloids, terpenoids, reducing sugar and cardiac glycosides. Acute toxicity test did not show toxicity or death at 5000 mg/kg. There was significant (p<0.005) reduction in white blood cell and lymphocyte counts, significant (p<0.05) increase in some liver and kidney biomarkers as well as alterations in liver and kidney histo-architecture on 91st days in animals that were treated with 250 and 500 mg/kg extract. However, toxicities observed on 91st day were reversible in recovery studies. The leaf extract of Dryopteris filix-mas may be hepatotoxic and nephrotoxic when used for long periods


Subject(s)
Animals , Male , Female , Rats , Plant Extracts/analysis , Acute Toxicity/adverse effects , Dryopteris/toxicity , Toxicity Tests, Subchronic/instrumentation , Ethanol/toxicity
6.
Rev. méd. Minas Gerais ; 28: [1-6], jan.-dez. 2018.
Article in Portuguese | LILACS | ID: biblio-970579

ABSTRACT

A ingesta crônica de álcool causa danos tóxicos diretos e indiretos e as principais alterações são causadas pelo seu próprio metabolismo. O etanol aumenta o estresse oxidativo principalmente no fígado, reduz a relação NAD+/NADH, aumenta a produção de acetaldeído e altera a função mitocondrial. Essas alterações são frequentemente associadas com o aumento de produtos da peroxidação lipídica, essenciais ao desenvolvimento da doença hepática alcóolica (DHA). Os exercícios físicos moderados parecem não influenciar significativamente as características morfológicas do tecido hepático ou a função hepática. Em exercícios pesados e prolongados, observam-se estresse oxidativo, alterações histológicas, prejuízo da farmacocinética e níveis alterados de enzimas hepáticas. Cessado o exercício alguns dias, parece havervrecuperação da função hepática normal. As alterações hepáticas com o exercício agudo parecem ser transitórias e possivelmente contribuem para a homeostase. A atividade física parece ter alguma influência direta na patologia hepática, além da simples modificação dos níveis de gordura no fígado e parece que a intensidade da atividade física é importante para prevenir a progressão da doença. Entender os mecanismos subjacentes da doença hepática auxiliaria na descoberta de intervenções para reduzir a progressão dessa doença de uma condição benigna, como a esteatose, para formas graves como esteatohepatite, fibrose e cirrose. Portanto, exercícios podem ser uma terapia útil para melhorar a performance e a capacidade funcional em indivíduos com doença hepática, porém não está claro na literatura se o exercício físico pode restaurar a saúde hepática e nem qual seria a quantidade e o tipo de exercício necessários. (AU)


Chronic alcohol intake causes direct and indirect toxic damage and major changes are caused by their own metabolism. Ethanol increases oxidative stress primarily in the liver, reduces NAD + / NADH ratio, increases the production of acetaldehyde and alters mitochondrial function. These changes are often associated with increased lipid peroxidation products that are essentiais to the development of alcoholic liver disease (ADH). The moderate intensity exercise does not seem to significantly influence the morphological characteristics of liver tissue or liver function. In heavy and prolonged exercise, oxidative stress, histological changes, impaired pharmacokinetics and altered levels of liver enzymes are noted. Liver function seems to improve a few days after the end of exercise. Hepatic changes with acute exercise appear to be transient and possibly contribute to homeostasis. Physical activity seems to have any direct influence on the liver pathology in addition to the simple modification of the levels of fat in the liver and it seems that the intensity of physical activity is important to prevent disease progression. Understanding the mechanisms underlying hepatic disease, this could help find interventions to slow the progression of liver disease of a benign condition, such as steatosis to severe forms, such as steatohepatitis, fibrosis and cirrhosis. Therefore, exercise can be a useful therapy to improve the performance and functional capacity in patients with liver disease, but it is not clear in the literature that the exercise can restore liver health and even what the quantity and type of needed exercise. (AU)


Subject(s)
Ethanol , Hepatitis, Alcoholic , Ethanol/toxicity , Exercise , Hepatitis, Alcoholic/prevention & control , Hepatitis, Alcoholic/therapy , Alcoholism
7.
Pesqui. vet. bras ; 38(3): 382-386, mar. 2018. ilus
Article in Portuguese | LILACS, VETINDEX | ID: biblio-964214

ABSTRACT

O presente trabalho descreve um surto de intoxicação por etanol que afetou um rebanho bovino de aptidão leiteira alimentado com o subproduto de cervejaria denominado bagaço de malte, resíduo úmido de cervejaria (RUC), resíduo de cevada maltada ou simplesmente "cevada". O surto iniciou cerca de 24 horas após ao fornecimento de uma nova partida do subproduto que apresentava odor alcoólico. Análise cromatográfica e microbiológica de amostra deste subproduto confirmou a presença de etanol e Saccharomyces spp., respectivamente, indicando a adição de outro subproduto de cervejaria, a levedura de cerveja ou levedo. Os principais sinais clínicos observados foram diarreia, salivação, andar cambaleante e decúbito. A morbidade foi de 12,2% (5/41) e mortalidade de 2,4% (1/41). Uma vaca que morreu após um curso clínico de 3 dias foi necropsiada. Não foram observadas lesões macroscópicas significativas, mas na histopatologia havia rumenite necrosupurativa aguda, multifocal, moderada, com colonização bacteriana e fúngica secundária, indicando acidose ruminal concomitante. Em análise cromatográfica de amostras de conteúdo ruminal e fígado deste bovino foram detectadas quantidades variáveis de etanol. Os dados do presente estudo indicam que a possibilidade de intoxicação por etanol deve ser considerada em bovinos com sinais neurológicos e digestivos alimentados com RUC quando a este acrescentado levedura de cerveja.(AU)


An outbreak of ethanol poisoning that affected a dairy cattle herd fed with the brewery by-product known as malt bagasse, wet brewery residue, malted barley waste or "barley". The outbreak began about 24 hours after a new product of the by-product was offered to cattle that had an alcoholic odor. Chromatographic and microbiological analysis of this by-product sample confirmed the presence of ethanol and Saccharomyces spp., respectively, indicating the addition of another by-product brewery, brewer's yeast or yeast. The main clinical signs observed were diarrhea, salivation, staggering gait and decubitus. Morbidity was 12.2% (5/41) and mortality was 2.4% (1/41). A cow that died after a 3-day of clinical course was necropsied. No significant macroscopic lesions were observed, but in the histopathology, there was acute, multifocal, moderate necrosupurative rumenitis with secondary bacterial and fungal colonization, indicating concomitant ruminal acidosis. In the chromatographic analysis of samples of rumen and liver contents of this bovine, variable amounts of ethanol were detected. The data from the present study indicate that the possibility of ethanol intoxication should be considered in cattle with neurological and digestive signs fed with RUC when added to brewer's yeast.(AU)


Subject(s)
Animals , Cattle , Seedlings/toxicity , Ethanol/toxicity , Alcoholic Intoxication/veterinary , Saccharomyces cerevisiae/metabolism , Cattle
8.
Int. j. morphol ; 35(3): 942-949, Sept. 2017.
Article in English | LILACS | ID: biblio-893078

ABSTRACT

Prolonged alcohol consumption has consequences on the liver, producing necrotic precipitates and fibrosis, on the pancreas, causing the pancreatic acini to atrophy and destroying insulin-producing cells, and on the central nervous system (CNS), causing the gray and white matter in the frontal lobes of the brain and cerebellum to atrophy. Generally, alcohol is metabolized via oxidative pathways, where the enzymes alcohol dehydrogenase and aldehyde dehydrogenase participate during its metabolization in the liver and CNS, or via non-oxidative pathways during its metabolization in the pancreas. Ethanol metabolism can produce oxidative stress and tissue damage mediated by free radicals, causing morphological and functional alterations in the liver. In the pancreas, it can cause progressive and irreversible damage affecting the endocrine and exocrine functions, a result of the activation of the stellate cells, which are activated directly by alcohol, causing pancreatic fibrosis. In the CNS ethanol can bind directly to proteins, nucleic acids and phospholipids to develop its pathogenesis. The effects produced by alcohol can be counteracted by supplementation with antioxidants, which reduce the inflammation and areas of focal necrosis in the liver, inhibit the activation of pancreatic stellate cells, and reduce oxidative stress in the CNS. Additionally, in order to reduce the negative effects associated with alcohol consumption, recent studies have suggested the administration of antioxidants as a treatment strategy.


El consumo prolongado de alcohol tiene consecuencias en hígado, produciendo precipitados necróticos y fibrosis; en páncreas, provocando atrofia del acino pancreático y destrucción de las células productoras de insulina, y en Sistema Nervioso Central (SNC) generando atrofia de la sustancia gris y blanca en lóbulos frontales del cerebro y cerebelo. En general, el metabolismo del alcohol se consigue mediante las vías oxidativas, donde participan las enzimas alcohol-deshidrogenasa y aldehído deshidrogenasa durante su metabolización en hígado y SNC; o bien, mediante las vías no oxidativas durante su metabolización en páncreas. El metabolismo del etanol es capaz de producir estrés oxidativo y daño tisular mediado por radicales libres, causando alteraciones morfológicas y funcionales del hígado; en el páncreas, puede causar daño progresivo e irreversible afectando las funciones endocrinas y exocrinas de este órgano producto de la activación de las células estrelladas que son activadas directamente por el alcohol generando fibrosis pancreática; mientras que, en SNC se puede unir directamente a proteínas, ácidos nucleicos y fosfolípidos para desarrollar su patogenia. Los efectos producidos por el alcohol pueden contrarrestarse mediante la suplementación con antioxidantes, que reducen la inflamación y las zonas de necrosis focal en el hígado, inhiben la activación de células pancreáticas estrelladas, y reducen el estrés oxidativo en SNC. Asimismo, para reducir los efectos negativos asociados al consumo de alcohol, estudios recientes han propuesto la administración de antioxidantes como estrategia terapéutica.


Subject(s)
Humans , Central Nervous System/drug effects , Ethanol/toxicity , Alcoholic Intoxication/drug therapy , Antioxidants/therapeutic use , Pancreas/drug effects , Pancreas/pathology , Central Nervous System/pathology , Oxidative Stress , Ethanol/metabolism , Liver/drug effects , Liver/pathology
9.
Braz. j. microbiol ; 47(1): 181-190, Jan.-Mar. 2016. tab, graf
Article in English | LILACS | ID: lil-775120

ABSTRACT

Abstract In the present work we isolated and identified various indigenous Saccharomyces cerevisiae strains and screened them for the selected oenological properties. These S. cerevisiae strains were isolated from berries and spontaneously fermented musts. The grape berries (Sauvignon blanc and Pinot noir) were grown under the integrated and organic mode of farming in the South Moravia (Czech Republic) wine region. Modern genotyping techniques such as PCR-fingerprinting and interdelta PCR typing were employed to differentiate among indigenous S. cerevisiae strains. This combination of the methods provides a rapid and relatively simple approach for identification of yeast of S. cerevisiae at strain level. In total, 120 isolates were identified and grouped by molecular approaches and 45 of the representative strains were tested for selected important oenological properties including ethanol, sulfur dioxide and osmotic stress tolerance, intensity of flocculation and desirable enzymatic activities. Their ability to produce and utilize acetic/malic acid was examined as well; in addition, H2S production as an undesirable property was screened. The oenological characteristics of indigenous isolates were compared to a commercially available S. cerevisiae BS6 strain, which is commonly used as the starter culture. Finally, some indigenous strains coming from organically treated grape berries were chosen for their promising oenological properties and these strains will be used as the starter culture, because application of a selected indigenous S. cerevisiae strain can enhance the regional character of the wines.


Subject(s)
Saccharomyces cerevisiae/classification , Saccharomyces cerevisiae/isolation & purification , Vitis/microbiology , Acetic Acid/metabolism , Bacterial Adhesion , Czech Republic , DNA Fingerprinting , Drug Tolerance , Ethanol/toxicity , Hydrogen Sulfide/metabolism , Molecular Typing , Mycological Typing Techniques , Malates/metabolism , Osmotic Pressure , Polymerase Chain Reaction , Stress, Physiological , Saccharomyces cerevisiae/genetics , Saccharomyces cerevisiae/physiology , Sulfur Dioxide/toxicity
10.
Pesqui. vet. bras ; 35(12): 956-964, dez. 2015. graf
Article in Portuguese | LILACS | ID: lil-771956

ABSTRACT

A utilização de subprodutos de cervejaria na alimentação de bovinos tem crescido nos últimos anos como uma excelente alternativa na manutenção ou aumento da produtividade na bovinocultura, sobretudo na Região Sudeste. Entre os resíduos mais empregados estão o bagaço de malte oriundo da "cevada" e o "levedo de cerveja", um subproduto líquido que contém álcool, muito utilizado no Estado do Rio de Janeiro. O uso incorreto ou sem os devidos cuidados, bem como o armazenamento de forma inadequada, contudo, podem ser responsáveis por quadros de intoxicação por etanol, neurotoxicose por Aspergillus clavatus, acidose ruminal e botulismo. Esse trabalho tem por intuito alertar para a importância dessas condições como causa de sérios prejuízos econômicos à pecuária e fornecer subsídios para o estabelecimento do diagnóstico, diagnóstico diferencial e profilaxia das mesmas...


The use of brewery by-products in cattle feed has grown in recent years as an excellent alternative for maintenance or increase in cattle productivity especially in Southeastern Brazil. Among the most employed by-products are malted barley waste and brewer's yeast, a liquid by-product that contains alcohol and is widely used in the State of Rio de Janeiro. Careless or incorrect use of these products, as well as inadequate storage, can cause ethanol poisoning, neurotoxicosis by Aspergillus clavatus, ruminal acidosis and botulism. This paper highlights the importance of these conditions as causes of severe economic losses to livestock, and provides support for the establishment of diagnosis, differential diagnosis and prophylaxis...


Subject(s)
Animals , Cattle , Edible Grain/toxicity , Hordeum/toxicity , Saccharomyces cerevisiae/pathogenicity , Acidosis/veterinary , Aspergillus/pathogenicity , Botulism/veterinary , Ethanol/toxicity , Rumen , Animal Feed/toxicity
11.
J. appl. oral sci ; 23(5): 497-507, Sept.-Oct. 2015. tab, graf
Article in English | LILACS, BBO | ID: lil-764156

ABSTRACT

The value of aesthetic dentistry has precipitated several developments in the investigation of dental materials related to this field. The free marketing of these products is a problem and it is subject to various interpretations regarding its legality. There are several techniques for tooth whitening, the most used one being the external bleaching. It is the later version of such technique that poses the greatest danger of ingesting the product. The present study analysed the systemic effect of these products when they are swallowed.Objective This experimental study aimed to observe the effects of a tooth whitening product, whose active agent is 6% hydrogen peroxide, on the gastric mucosa of healthy and non-tumour gastric pathology animals.Material and Methods Fifty Wistar-Han rats were used and then distributed into 5 groups, one for control and four test groups in which the bleaching product was administered in animals with and without non-tumour gastric pathology (induced by the administration of 1 sample of 50% ethanol and 5% of drinking water during 6 days) at different times of study by gavage. There was a decrease in body weight in animals of groups handled during the study period, which was most pronounced in IV and VA groups. Changes in spleen weight relative to body weight revealed no statistically significant changes. An analysis of the frequency was performed on the results of macroscopic observation of the gastric mucosa.Results The gastric mucosa revealed lesions in all manipulated groups, being more frequent in groups III and IV. It appears that there is a synergism when using hydrogen peroxide and 50% ethanol in the same group.Conclusion Therefore, it seems that there are some signs of toxicity 3 to 4 days after administration of 6% hydrogen peroxide. The prescription of these therapies must be controlled by the clinician and the risks must be minimized.


Subject(s)
Animals , Gastric Mucosa/drug effects , Hydrogen Peroxide/toxicity , Tooth Bleaching Agents/toxicity , Tooth Bleaching/adverse effects , Body Weight , Ethanol/toxicity , Gastric Mucosa/pathology , Organ Size , Rats, Wistar , Spleen/drug effects , Spleen/pathology , Time Factors
12.
Rev. cuba. farm ; 49(3)jul.-set. 2015. tab
Article in English | LILACS, CUMED | ID: lil-779731

ABSTRACT

Introduction: D-002, a mixture of beeswax alcohols, has been effective in osteoarthritis models and for reducing osteoarthritis symptoms. Unlike the classic anti-inflammatory drugs, D-002 elicits gastroprotective rather than gastrotoxic effects. Lyprinol, used for ameliorating inflammation and arthritic symptoms, improves gastrointestinal dysfunction symptoms in osteoarthritis subjects. Both D-002 and Lyprinol inhibit cyclooxygenase and 5?lipoxygenase activities, and have been similarly effective for reducing inflammation experimentally. Objective: to compare the effects of D-002 and Lyprinol on gastric mucosa of normal and experimentally-induced ulcer rats. Methods: ulcer indexes were measured in normal rats and in rats with ethanol or pylorus ligation-induced ulcers, in which gastric volume and mucus secretion were also measured. Normal rats were randomized into a vehicle control, one acetic salicylic acid (150 mg/kg), three D-002, three Lyprinol groups; rats with ethanol-ulcers into a vehicle control, three D-002 and three Lyprinol-treated groups; and the experiment on pylorus ligation included a negative control and eight pylorus-ligated groups: one vehicle control, three D-002, three Lyprinol, one omeprazole 10 mg/kg. In all cases, D-002 and Lyprinol (50, 200 and 400 mg/kg) were given orally. Results: unlike D-002 and Lyprinol (50-400 mg/kg), acetic salicylic acid increased ulcer indexes and the incidence of ulcers versus the vehicle control. Single oral doses of D-002 (50-400 mg/kg) or Lyprinol (200 and 400 mg/kg) decreased significantly (p<0.01) and in a similar way ulcer indexes versus the ethanol-positive control. D-002 and Lyprinol (50-400 mg/kg) lowered significantly (p<0.01) and comparably ulcer indexes in rats with pylorus ligation versus the positive controls. D-002 (200 and 400 mg/kg) decreased gastric volume and increased gastric mucus secretion versus the positive control whereas only Lyprinol 400 mg/kg increased the gastric mucus secretion but without modifying the gastric volume. Omeprazole significantly reduced ulcer index (p<0.05) and gastric volume (p< 0.01), with no change in mucus secretion. Conclusion: D-002 and Lyprinol did not show gastrotoxic effects and similar efficacy in protecting against ethanol and pylorus ligation-induced gastric ulceration in rats(AU)


Introducción: el D‒002, una mezcla de alcoholes de la cera de abejas, efectivo en modelos de osteoartritis y para reducir los síntomas de la misma. A diferencia de los medicamentos antiinflamatorios clásicos el D‒002 produce efectos gastroprotectores más que efectos gastrotóxicos. El Lyprinol, usado para disminuir la inflamación y los síntomas artríticos, mejora los síntomas de disfunción gastrointestinal en sujetos con dicha enfermedad. D‒002 y Lyprinol inhiben las actividades de cyclooxigenasa y 5‒lipooxigenasa, y son similarmente efectivos para reducir la inflamación en modelos experimentales. Objetivo: comparar los efectos del D‒002 y el Lyprinol sobre la mucosa gástrica de ratas normales y de ratas con úlcera gástrica inducida experimentalmente. Métodos: se determinó el índice de úlcera en ratas normales y en ratas con úlceras gástricas inducidas por etanol e inducidas por ligadura de píloro, en las cuales se midió el volumen gástrico y la secreción de mucus. Las ratas normales se distribuyeron en un grupo control (vehículo), uno con ácido acetil salicílico (150 mg/kg), tres con D‒002 y tres con Lyprinol; las ratas con úlcera inducida por etanol en un grupo control (vehículo), tres con D‒002 y tres con Lyprinol; y el experimento con ligadura de píloro en un grupo control (vehículo), tres D‒002, tres Lyprinol y uno con omeprazol (10 mg/kg). En todos los casos, el D‒002 y el Lyprinol (50, 200 y 400 mg/kg) se administraron por vía oral. Resultados: el ácido acetil salicílico, no el D‒002 ni el Lyprinol (50‒400 mg/kg), incrementó el índice de úlceras y la incidencia de úlceras comparadas con el grupo control. Dosis orales únicas de D‒002 (50‒400 mg/kg) o Lyprinol (200 y 400 mg/kg) redujeron significativa (p<0,01) y similarmente el índice de úlceras comparado con el grupo control positivo con úlceras por etanol. El D‒002 y el Lyprinol (50‒400 mg/kg) redujeron significativamente (p<0,01) y comparablemente el índice de úlceras en ratas con ligadura de píloro comparado con el grupo control positivo. El D‒002 (200 y 400 mg/kg) redujo el volumen gástrico e incrementó la secreción de mucus gástrico respecto al grupo control positivo; mientras solo el Lyprinol 400 mg/kg aumentó la secreción de mucus gástrico pero sin modificar el volumen gástrico. El omeprazol redujo significativamente el índice de úlcera (p<0,05) y el volumen gástrico (p<0,01), sin modificar la secreción de mucus. Conclusiones: el D‒002 y el Lyprinol no presentaron efectos gastrotóxicos, y protegieron con eficacia similar de las úlceras gástricas inducidas por etanol y por ligadura del píloro en ratas(AU)


Subject(s)
Rats , Stomach Ulcer/complications , Gastrointestinal Agents/therapeutic use , Aspirin/adverse effects , Ethanol/toxicity
13.
Rev. méd. Chile ; 143(3): 320-328, mar. 2015. tab
Article in Spanish | LILACS | ID: lil-745629

ABSTRACT

Background: Suicide mortality rates are increasing among teenagers. Aim: To study the prevalence and predictive factors of suicide attempts among Chilean adolescents. Material and Methods: A random sample of 195 teenagers aged 16 ± 1 years (53% males) answered an anonymous survey about their demographic features, substance abuse, the Osaka suicidal ideation questionnaire, Smilksten familial Apgar. Beck hopelessness scale, Beck depression scale and Coppersmith self-esteem inventory. Results: Twenty five percent of respondents had attempted suicide at least in one occasion during their lives. These attempts were significantly associated with female gender, absent parents, family dysfunction, drug abuse, smoking, low self-esteem, hopelessness, depression and recent suicidal ideation. A logistic regression analysis accepted female gender, smoking and recent suicidal ideation as significant independent predictors of suicide attempt. Conclusions: Suicide attempted is common among teenagers and its predictors are female sex, smoking and previous suicidal ideation.


Subject(s)
Animals , Female , Humans , Mice , Pregnancy , Acetaldehyde/metabolism , Aldehyde Dehydrogenase/genetics , Aldehyde Dehydrogenase/metabolism , Embryo, Mammalian/metabolism , Ethanol/toxicity , Fanconi Anemia Complementation Group A Protein/genetics , Fanconi Anemia/pathology , Animals, Newborn , Acetaldehyde/toxicity , Disease Models, Animal , DNA Damage , Embryo, Mammalian/embryology , Genome , Hematopoietic Stem Cells/metabolism , Isoenzymes/genetics , Isoenzymes/metabolism , Retinal Dehydrogenase/genetics , Retinal Dehydrogenase/metabolism
14.
Indian J Exp Biol ; 2015 Feb; 53(2): 93-97
Article in English | IMSEAR | ID: sea-158383

ABSTRACT

Though there are literature indicating the bone loss due to alcohol consumption, studies on the association between ethanol consumption and periodontal breakdown in animals are either scarce or have provided conflicting results. Here, we investigated the effects of chronic alcohol exposure from adolescence to adulthood on the alveolar bone in rats. Wistar rats were exposed to ethanol (6.5 g/kg/day) in a solution of 22.5% (w/v) or distilled water (control) by gavage from 35 days of age (adolescent) until 90 days (adulthood). Evaluation of the bone loss was performed using scanning electronic microscopy, in which the distances between the cement-enamel junction and the alveolar bone crest from the palatal side of the first molar mandibular were measured. The measurements obtained were tabulated and analyzed using Student’s t-test. Alcohol-treated group revealed greater bone loss in comparison to the control group. These findings indicate that heavy chronic alcohol exposure from adolescent to adulthood can induce alveolar bone loss in rats associated to absence of periodontitis.


Subject(s)
Age Factors , Alveolar Bone Loss/chemically induced , Alveolar Bone Loss/drug effects , Alveolar Process/drug effects , Alveolar Process/pathology , Alveolar Process/ultrastructure , Analysis of Variance , Animals , Body Weight/drug effects , Central Nervous System Depressants/administration & dosage , Central Nervous System Depressants/toxicity , Ethanol/administration & dosage , Ethanol/toxicity , Mandibular Diseases/chemically induced , Mandibular Diseases/diagnosis , Microscopy, Electron, Scanning , Rats , Rats, Wistar , Time Factors
15.
Article in English | WPRIM | ID: wpr-53689

ABSTRACT

Diabetes is related with a number of cystopathic complications. However, there have been no studies about the influence of alcohol consumption in the bladder of type 2 diabetes. Thus, we investigated the effect of moderate alcohol intake in the bladder of the Otsuka Long Evans Tokushima Fatty (OLETF) diabetic rat. The non-diabetic Long-Evans Tokushima Otsuka (LETO, n=14) and the OLETF control group (n=14) were fed an isocaloric diet; the LETO (n=14) and the OLETF ethanol group (n=14) were fed 36% ethanol 7 g/kg/day. After ten weeks, muscarinic receptors, RhoGEFs, myogenic change, and the level of oxidative stress were evaluated. Moderate alcohol intake significantly decreased excessive muscarinic receptor and Rho kinase expressions in the OLETF rats compared with the LETO rats. In addition, iNOS and collagen expression were not changed in the OLETF rats in spite of alcohol consumption. Superoxide dismutase levels, which is involved in antioxidant defense, in the LETO rats were significantly decreased after alcohol consumption, however those in the OLETF rats were similar. Moderate alcohol consumption reduces the oxidative stress, and may prevent molecular and pathologic changes of the bladder of rats with type 2 diabetes.


Subject(s)
Alcohol Drinking/adverse effects , Animals , Diabetes Mellitus, Type 2/complications , Ethanol/toxicity , Humans , Rats , Rats, Inbred OLETF , Reactive Oxygen Species/metabolism , Urinary Bladder/drug effects
16.
Acta toxicol. argent ; 22(3): 122-135, dic. 2014. ilus, tab
Article in Spanish | LILACS | ID: lil-750436

ABSTRACT

El etanol y el isopropanol son, de los alcoholes alifáticos de cadena corta, los más frecuentemente asociados a la actividad humana tanto a nivel industrial como en el entorno doméstico. En este trabajo se presentan los principales hallazgos reportados en la literatura para ensayos de genotoxicidad y teratogénesis en modelos experimentales de distinto nivel de complejidad, con especial énfasis en Drosophila melanogaster. El metabolismo de estos alcoholes es semejante en Drosophila y en humanos por lo cual la mosca es un buen modelo in vivo para la evaluación de sus potenciales efectos tóxicos, genotóxicos y teratogénicos.


Ethanol and isopropanol are two of the short chain aliphatic alcohols more frequently associated to the human environment, both in the industrial and domestic conditions. The aim of this work was to present the main findings reported in the literature about their genotoxicity and teratogenicity in experimental models of different level of complexity, with special emphasis in Drosophila melanogaster. Taking into account that the metabolism of both alcohols in Drosophila and humans is similar, the fly is a good model for the evaluation of their potentially toxic, genotoxic and teratogenic effects.


Subject(s)
Animals , 2-Propanol/metabolism , 2-Propanol/toxicity , Ethanol/metabolism , Ethanol/toxicity , Drosophila melanogaster/drug effects , Genotoxicity/analysis , Teratogens/analysis , Toxicogenetics/methods
17.
Indian J Biochem Biophys ; 2014 Jun; 51(3): 215-222
Article in English | IMSEAR | ID: sea-154231

ABSTRACT

Alcoholism and obesity are strongly associated with several disorders including heart and liver diseases. This study evaluated the effects of rutin treatment in serum, heart and liver tissues of rats subjected to a combination of hypercaloric diet (HD) and chronic ethanol consumption. Rats were divided into three groups: Control: rats fed a standard diet and drinking water ad libitum; G1: rats fed the HD and receiving a solution of 10% (v/v) ethanol; and G2: rats fed the HD and ethanol solution, followed by injections of 50 mg/kg-1 rutin as treatment. After 53 days of HD and ethanol exposure, the rutin was administered every three days for nine days. At the end of the experimental period (95 days), biochemical analyses were carried out on sera, cardiac and hepatic tissues. Body weight gain and food consumption were reduced in both the G1 and G2 groups compared to control animals. Rutin effectively reduced the total lipids (TL), triglycerides (TG), total cholesterol (TC), VLDL, LDL-cholesterol and glucose levels, while it increased the HDL-cholesterol in the serum of G2 rats, compared to G1. Although rutin had no effect on total protein, albumin, uric acid and cretinine levels, it was able to restore serum activities of alkaline phosphatase (ALP), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatine kinase (CK) in animals fed HD and receiving ethanol. Glycogen stores were replenished in both hepatic and cardiac tissues after rutin treatment. Moreover, rutin consistently reduced hepatic levels of TG and TC and cardiac AST, ALT and CK activities. Thus, rutin treatment was effective in reducing the risk factors for cardiac and hepatic disease caused by both HD and chronic ethanol consumption.


Subject(s)
Alanine Transaminase/metabolism , /metabolism , Animals , Aspartate Aminotransferases/metabolism , Central Nervous System Depressants/toxicity , /metabolism , Biomarkers/metabolism , /adverse effects , Ethanol/toxicity , Glycemic Index/drug effects , Heart/drug effects , Heart/physiology , L-Lactate Dehydrogenase/metabolism , Lipids/analysis , Liver/cytology , Liver/metabolism , Male , Rats , Rats, Wistar , Rutin/pharmacology
18.
Rio de Janeiro; s.n; 2014. 138 f p.
Thesis in Portuguese | LILACS | ID: lil-751072

ABSTRACT

Uma questão particularmente relevante é o fato de exposições precoces a drogas de abuso durante o desenvolvimento potencialmente aumentarem a susceptibilidade a estas drogas posteriormente durante o desenvolvimento. No presente estudo utilizando estudos comportamentais e eletrofisiológicos, investigamos efeitos tardios da exposição de camundongos à fumaça de cigarro, à nicotina e ao etanol durante o período que corresponde à gestação em humanos. Para tal, esta tese foi dividida em 2 estudos. No Estudo 1, submetemos camundongos durante o período que corresponde à gestação de humanos à fumaça de cigarro e/ou etanol visando investigar se a estas drogas de abuso, separadamente ou quando combinadas, programam maior susceptibilidade aos efeitos da nicotina durante a adolescência (PN30) ou idade adulta (PN90). Para avaliar a susceptibilidade, utilizamos 3 testes: campo aberto (CA), preferencia pela nicotina (PPN) e preferencia condicionada por lugar (CPP). No Estudo 2, os animais foram expostos a nicotina durante o período gestacional e, no período que corresponde à infância (PN9 a PN20), fatias de cérebro contendo o núcleo tegumental laterodorsal (LDT) foram expostas a etanol. Este núcleo foi escolhido uma vez que estudos recentes indicam sua participação em mecanismos de toxicodependência. Foram realizados registros eletrofisiológicos de uma única célula. No Estudo 1, identificamos maior sensibilidade para os efeitos da reexposição à nicotina na adolescência quando comparada com a idade adulta . Em animais testados no CA durante a adolescência, a nicotina foi capaz de causar aumento da atividade locomotora nos animais controle, previamente expostos à fumaça de cigarro e ao etanol. Contudo, em animais expostos à fumaça combinada com etanol, não houve aumento da locomoção. Na idade adulta, a nicotina causou um aumento da atividade locomotora no CA somente nos animais expostos à fumaça de cigarro...


Particularly relevant is the fact that early exposure to drugs of abuse during development potentially increases drug susceptibility later during development. In the present study we used mice models to investigate postnatal behavioral and electrophysiological effects of exposure to cigarette smoke, nicotine and ethanol during the period that corresponds to pregnancy in humans. To this end, this thesis was divided into two studies. In Study 1, we submitted mice to cigarette smoke and / or ethanol in order during the period that corresponds to human pregnancy to investigate whether these drugs of abuse, alone or when combined, programs increased susceptibility to the effects of nicotine during adolescence (PN30) or adulthood (PN90). To evaluate susceptibility, we use three tests: open field (OF), preference for nicotine (PFN) and conditioned place preference (CPP). In Study 2, the animals were exposed to nicotine during pregnancy and, in the period corresponding to childhood (PN9 to PN20), brain slices containing the laterodorsal tegmental nucleus (LDT) were exposed to ethanol. This nucleus was chosen based on recent studies that indicate that it participates in mechanisms of addiction. Whole cell patch clamp recordings were performed. In Study 1, a higher sensitivity to the effects of nicotine exposure was identified during adolescence when compared to adulthood. In animals tested in the OF during adolescence, nicotine was able to cause an increase in locomotor activity in controls, in mice previously exposed to cigarette smoke, and in those exposed to ethanol. However, nicotine failed to increase locomotion in mice previously exposed to smoke combined with ethanol. In adulthood, nicotine caused an increase in OF locomotor activity only in animals exposed to cigarette smoke...


Subject(s)
Animals , Male , Female , Infant , Adolescent , Mice , Motor Activity , Adolescent Behavior , Ethanol/adverse effects , Maternal Exposure/adverse effects , Nicotine/adverse effects , Alcohol-Related Disorders , Ethanol/toxicity , Nicotine/toxicity , Tobacco Use Disorder
19.
Article in English | WPRIM | ID: wpr-56423

ABSTRACT

Betulinic acid (BA), a pentacyclic lupane-type triterpene, has a wide range of bioactivities. The main objective of this work was to evaluate the hepatoprotective activity of BA and the potential mechanism underlying the ability of this compound to prevent liver damage induced by alcohol in vivo. Mice were given oral doses of BA (0.25, 0.5, and 1.0 mg/kg) daily for 14 days, and induced liver injury by feeding 50% alcohol orally at the dosage of 10 ml/kg after 1 h last administration of BA. BA pretreatment significantly reduced the serum levels of alanine transaminase, aspartate transaminase, total cholesterol, and triacylglycerides in a dose-dependent manner in the mice administered alcohol. Hepatic levels of glutathione, superoxide dismutase, glutathione peroxidase, and catalase were remarkably increased, while malondialdehyde contents and microvesicular steatosis in the liver were decreased by BA in a dose-dependent manner after alcohol-induced liver injury. These findings suggest that the mechanism underlying the hepatoprotective effects of BA might be due to increased antioxidant capacity, mainly through improvement of the tissue redox system, maintenance of the antioxidant system, and decreased lipid peroxidation in the liver.


Subject(s)
Animals , Antioxidants/pharmacology , Blood Chemical Analysis , Enzymes/blood , Ethanol/toxicity , Lipid Peroxidation/drug effects , Liver/drug effects , Male , Mice , Random Allocation , Triterpenes/pharmacology
20.
Braz. j. microbiol ; 44(4): 1067-1074, Oct.-Dec. 2013. graf, tab
Article in English | LILACS | ID: lil-705252

ABSTRACT

The aim of our study was to select the optimal operating conditions to permeabilize Kluyveromyces lactis cells using ethanol as a solvent as an alternative to cell disruption and extraction. Cell permeabilization was carried out by a non-mechanical method consisting of chemical treatment with ethanol, and the results were expressed as β-galactosidase activity. Experiments were conducted under different conditions of ethanol concentration, treatment time and temperature according to a central composite rotatable design (CCRD), and the collected results were then worked out by response surface methodology (RSM). Cell permeabilization was improved by an increase in ethanol concentration and simultaneous decreases in the incubation temperature and treatment time. Such an approach allowed us to identify an optimal range of the independent variables within which the β-galactosidase activity was optimized. A maximum permeabilization of 2,816 mmol L-1 oNP min-1 g-1 was obtained by treating cells with 75.0% v/v of ethanol at 20.0 °C for 15.0 min. The proposed methodology resulted to be effective and suited for K. lactis cells permeabilization at a lab-scale and promises to be of possible interest for future applications mainly in the food industry.


Subject(s)
Cell Membrane/drug effects , Ethanol/toxicity , Kluyveromyces/drug effects , Permeability/drug effects , Cell Membrane/physiology , Kluyveromyces/physiology , Models, Statistical , Temperature , Time Factors , beta-Galactosidase/analysis
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