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Título del libro: Alcohol And The Liver: Role Of Mitochondria

Autores UNAM:
HECTOR RIVEROS ROSAS;

Autores externos:

Idioma:
Inglés

Año de publicación:
2016

Resumen:

Alcohol consumption, abuse, and dependence are social problems that emerged as a consequence of industrialization. Ethanol itself is a toxic metabolite that produces deleterious effects like fatty liver despite adequate diets. It is evident that the net effect of alcohol consumption on health is detrimental and is a causal factor in 60 types of diseases and injuries, and a component that causes in 200 others. The liver is the main site of ethanol oxidation, and is extremely vulnerable to alcoholic damage. The most prevalent types of alcoholic liver diseases are fatty liver, alcoholic hepatitis, and cirrhosis. Heavy drinkers and alcoholics may progress from fatty liver to alcoholic hepatitis to cirrhosis, and it is estimated that 10 percent to 15 percent of alcoholics will develop cirrhosis. A number of mechanisms have been postulated for the pathogenesis of alcoholic injuries and diseases, including toxicity of ethanol and its metabolite acetaldehyde, the primary metabolic product of ethanol. In addition, oxidative stress, and accumulation of fatty acid ethyl esters also contribute to alcohol-associated complications. Interestingly, in all these mechanisms of toxicity, mitochondria play a central role. Oxidative pathways are by far the main pathways responsible of ethanol clearance. Currently, in animals there are three non homologous NAD(P)+-dependent alcohol dehydrogenases (ADH) protein families that possess different structures and mechanisms of reaction. The Microsomal Ethanol Oxidizing System (MEOS) system catalyzes the oxidation from ethanol to acetaldehyde, coupling this reaction to the oxidation of an NADPH molecule, and the reduction of an oxygen molecule to form hydrogen peroxide. Mitochondria participate with the conversion of acetaldehyde into acetate and the generation of increased amounts of NADH. Mitochondria play an important role in the alcohol metabolism via the enzyme ALDH; this enzyme catalyzes the oxidation of acetaldehyde into acetate. The acetaldehyde is capable of escape into the blood stream and leads to damage to biomolecules such as lipids, proteins and nucleic acids, which results in the toxic side effects that are associated with alcohol consumption. Mitochondrial dysfunction results in decreased ATP synthesis and increased reactive oxygen species (ROS) production, which can compromise the survival, function and regeneration capacity of hepatocytes, especially in pathological conditions such as cirrhosis, in which chronic damage in liver causes changes in mitochondria. In cells, the mitochondrial electron transport chain (ETC) is one of the most important sources of ROS. Ethanol metabolism executes conditions that promote ROS formation by mitochondria, effects that may be enhanced by a decrease in the mitochondrial antioxidant systems. Either acute or chronic ethanol consumption produces excessive ROS, mitochondrial dysfunction and endoplasmic reticulum stress in liver. It is clear that antioxidants may play a role in the treatment of alcoholic liver disease. Plants and plant derived compounds have been shown to to improve symptoms. However clinical benefit is still far from proven. © 2016 by Nova Science Publishers, Inc.

Entidades citadas de la UNAM:

Fuente:

ISBN:
9781634844154
Editorial:
Nova Science Publishers, Inc. Nombre de la publicación:
Alcohol and the liver: Role of mitochondria
Página inicial:
119
Página final:
158