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Effect of Si-based agent on alcohol hangovers and liver damage caused by acute ethanol overdose
Yoshihisa Koyama1,2, Xin Ye1, Yuki Kobayashi3
1Department of Neuroscience and Cell Biology, Graduate School of Medicine, The University of Osaka, Osaka, 565-0871, Japan.
Abstract:
Excessive alcohol consumption induces hangover symptoms such as headaches, sleep disorders, nausea, cognitive and sensory impairments, depression, and autonomic nervous system dysfunction, as well as liver damage. Additionally, alcohol hangovers cause an altered state of consciousness referred to as intoxication, which may lead to decreased work performance and a higher risk of workplace accidents. Furthermore, liver damage resulting from excessive alcohol consumption has significant health implications. Therefore, developing an effective treatment for alcohol hangovers and alcohol-induced liver damage is highly desirable. A silicon (Si)-based agent reacts with water to continuously generate a substantial amount of hydrogen. In fact, oral administration of the Si-based agent to mice has been shown to increase hydrogen concentration in the intestine. Reports indicate that hydrogen gas alleviates acute alcohol-induced liver injury, suggesting that the Si-based agent could serve as an effective treatment for excessive alcohol consumption. This study evaluated the Si-based agent's ability to alleviate motor impairment associated with hangover and prevent ethanol-induced liver damage in acute overdose mouse models. A comparative analysis between the Si-based agent-treated group and untreated group demonstrated that the Si-based agent mitigated reductions in spontaneous activity, behavioral performance, and motor coordination associated with alcohol consumption. Moreover, morphological analysis showed that the Si-based agent-treated group exhibited significantly less ethanol-induced liver damage compared to the untreated group. Aldehyde dehydrase activation showed to persist in the untreated group, but not in the Si-based agent-treated group. Furthermore, in the Si-based agent-treated group, antioxidant capacity exhibited a slight increase after ethanol administration; however, this change did not reach statistical significance. In conclusion, our findings indicate that the Si-based agent alleviates motor impairment associated with hangover and liver damage by alleviating the increase in oxidative stress and promoting the ethanol metabolize caused by excessive alcohol intake. This study suggests that the Si-based agent has potential as an effective treatment for alcohol hangovers and alcohol-induced liver damage in the future.
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