Abstract

The liver can be affected by a wide range of therapeutic and environmental chemicals and here we want to provide a summary of the complex effects of alcohol, cannabinoids and nicotine on liver function. Alcohol is the most important agent that produces liver injury, manifesting as alcoholic fatty liver disease. In addition, it is one of the main etiologic agents for hepatocellular carcinoma development. Studies reviewed in this article regarding cannabinoids, show that Delta9-THC does not produce any harmful effects on the liver, while cannabidiol has hepatoprotective effects inischemia/reperfusion and alcohol-induced liver injuries. The liver is negatively affected by nicotine exposure, but surprisingly nicotine was shown to have a positive effect on the liver in the diet-induced obese animal model, which should be confirmed by future research.
Lingua originaleEnglish
pagine (da-a)132-136
Numero di pagine5
RivistaDefault journal
Stato di pubblicazionePublished - 2017

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Cannabinoids
Nicotine
Alcohols
Liver
Alcoholic Fatty Liver
Cannabidiol
Alcoholic Liver Diseases
Dronabinol
Wounds and Injuries
Reperfusion
Hepatocellular Carcinoma
Animal Models
Diet

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abstract = "The liver can be affected by a wide range of therapeutic and environmental chemicals and here we want to provide a summary of the complex effects of alcohol, cannabinoids and nicotine on liver function. Alcohol is the most important agent that produces liver injury, manifesting as alcoholic fatty liver disease. In addition, it is one of the main etiologic agents for hepatocellular carcinoma development. Studies reviewed in this article regarding cannabinoids, show that Delta9-THC does not produce any harmful effects on the liver, while cannabidiol has hepatoprotective effects inischemia/reperfusion and alcohol-induced liver injuries. The liver is negatively affected by nicotine exposure, but surprisingly nicotine was shown to have a positive effect on the liver in the diet-induced obese animal model, which should be confirmed by future research.",
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T1 - Alcohol, Cannabinoids and Nicotine in Liver Pathophysiology

AU - Cappello, Francesco

AU - Barone, Rosario

AU - Crescimanno, Giuseppe

AU - Radic, Manuela

AU - Casarrubea, Maurizio

AU - Marino Gammazza, Antonella

AU - Rappa, Francesca

PY - 2017

Y1 - 2017

N2 - The liver can be affected by a wide range of therapeutic and environmental chemicals and here we want to provide a summary of the complex effects of alcohol, cannabinoids and nicotine on liver function. Alcohol is the most important agent that produces liver injury, manifesting as alcoholic fatty liver disease. In addition, it is one of the main etiologic agents for hepatocellular carcinoma development. Studies reviewed in this article regarding cannabinoids, show that Delta9-THC does not produce any harmful effects on the liver, while cannabidiol has hepatoprotective effects inischemia/reperfusion and alcohol-induced liver injuries. The liver is negatively affected by nicotine exposure, but surprisingly nicotine was shown to have a positive effect on the liver in the diet-induced obese animal model, which should be confirmed by future research.

AB - The liver can be affected by a wide range of therapeutic and environmental chemicals and here we want to provide a summary of the complex effects of alcohol, cannabinoids and nicotine on liver function. Alcohol is the most important agent that produces liver injury, manifesting as alcoholic fatty liver disease. In addition, it is one of the main etiologic agents for hepatocellular carcinoma development. Studies reviewed in this article regarding cannabinoids, show that Delta9-THC does not produce any harmful effects on the liver, while cannabidiol has hepatoprotective effects inischemia/reperfusion and alcohol-induced liver injuries. The liver is negatively affected by nicotine exposure, but surprisingly nicotine was shown to have a positive effect on the liver in the diet-induced obese animal model, which should be confirmed by future research.

KW - alcohol

KW - cannabinoids

KW - liver

KW - nicotine

UR - http://hdl.handle.net/10447/254000

M3 - Article

SP - 132

EP - 136

JO - Default journal

JF - Default journal

ER -