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Alcohol addiction is recognized as a serious public health issue today. The World Health Organization classifies alcohol as substances that cause both physiological and psychological dependence when consumed over prolonged periods. Studies clearly indicate that chronic alcohol consumption has detrimental effects on the male reproductive system, suggesting that it is a risk factor for male fertility with reproductive and endocrine problems. Acetaldehyde, which is formed by the metabolism of alcohol, causes the production of free radicals when oxidized, which triggers apoptotic processes and oxidative stress. It is known that chronic alcohol use results in oxidative stress. However, various studies have shown that acetyl-L-carnitine (ALCAR) has antioxidant effects on several biological mechanisms under different conditions. Therefore, we aimed to investigate the potential effects of ALCAR administration on sperm motility, testicular histopathology, apoptosis, and oxidative stress in rats chronically exposed to ethanol (EtOH). Rats were randomly separated into 4 groups. Over the course of the 4-week period, EtOH (5 g/kg, 25% w/v), ALCAR (50 mg/kg), and EtOH (5 g/kg, 25% w/v) + ALCAR (50 mg/kg) were given to rats by oral gavage daily (n=10/group). However, the control group received only distilled water. Epididymal sperm motility and testicular weight index were measured in line with testicular histopathology and modified Johnsen scoring. TUNEL assay was used for the assessment of the apoptotic index. Total oxidants and antioxidant status were analyzed with ELISA. Sperm motility and testicular modified Johnsen scores were decreased in the EtOH group (p<0.001). However, the EtOH+ALCAR group showed similar levels as to the control group. Even though no significant difference was determined for testicular weight index, immature germ cells spilled into the lumen, vacuolization in the intertubular area, and expansion in the interstitial area were observed in the EtOH group in contrast to normal testicular histology in the EtOH+ALCAR group. Chronic alcohol administration caused a significant increase in the apoptotic index (p<0.05) and oxidative stress (p<0.001). Nevertheless, we detected decreased apoptotic index and oxidative stress levels in the EtOH+ALCAR group compared to the EtOH group. Our results indicate that ALCAR, an antioxidant compound, may have beneficial effects against the damages caused by chronic use of alcohol, such as poor sperm motility, testicular atrophy, and increased oxidative stress. However, the exact efficacy of ALCAR on the treatment for male infertility and metabolic consequences of chronic alcohol consumption needs to be confirmed by further investigations. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]