Acetyl-L-carnitine attenuates chronic ethanol-induced oxidative stress, ER stress and apoptosis in rat gastric tissue

Consuming alcohol affects almost all organs. Acetaldehyde, formed as the main product as a result of alcohol metabolism, causes the production of free superoxide radicals when oxidized, and accordingly oxidative and apoptotic processes are triggered. There are studies showing that carnitine has effe...

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Published in:Alcohol (Fayetteville, N.Y.) N.Y.), 2023-11, Vol.112, p.51-59
Main Authors: Er, Hakan, Gemici, Ayşegül, Tas, Gizem Gamze, Sati, Leyla, Zengin, Gamze, Bilmen, Süreyya, Derin, Narin, Kelek, Sevim Ercan
Format: Article
Language:English
Subjects:
Abdomen
Acetaldehyde
Acetyl-L-carnitine
Alcohol
Antigens
Antioxidants
Apoptosis
Carnitine
Chronic ethanol
DNA nucleotidylexotransferase
Drinking water
Endoplasmic reticulum
Enzyme-linked immunosorbent assay
ER stress
Ethanol
Free radicals
Homeostasis
Molecular modelling
Oxidants
Oxidation
Oxidative stress
Proteins
Rodents
Western blotting
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cited_by cdi_FETCH-LOGICAL-c393t-bf0dd764d959fcbb0b61bca7135951c8112dc0b4c0f841f069da55cb34ccc0983
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container_title Alcohol (Fayetteville, N.Y.)
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creator Er, Hakan
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Kelek, Sevim Ercan
description Consuming alcohol affects almost all organs. Acetaldehyde, formed as the main product as a result of alcohol metabolism, causes the production of free superoxide radicals when oxidized, and accordingly oxidative and apoptotic processes are triggered. There are studies showing that carnitine has effects on oxidative and apoptotic processes that occur in various conditions. However, the mechanisms showing the effects of L-carnitine on these effects of alcohol have not been fully elucidated. In our study, the effects of acetyl-L-carnitine administration on the molecular mechanisms of oxidative stress, endoplasmic reticulum stress, and apoptotic parameters in gastric tissue of rats chronically exposed to alcohol were investigated. Hematoxylin-eosin staining was used for histopathological studies. Endoplasmic reticulum stress markers were detected with immunohistochemical staining and western blotting. Apoptotic index was evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. Total oxidant and antioxidant status were examined by ELISA. Our results showed that chronic alcohol administration caused a significant increase in TOS levels, an indicator of oxidative stress, the levels of ER-stress-associated proteins XBP1, GRP78, and CHOP, and % apoptotic index values in rat gastric tissues. Additionally, it was determined that acetyl-L-carnitine administration caused an improvement in those values. Based on our data, we can conclude that acetyl-L-carnitine has a tissue protective effect by scavenging free oxygen radicals and reducing ER stress-related proteins XBP1, GRP78, and CHOP and apoptosis in chronic ethanol-administered rats, and that this natural antioxidant may be beneficial in the treatment of oxidative stress-induced diseases. •Consuming alcohol affects almost all organs.•Alcohol causes apoptosis, as well as oxidative and endoplasmic reticulum stress.•L-carnitine has important intracellular functions and pharmacological effects.•Acetyl-L-carnitine administration may attenuate alcohol-induced gastric damage.
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Acetaldehyde, formed as the main product as a result of alcohol metabolism, causes the production of free superoxide radicals when oxidized, and accordingly oxidative and apoptotic processes are triggered. There are studies showing that carnitine has effects on oxidative and apoptotic processes that occur in various conditions. However, the mechanisms showing the effects of L-carnitine on these effects of alcohol have not been fully elucidated. In our study, the effects of acetyl-L-carnitine administration on the molecular mechanisms of oxidative stress, endoplasmic reticulum stress, and apoptotic parameters in gastric tissue of rats chronically exposed to alcohol were investigated. Hematoxylin-eosin staining was used for histopathological studies. Endoplasmic reticulum stress markers were detected with immunohistochemical staining and western blotting. Apoptotic index was evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. Total oxidant and antioxidant status were examined by ELISA. Our results showed that chronic alcohol administration caused a significant increase in TOS levels, an indicator of oxidative stress, the levels of ER-stress-associated proteins XBP1, GRP78, and CHOP, and % apoptotic index values in rat gastric tissues. Additionally, it was determined that acetyl-L-carnitine administration caused an improvement in those values. Based on our data, we can conclude that acetyl-L-carnitine has a tissue protective effect by scavenging free oxygen radicals and reducing ER stress-related proteins XBP1, GRP78, and CHOP and apoptosis in chronic ethanol-administered rats, and that this natural antioxidant may be beneficial in the treatment of oxidative stress-induced diseases. •Consuming alcohol affects almost all organs.•Alcohol causes apoptosis, as well as oxidative and endoplasmic reticulum stress.•L-carnitine has important intracellular functions and pharmacological effects.•Acetyl-L-carnitine administration may attenuate alcohol-induced gastric damage.</description><identifier>ISSN: 0741-8329</identifier><identifier>EISSN: 1873-6823</identifier><identifier>DOI: 10.1016/j.alcohol.2023.07.003</identifier><identifier>PMID: 37499932</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Abdomen ; Acetaldehyde ; Acetyl-L-carnitine ; Alcohol ; Antigens ; Antioxidants ; Apoptosis ; Carnitine ; Chronic ethanol ; DNA nucleotidylexotransferase ; Drinking water ; Endoplasmic reticulum ; Enzyme-linked immunosorbent assay ; ER stress ; Ethanol ; Free radicals ; Homeostasis ; Molecular modelling ; Oxidants ; Oxidation ; Oxidative stress ; Proteins ; Rodents ; Western blotting</subject><ispartof>Alcohol (Fayetteville, N.Y.), 2023-11, Vol.112, p.51-59</ispartof><rights>2023 Elsevier Inc.</rights><rights>Copyright © 2023 Elsevier Inc. 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Acetaldehyde, formed as the main product as a result of alcohol metabolism, causes the production of free superoxide radicals when oxidized, and accordingly oxidative and apoptotic processes are triggered. There are studies showing that carnitine has effects on oxidative and apoptotic processes that occur in various conditions. However, the mechanisms showing the effects of L-carnitine on these effects of alcohol have not been fully elucidated. In our study, the effects of acetyl-L-carnitine administration on the molecular mechanisms of oxidative stress, endoplasmic reticulum stress, and apoptotic parameters in gastric tissue of rats chronically exposed to alcohol were investigated. Hematoxylin-eosin staining was used for histopathological studies. Endoplasmic reticulum stress markers were detected with immunohistochemical staining and western blotting. Apoptotic index was evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. Total oxidant and antioxidant status were examined by ELISA. Our results showed that chronic alcohol administration caused a significant increase in TOS levels, an indicator of oxidative stress, the levels of ER-stress-associated proteins XBP1, GRP78, and CHOP, and % apoptotic index values in rat gastric tissues. Additionally, it was determined that acetyl-L-carnitine administration caused an improvement in those values. 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subjects Abdomen
Acetaldehyde
Acetyl-L-carnitine
Alcohol
Antigens
Antioxidants
Apoptosis
Carnitine
Chronic ethanol
DNA nucleotidylexotransferase
Drinking water
Endoplasmic reticulum
Enzyme-linked immunosorbent assay
ER stress
Ethanol
Free radicals
Homeostasis
Molecular modelling
Oxidants
Oxidation
Oxidative stress
Proteins
Rodents
Western blotting
title Acetyl-L-carnitine attenuates chronic ethanol-induced oxidative stress, ER stress and apoptosis in rat gastric tissue
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