“…The production of ROS by ethanol and aldehydes occurs not only as a result of mitochondrial damage, but also as a major product or byproduct of various enzymatic reactions associated with alcohol degradation. In addition, it is known to induce disruption of the antioxidant system [ 19 ], suggesting that H 2 molecules suppress ROS generation by acting on the intracellular ROS production mechanism caused by ethanol metabolism and aldehyde toxicity. On the other hand, since H 2 O 2 is a precursor of hydroxyl radicals, components other than molecular hydrogen in EHW may act more strongly to scavenge intracellular reactive oxygen species caused by hydroxyl radicals [ 20 ].…”
Excessive alcohol consumption can cause multi-systemic diseases. Among them, alcoholic liver disease is the most frequent and serious disease. Electrolytic hydrogen water (EHW) is produced at the cathode during electrolysis of water and contains a large amount of molecular hydrogen and a low content of platinum nanoparticles with alkaline properties. In this study, we found that EHW inhibits ethanol-induced cytotoxicity by decreasing the intracellular acetaldehyde, a toxic substance produced by ethanol degradation, in hepatocyte cell lines HepG2. Analysis of the mechanism of action revealed that EHW inhibits the metabolism of ethanol to acetaldehyde by suppressing alcohol dehydrogenase. EHW also promotes the metabolism of acetaldehyde to acetic acid by activating aldehyde dehydrogenase, which plays to reduce aldehyde toxicity and intracellular reactive oxygen species in HepG2 cells. These functions were correlated with the concentration of molecular hydrogen in EHW, and were abolished by degassing treatment, suggesting that molecular hydrogen may contribute as a functional factor in the suppression of ethanol-induced hepatocellular damage. Furthermore, hydrogen water with high dissolved hydrogen molecule showed the same hepatocellular protective effect against ethanol as the EHW. These results suggest that EHW may be useful in the prevention of alcoholic liver disease.
“…The production of ROS by ethanol and aldehydes occurs not only as a result of mitochondrial damage, but also as a major product or byproduct of various enzymatic reactions associated with alcohol degradation. In addition, it is known to induce disruption of the antioxidant system [ 19 ], suggesting that H 2 molecules suppress ROS generation by acting on the intracellular ROS production mechanism caused by ethanol metabolism and aldehyde toxicity. On the other hand, since H 2 O 2 is a precursor of hydroxyl radicals, components other than molecular hydrogen in EHW may act more strongly to scavenge intracellular reactive oxygen species caused by hydroxyl radicals [ 20 ].…”
Excessive alcohol consumption can cause multi-systemic diseases. Among them, alcoholic liver disease is the most frequent and serious disease. Electrolytic hydrogen water (EHW) is produced at the cathode during electrolysis of water and contains a large amount of molecular hydrogen and a low content of platinum nanoparticles with alkaline properties. In this study, we found that EHW inhibits ethanol-induced cytotoxicity by decreasing the intracellular acetaldehyde, a toxic substance produced by ethanol degradation, in hepatocyte cell lines HepG2. Analysis of the mechanism of action revealed that EHW inhibits the metabolism of ethanol to acetaldehyde by suppressing alcohol dehydrogenase. EHW also promotes the metabolism of acetaldehyde to acetic acid by activating aldehyde dehydrogenase, which plays to reduce aldehyde toxicity and intracellular reactive oxygen species in HepG2 cells. These functions were correlated with the concentration of molecular hydrogen in EHW, and were abolished by degassing treatment, suggesting that molecular hydrogen may contribute as a functional factor in the suppression of ethanol-induced hepatocellular damage. Furthermore, hydrogen water with high dissolved hydrogen molecule showed the same hepatocellular protective effect against ethanol as the EHW. These results suggest that EHW may be useful in the prevention of alcoholic liver disease.
“…MetHb formation suggests that phthalates target Hb and its heme groups. Heme degradation usually leads to an increase in the level of free iron ions, which are active in redox reactions and can react with H 2 O 2 to form highly reactive hydroxyl radicals [ 56 , 57 , 58 , 59 , 60 ]. Therefore, we determined the level of ROS, including that of hydroxyl radical.…”
Phthalates used as plasticizers have become a part of human life because of their important role in various industries. Human exposure to these compounds is unavoidable, and therefore their mechanisms of toxicity should be investigated. Due to their structure and function, human erythrocytes are increasingly used as a cell model for testing the in vitro toxicity of various xenobiotics. Therefore, the purpose of our study was to assess the effect of selected phthalates on methemoglobin (metHb), reactive oxygen species (ROS) including hydroxyl radical levels, as well as the activity of antioxidative enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), in human erythrocytes. Erythrocytes were incubated with di-n-butyl phthalate (DBP), butylbenzyl phthalate (BBP), and their metabolites, i.e., mono-n-butyl phthalate (MBP) and monobenzyl phthalate (MBzP), at concentrations ranging from 0.5 to 100 µg/mL for 6 or 24 h. This study shows that the analyzed phthalates disturbed the redox balance in human erythrocytes. DBP and BBP, at much lower concentrations than their metabolites, caused a statistically significant increase of metHb and ROS, including hydroxyl radical levels, and changed the activity of antioxidant enzymes. The studied phthalates disturbed the redox balance in human erythrocytes, which may contribute to the accelerated removal of these cells from the circulation.
“…First, the alcohol metabolite, acetaldehyde, can increase the generation of free radicals, such as reactive oxygen and nitrogen, causing damage to cells or tissues (Wakabayashi, 2019; Yan and Zhao, 2020). Acetaldehyde affects the normal development of red blood cells, reduces their oxygen‐carrying capacity, and shortens the life of these cells (Waris et al, 2020). Second, the levels of tumor necrosis factor‐α, interleukin‐1β, and interleukin‐6 are increased in patients with AUD (Ansari et al, 2016).…”
Background: Patients with alcohol use disorder (AUD) are common attendees of the intensive care unit (ICU). Early assessment of the prognosis for critically ill patients with AUD is conducive for formulating comprehensive treatment measures and improving survival rates. The purpose of this study was to explore the predictive value of red blood cell distribution width (RDW) for 28-day mortality in critically ill patients with AUD. Methods: 2,884 patients with AUD were recruited retrospectively. Data from the MIMIC-III database were collected and analyzed. A receiver operating characteristic (ROC) curve was used to determine the optimal cutoff value of RDW. The Kaplan-Meier method and Cox regression models were used to evaluate prognostic factors. Results: Of the 2,884 patients, there were 344 nonsurvivors (11.9%). The nonsurvivors had a higher RDW than the survivors (p < 0.001). According to ROC curve analysis, the area under the curve predicted by RDW for 28-day mortality was 0.728 (95% CI, 0.700 to 0.755) and the optimal cutoff value was 15.45% (sensitivity: 67.2%; specificity: 67.3%). Length of stay in ICU, length of stay in hospital, in-hospital mortality, and 28-day mortality in patients with an RDW > 15.45% were significantly higher than in those with an RDW ≤ 15.45% (p < 0.001). Cox regression analysis showed that an RDW > 15.45% was an independent prognostic indicator for 28-day mortality in critically ill patients with AUD (HR = 1.964, 95% CI: 1.429 to 2.698). Conclusions: High RDW was associated with increased short-term mortality risks in critically ill patients with AUD.
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