scholarly journals Electrolyzed Hydrogen Water Protects against Ethanol-Induced Cytotoxicity by Regulating Aldehyde Metabolism-Associated Enzymes in the Hepatic Cell Line HepG2

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 801
Author(s):  
Satoshi Yano ◽  
Jinyun Wang ◽  
Shigeru Kabayama ◽  
Taichi Hara
Keyword(s):  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Molecular Hydrogen ◽  
Toxic Substance ◽  
Excessive Alcohol Consumption ◽  
Hydrogen Water ◽  
Hepatocellular Damage ◽  
Electrolytic Hydrogen ◽  
Excessive Alcohol ◽  
Serious Disease

Excessive alcohol consumption can cause multi-systemic diseases. Among them, alcoholic liver disease is the most frequent and serious disease. Electrolytic hydrogen water (EHW) is produced at the cathode during electrolysis of water and contains a large amount of molecular hydrogen and a low content of platinum nanoparticles with alkaline properties. In this study, we found that EHW inhibits ethanol-induced cytotoxicity by decreasing the intracellular acetaldehyde, a toxic substance produced by ethanol degradation, in hepatocyte cell lines HepG2. Analysis of the mechanism of action revealed that EHW inhibits the metabolism of ethanol to acetaldehyde by suppressing alcohol dehydrogenase. EHW also promotes the metabolism of acetaldehyde to acetic acid by activating aldehyde dehydrogenase, which plays to reduce aldehyde toxicity and intracellular reactive oxygen species in HepG2 cells. These functions were correlated with the concentration of molecular hydrogen in EHW, and were abolished by degassing treatment, suggesting that molecular hydrogen may contribute as a functional factor in the suppression of ethanol-induced hepatocellular damage. Furthermore, hydrogen water with high dissolved hydrogen molecule showed the same hepatocellular protective effect against ethanol as the EHW. These results suggest that EHW may be useful in the prevention of alcoholic liver disease.

scholarly journals Crosstalk between Oxidative Stress and Inflammatory Liver Injury in the Pathogenesis of Alcoholic Liver Disease

2022 ◽  
Vol 23 (2) ◽  
pp. 774
Author(s):  
Yoon Mee Yang ◽  
Ye Eun Cho ◽  
Seonghwan Hwang
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
Pathological Features ◽  
Excessive Alcohol Consumption ◽  
Excessive Alcohol ◽  
The Relationship

Alcoholic liver disease (ALD) is characterized by the injury, inflammation, and scarring in the liver owing to excessive alcohol consumption. Currently, ALD is a leading cause for liver transplantation. Therefore, extensive studies (in vitro, in experimental ALD models and in humans) are needed to elucidate pathological features and pathogenic mechanisms underlying ALD. Notably, oxidative changes in the liver have been recognized as a signature trait of ALD. Progression of ALD is linked to the generation of highly reactive free radicals by reactions involving ethanol and its metabolites. Furthermore, hepatic oxidative stress promotes tissue injury and, in turn, stimulates inflammatory responses in the liver, forming a pathological loop that promotes the progression of ALD. Accordingly, accumulating further knowledge on the relationship between oxidative stress and inflammation may help establish a viable therapeutic approach for treating ALD.

scholarly journals A study of alanine aminotransferase - aspartate aminotransferase as a marker of advanced alcoholic liver disease

2020 ◽  
Vol 7 (4) ◽  
pp. 551
Author(s):  
Aravind G. N. ◽  
Abhilash K. ◽  
Syed Umar Farooq
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Chronic Liver Disease ◽  
Alcoholic Liver Disease ◽  
Alcohol Withdrawal ◽  
Chronic Liver ◽  
Outpatient Basis ◽  
Excessive Alcohol Consumption ◽  
Excessive Alcohol ◽  
The Mean

Background: Alcohol is one of the most common etiology for chronic liver disease. There are several enzymes which remain elevated in both excessive Alcohol consumption and Alcohol induced liver cirrhosis1.  But none is sensitive or specific.  The ratio of Aspartate transaminase (AST) with Alanine transaminase (ALT) is one of the best marker for alcohol liver disease. Current study mainly compares the ratio of AST/ALT with both Alcoholic liver disease and excessive Alcohol consumption patients.Methods: Observational, cross sectional study conducted on 50 patients diagnosed with alcoholic liver disease and 50 patients of alcohol withdrawal syndrome.  Either admitted or seen on outpatient basis at Bangalore medical college and research institute and data was compared among the groups and appropriate statistical methods are applied.Results: The mean ratio of AST/ALT ratio in 50 patients of alcoholic liver disease group was 3.45, whereas the mean ratio in 50 patient of alcohol withdrawal was about 99. When compared statistically this ratio was significant in chronic liver disease group.Conclusions: Most of the patients with heavy alcohol drinking had high AST and alt levels. But ratio of AST/ALT levels was significant high and suggest chronic liver disease secondary to alcohol.

scholarly journals Genetic and Epigenetic Modifiers of Alcoholic Liver Disease

2018 ◽  
Vol 19 (12) ◽  
pp. 3857 ◽  
Author(s):  
Marica Meroni ◽  
Miriam Longo ◽  
Raffaela Rametta ◽  
Paola Dongiovanni
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Alcoholic Liver Disease ◽  
Complex Disease ◽  
Wide Spectrum ◽  
Association Studies ◽  
Phenotypic Variability ◽  
Genome Wide Association Studies ◽  
Epigenetic Factors ◽  
Excessive Alcohol Consumption

Alcoholic liver disease (ALD), a disorder caused by excessive alcohol consumption is a global health issue. More than two billion people consume alcohol in the world and about 75 million are classified as having alcohol disorders. ALD embraces a wide spectrum of hepatic lesions including steatosis, alcoholic steatohepatitis (ASH), fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). ALD is a complex disease where environmental, genetic, and epigenetic factors contribute to its pathogenesis and progression. The severity of alcohol-induced liver disease depends on the amount, method of usage and duration of alcohol consumption as well as on age, gender, presence of obesity, and genetic susceptibility. Genome-wide association studies and candidate gene studies have identified genetic modifiers of ALD that can be exploited as non-invasive biomarkers, but which do not completely explain the phenotypic variability. Indeed, ALD development and progression is also modulated by epigenetic factors. The premise of this review is to discuss the role of genetic variants and epigenetic modifications, with particular attention being paid to microRNAs, as pathogenic markers, risk predictors, and therapeutic targets in ALD.

scholarly journals Emerging role of circadian clock disruption in alcohol-induced liver disease

2018 ◽  
Vol 315 (3) ◽  
pp. G364-G373 ◽  
Author(s):  
Shannon M. Bailey
Keyword(s):  
Liver Disease ◽  
Circadian Clock ◽  
Therapeutic Approaches ◽  
Excessive Alcohol Consumption ◽  
Peripheral Tissues ◽  
New Therapeutic Approaches ◽  
Timing System ◽  
Excessive Alcohol ◽  
The Impact

The detrimental health effects of excessive alcohol consumption are well documented. Alcohol-induced liver disease (ALD) is the leading cause of death from chronic alcohol use. As with many diseases, the etiology of ALD is influenced by how the liver responds to other secondary insults. The molecular circadian clock is an intrinsic cellular timing system that helps organisms adapt and synchronize metabolism to changes in their environment. The clock also influences how tissues respond to toxic, environmental, and metabolic stressors, like alcohol. Consistent with the essential role for clocks in maintaining health, genetic and environmental disruption of the circadian clock contributes to disease. While a large amount of rich literature is available showing that alcohol disrupts circadian-driven behaviors and that circadian clock disruption increases alcohol drinking and preference, very little is known about the role circadian clocks play in alcohol-induced tissue injuries. In this review, recent studies examining the effect alcohol has on the circadian clock in peripheral tissues (liver and intestine) and the impact circadian clock disruption has on development of ALD are presented. This review also highlights some of the rhythmic metabolic processes in the liver that are disrupted by alcohol and potential mechanisms through which alcohol disrupts the liver clock. Improved understanding of the mechanistic links between the circadian clock and alcohol will hopefully lead to the development of new therapeutic approaches for treating ALD and other alcohol-related organ pathologies.

Plasma Protein C as a Marker of Hepatocellular Damage in Alcoholic Liver Disease

1992 ◽  
Vol 22 (6) ◽  
pp. 340-344 ◽  
Author(s):  
J. Kłoczko ◽  
M. Mian ◽  
M.Z. Wojtukiewicz ◽  
L. Babiuch ◽  
M. Bielawiec ◽  
...  
Keyword(s):  
Liver Disease ◽  
Plasma Protein ◽  
Alcoholic Liver Disease ◽  
Protein C ◽  
Hepatocellular Damage

scholarly journals Animals Models of Gastrointestinal and Liver Diseases. Animal models of alcohol-induced liver disease: pathophysiology, translational relevance, and challenges

2014 ◽  
Vol 306 (10) ◽  
pp. G819-G823 ◽  
Author(s):  
Stephanie Mathews ◽  
Mingjiang Xu ◽  
Hua Wang ◽  
Adeline Bertola ◽  
Bin Gao
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Neutrophil Infiltration ◽  
Alcoholic Liver Injury ◽  
Drinking Patterns ◽  
Excessive Alcohol Consumption ◽  
Ethanol Feeding ◽  
History Of ◽  
Excessive Alcohol ◽  
Binge Ethanol

Over the last four decades, chronic ethanol feeding studies in rodents using either ad libitum feeding or intragastric infusion models have significantly enhanced our understanding of the pathogenesis of alcoholic liver disease (ALD). Recently, we developed a chronic plus binge alcohol feeding model in mice that is similar to the drinking patterns of many alcoholic hepatitis patients: a history of chronic drinking and recent excessive alcohol consumption. Chronic+binge ethanol feeding synergistically induced steatosis, liver injury, and neutrophil infiltration in mice, which may be useful for the study of early alcoholic liver injury and inflammation. Using this chronic+binge model, researchers have begun to identify novel mechanisms that participate in the pathogenesis of alcoholic liver injury, thereby revealing novel therapeutic targets. In this review article, we briefly discuss several mouse models of ALD with a focus on the chronic+binge ethanol feeding model.

scholarly journals The effect of moderate alcohol drinking in nonalcoholic fatty liver disease

2020 ◽  
Vol 26 (4) ◽  
pp. 662-669
Author(s):  
Jong Hwa Choi ◽  
Won Sohn ◽  
Yong Kyun Cho
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Alcohol Consumption ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Moderate Alcohol Consumption ◽  
Excessive Alcohol Consumption ◽  
Nonalcoholic Fatty Liver ◽  
Safe Limits ◽  
Excessive Alcohol

Nonalcoholic fatty liver disease (NAFLD) is defined by fat accumulation in liver that is not caused by excessive alcohol consumption. Safe limits of alcohol consumption in NAFLD are usually defined as alcohol consumption of less than 210 g per week for men and 140 g per week for women (30 g/day in men, 20 g/day in women) and alcohol consumption below safe limits is generally regarded as moderate alcohol consumption. Many studies have investigated the effects of moderate alcohol consumption on NAFLD patients. Some studies showed that moderate alcohol consumption prevented the progression of fibrosis in the liver, whereas other reports showed worsening of fibrosis in the liver based on serologic, radiologic and liver biopsy findings compared with effects on total abstainers. NAFLD is also thought to be a hepatic manifestation of metabolic syndrome, and when combined with excessive alcohol consumption results in the development of components of metabolic syndrome and systemic harmful effects. The effects of moderate alcohol consumption on NAFLD have yet to be established.

scholarly journals Hepatocellular damage and inflammation in various forms of alcoholic liver disease

2021 ◽  
Vol 93 (1) ◽  
pp. 15-19
Author(s):  
Alisa S. Rodina ◽  
Marina E. Shubina ◽  
Irina V. Kurbatova ◽  
Ludmila V. Topchieva ◽  
Olga P. Dudanova
Keyword(s):  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Clinical Laboratory ◽  
Cell Damage ◽  
Liver Steatosis ◽  
Hepatic Cell ◽  
Control Group ◽  
Healthy Individuals ◽  
Hepatocellular Damage ◽  
Immune Inflammation

Aim. The aim of the study was to evaluate hepatocellular damage and immune inflammation in various forms of alcoholic liver disease (ALD). Materials and methods. 104 patients with ALD were examined: 15 (14.4%) with liver steatosis (LS), 19 (18.3%) with steatohepatitis and 70 (67.3%) with liver cirrhosis (LC); men 50 (48.1%), women 54 (51.9%); age 45.78.4 years. Traditional clinical, laboratory, instrumental studies were performed, the levels of fragments of cytokeratin-18 (FCK-18), cytokines IL-1, TNF-, IL-4, IL-6, IL-8 were determined by ELISA. The control group consisted of 39 healthy individuals: men 20 (51.2%), women 19 (48.7%), age 48.58.3 years. Results. In LS, an increase in the level of FCK-18 was noted with normal aminotransferase activity, the content of TNF-, IL-6, IL-1, IL-8 increased and the level of IL-4 decreased compared to those in healthy individuals. In steatohepatitis, a triple increase in aminotransferases and FCK-18 was observed compared with LS, as well as an increase in the level of inflammatory mediators, to a greater extent IL-6, to a lesser extent IL-8, TNF-, a decrease in IL-4, IL-1 remained at the same level. In LC, there was a further increase in FCK-18, significantly more pronounced than an increase in AST, and the increase in cytokines continued to the same extent, the levels of IL-6 and IL-8, to a lesser extent IL-1 and TNF-, and the level of IL-4. Conclusion. With the progression of ALD from LS to steatohepatitis, hepatic cell damage was carried out by equally pronounced processes of hepatocyte necrosis and apoptosis, with the development of cirrhosis of the liver, parenchyma damage occurred mainly due to hepatocyte apoptosis. The immuno-inflammatory process progressively increased from the stage of LS to LC with IL-6 and IL-8 undergoing the greatest dynamics. FCK-18 can serve as a non-invasive marker of hepatic cell damage, and IL-6 and IL-8 markers of immune inflammation in ALD.

scholarly journals Spectrum of Alcoholic Liver Disease in Tribal Alcoholics of Chittagong Hill Tracts of Bangladesh

1970 ◽  
Vol 12 (1) ◽  
pp. 7-11 ◽  
Author(s):  
Sarmistha Biswas ◽  
Sujat Paul ◽  
Abu Syeed ◽  
Md Shahriar Mahbub ◽  
Mohammad Ashik Imran Khan ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Liver Disease ◽  
Fatty Liver ◽  
Alcoholic Liver Disease ◽  
Small Scale ◽  
Alcoholic Liver Cirrhosis ◽  
Alcoholic Fatty Liver ◽  
Usual Practice ◽  
Hepatocellular Damage ◽  
The Common

Background: Alcohol is one of the most important causes of liver disease. In Bangladesh, alcoholism is not a usual practice among the general population as there are social and religious barriers against it. But in the Hill tracts, there is no social stigma in taking alcohol. Relatively little is known about this aspect in Bangladesh. This small-scale study was done to identify the spectrum of liver disease among tribal people. Material and Methods: A descriptive, observational clinical study was conducted for a period of six months (1st July, 2007 to 31st December, 2007) on a series of 50 tribal alcoholic people, collected from General Hospital and the tribal community of Rangamati Hill District. Subjects were included from both the urban and rural area of different socioeconomic classes. History, meticulous clinical examination and investigations were done to detect the pattern of alcohol induced liver injury. Results: Among the 50 cases, 47 patients were male and 3 were female cases. Both regular and irregular drinkers were included. The common symptoms of liver disease among tribal alcoholics were yellow coloration of sclera (24%), nausea & vomiting (20%) and weight loss (14%). The common findings were jaundice (24%), anemia (20%), ascites (10%), edema (10%) and hepatosplenomegaly (20%). Liver function tests revealed only 17 patients had mild to severe form of hepatocellular damage. Hyperbilirubinemia was found in 34% participants. AST/ALT ratio more than 2 was found in 32% subjects. Ultrasonography was done in 46 out of 50 subjects: 29 cases reported as normal (63.04%), fatty liver in 5 (10.87%), acute hepatitis in 5 (10.87%) and chronic liver disease in 7 (15.22%) cases. Liver biopsy was possible in 4 suspected cases (clinically and biochemically) of alcoholic liver cirrhosis and histology supported the clinical diagnosis in these cases. So, alcohol induced liver damage was noticed only in 17 cases. Nearly two-thirds of the participants were free from any form of liver disease. Conclusion: Despite the presence of risk factors for developing alcoholic liver disease, the prevalence was found to be low among the tribal alcoholic participants in this study. Keyword: Alcoholic liver disease; alcoholic fatty liver; alcoholic hepatitis; alcoholic liver cirrhosis; tribal population; Bangladesh DOI: 10.3329/jom.v12i1.6925J Medicine 2011; 12 : 7-11

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