ABSTRACT
AIMS: Antioxidant system abnormalities have been associated with ethanol consumption. This study examines the effects of chronic ethanol consumption on oxidative balance, including selenium (Se) levels in alcoholic patients with or without liver disease, and if these measurements could be indicative of liver disease. MAIN METHODS: Serum Se levels, antioxidant enzymes' activities, malondialdehyde (MDA) and protein carbonyl (PC) were determined in three groups of patients: alcoholics without liver disease, alcoholics with liver disease, and non-alcoholics with liver disease; and in healthy volunteers. KEY FINDINGS: Serum Se levels were lower in alcoholic patients and in patients affected by liver disease and especially lower in the alcoholic liver disease group. These values were correlated with the activity of glutathione peroxidase (GPx), the antioxidant selenoprotein. The antioxidant activities of the glutathione reductase (GR) and superoxide dismutase (SOD) were also lower in the three non-healthy groups. However, GR activity decreased and SOD activity increased in the non-alcoholic liver disease group versus alcoholic groups. Higher concentrations of PC in serum were found in non-healthy groups and were higher in alcoholic patients who also showed higher MDA levels. The highest MDA and PC levels were found in the alcoholic liver disease group. SIGNIFICANCE: We conclude that serum Se levels are drastically decreased in alcoholic liver disease patients, showing that this element has a direct correlation with GPx activity, and lipid oxidation, suggesting that the serum Se/MDA ratio could be an indicator of hepatic damage caused by alcohol consumption, and pointing to Se as a possible antioxidant therapy.
Subject(s)
Liver Diseases, Alcoholic/blood , Oxidative Stress/drug effects , Selenium/blood , Adult , Aged , Alcoholism/blood , Alcoholism/metabolism , Biomarkers/blood , Case-Control Studies , Glutathione Peroxidase/blood , Glutathione Reductase/blood , Humans , Liver Diseases/blood , Liver Diseases/metabolism , Liver Diseases, Alcoholic/metabolism , Male , Middle Aged , Oxidation-Reduction/drug effects , Selenium/deficiency , Superoxide Dismutase/bloodABSTRACT
Las causas más comunes de esteatohepatitis son el consumo de alcohol y los trastornos metabólicos. Existen diversos métodos basados en determinaciones bioquímicas (transferrina deficiente en hidratos de carbono) y en la realización de cuestionarios (AUDIT, CAGE, MALT) útiles para la detección del consumo subrepticio de alcohol. A pesar de que se están desarrollando nuevos métodos no invasivos tanto basados en lipidómica (Owl-Liver(R)) como en determinaciones bioquímicas y parámetros antropométricos (NAFLD Fibrosis score) o en métodos de imagen (DeMILI NASH-MRi(R)), ninguno se ha postulado como definitivo, y la biopsia hepática constituye el método de referencia. La patogenia de la esteatohepatitis alcohólica y no alcohólica presenta elementos comunes como la resistencia a la insulina, el estrés oxidativo mediado por el citocromo CYP2E1, la adiponutrina y su gen PNPLA3 y la microbiota. Los cambios en el estilo de vida, incluido el abandono del consumo de alcohol, la dieta y el ejercicio constituyen la primera línea de tratamiento
The most common causes of steatohepatitis are alcohol intake and metabolic disorders. Several methods based on biochemical determinations (carbohydrate deficient transferrin) and questionnaires (AUDIT, CAGE, MALE) are useful for detecting surreptitious alcohol intake. Although new non-invasive methods are under development, based both on lipidomics (Owl-Liver(R)) and on biochemical determinations and anthropometric parameters (NAFLD Fibrosis score) or imaging methods (DeMILI NASH-MRi(R)), none has been proposed as definitive and the gold standard continues to be liver biopsy. The pathogenesis of alcoholic and non-alcoholic steatohepatitis shares some elements such as insulin resistance, cytochrome CYP2E1-mediated oxidative stress, adiponutrin and its PNPLA3 gene, and the microbiota. The first-line treatment consists of lifestyle changes, including giving up alcohol, diet and exercise
Subject(s)
Humans , Fatty Liver/physiopathology , Fatty Liver, Alcoholic/physiopathology , Alcohol Drinking/adverse effects , Metabolic Diseases/complications , Biopsy , Life Style , Risk FactorsABSTRACT
The most common causes of steatohepatitis are alcohol intake and metabolic disorders. Several methods based on biochemical determinations (carbohydrate deficient transferrin) and questionnaires (AUDIT, CAGE, MALE) are useful for detecting surreptitious alcohol intake. Although new non-invasive methods are under development, based both on lipidomics (Owl-Liver(®)) and on biochemical determinations and anthropometric parameters (NAFLD Fibrosis score) or imaging methods (DeMILI NASH-MRi(®)), none has been proposed as definitive and the gold standard continues to be liver biopsy. The pathogenesis of alcoholic and non-alcoholic steatohepatitis shares some elements such as insulin resistance, cytochrome CYP2E1-mediated oxidative stress, adiponutrin and its PNPLA3 gene, and the microbiota. The first-line treatment consists of lifestyle changes, including giving up alcohol, diet and exercise.
