Acetaldehyde Adducts in Alcoholic Liver Disease

Setshedi, Mashiko; Wands, Jack R.; Monte, Suzanne M. de la

doi:10.4161/oxim.3.3.12288

Cited by 289 publications

(235 citation statements)

References 113 publications

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“…The metabolism of ethanol is mainly performed in liver by hepatic alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) [18]. The accumulation of ethanol metabolites, especially acetaldehyde, in liver severely injured hepatic tissues, leading to alcoholic liver disease (ALD) which is one of the leading causes of death wordwide [19]. Therefore, accelerating the clearance of blood alcohol, thereby reducing the accumulation of its metabolites, helps to alleviate the toxic effect of alcohol in humans, especially on the liver.…”

Section: Discussionmentioning

confidence: 99%

Effect of <i>Elaeagnus Conferta</i> Roxb (Elaeagnaceae) Dry Fruit on the Activities of Hepatic Alcohol Dehydrogenase and Aldehyde Dehydrogenase in Mice

Wu¹,

Dai²,

Bai³

et al. 2011

Trop. J. Pharm Res

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Purposes: To determine the effect of Elaeagnus conferta Roxb dry fruit powder (ECR) on blood alcohol clearance and on the activities of hepatic alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). Methods:In a randomized controlled study, acute alcohol intoxication was induced in mice with Hongxing liquor containing 65 % v/v ethanol orally. The effect of ECR on blood alcohol clearance and on the activities of hepatic alcohol dehydrogenase and aldehyde dehydrogenase in the mice was then investigated. Results: A 30-min pretreatment with ECR at 400 and 800 mg/kg led to a faster clearance of blood alcohol after the alcohol ingestion. The concentration of blood alcohol at 4 h after alcohol ingestion decreased by 21.2 % in mice pretreated with 800 mg/kg ECR. The activities of hepatic alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) were enhanced by ECR. Conclusion: These results suggest that pretreatment with ECR might stimulate the clearance of blood alcohol by increasing the activities of hepatic alcohol dehydrogenase and aldehyde dehydrogenase.

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Section: Discussionmentioning

confidence: 99%

Effect of <i>Elaeagnus Conferta</i> Roxb (Elaeagnaceae) Dry Fruit on the Activities of Hepatic Alcohol Dehydrogenase and Aldehyde Dehydrogenase in Mice

Wu¹,

Dai²,

Bai³

et al. 2011

Trop. J. Pharm Res

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“…The resulting acetate formed in step (b) being unstable gets readily converted to water and carbon dioxide. Acetaldehyde accumulated in excess turns toxic and forms adducts with DNA, lipids and proteins [26][27][28][29]. This could result in the formation of acetaldehyde derived-AGEs termed as AA-AGEs via Maillard reaction [30].…”

Section: Plausible Link Between Alcohol and Agesmentioning

confidence: 99%

Association of Advanced Glycation End Products (AGEs) with Diabetic Nephropathy and Alcohol Consumption

Parwani¹,

Mandal²

2017

J Alcohol Drug Depend

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The occurrence of diabetes is accelerating worldwide, with consequent increase in the secondary complication like diabetic nephropathy (DN). Diabetic nephropathy refers to a set of structural and functional abnormalities of kidney in patients with diabetes. Detrimental changes like glomerular hypertrophy, glomerulosclerosis, hyperfiltration, proteinuria, etc. occur in DN. One of the major pathways suggested for the pathogenesis is formation of Advanced Glycation End Products (AGEs) via non enzymatic glycation (NEG). NEG is the process in which reducing sugars irreversibly modify free amino groups of proteins, by various events leading to the formation of a Schiff base resulting in Amadori products, culminating into AGEs. AGEs activate several cascades of intracellular signaling via interaction with Receptor for AGEs (RAGE) that results in responses like release of pro-inflammatory cytokines resulting in inflammation, autophagy and programmed cell death. AGEs can also come into circulation from baked food and processed food items. AGEs can also be formed through various oxidative reactions, including the chronic use of alcohol. Alcohol in excess could result in accumulation of acetaldehyde that would lead to insulin resistance. Many risk factors like race, genetic susceptibility, hypertension, hyperglycemia, hyper filtration, smoking, advanced age, male sex, and high-protein diet account for development of DN. Therapeutic interventions include glycemic control, control of blood pressure. This review focuses on the formation of AGEs via non enzymatic glycation, its implications in pathogenesis of DN and therapies designed to break AGEs so as to prevent the development of DN.

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“…It forms adducts with proteins and DNA and therefore impairs microtubules, decreases protein secretion and causes protein retention and ballooning of the hepatocyte. Acetaldehyde exerts toxicity also with regard to other key cellular functions, particularly in the mitochondria, and it may promote the peroxidation of the cellular membranes (55)(56)(57).…”

Section: Alcohol Metabolites and Ros-associated Alcoholinduced Hepatimentioning

confidence: 99%

Alcohol and hepatocyte-Kupffer cell interaction (Review)

Ajakaiye

Jacob

et al. 2011

Mol Med Rep

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Abstract. Alcoholic liver disease accounts for 12,000 deaths per year in the United States and is the second leading indication for liver transplantation. It covers a spectrum of disease conditions ranging from steatosis and cirrhosis to hepatic malignancies. Epidemiological data clearly show a strong correlation between alcohol consumption and liver diseases. A large body of evidence has accumulated over the years in determining the molecular mediators of alcohol-induced liver injury. In this review, we provide an overview of such mediators, which include alcohol metabolites and reactive oxygen/ nitrogen species, endotoxin via bacterial translocation from the gut and TNF-α, and highlight the role of the sympathetic nervous stimuli, norepinephrine and the α 2A -adrenergic receptors in contributing to the deleterious effect observed in alcohol-induced hepatic dysfunction.

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Acetaldehyde Adducts in Alcoholic Liver Disease

Cited by 289 publications

References 113 publications

Effect of <i>Elaeagnus Conferta</i> Roxb (Elaeagnaceae) Dry Fruit on the Activities of Hepatic Alcohol Dehydrogenase and Aldehyde Dehydrogenase in Mice

Effect of <i>Elaeagnus Conferta</i> Roxb (Elaeagnaceae) Dry Fruit on the Activities of Hepatic Alcohol Dehydrogenase and Aldehyde Dehydrogenase in Mice

Association of Advanced Glycation End Products (AGEs) with Diabetic Nephropathy and Alcohol Consumption

Alcohol and hepatocyte-Kupffer cell interaction (Review)

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