Chronic Alcoholism and Its Health Implications: A Case Report&#x0D;

Arbabi, Amirmohsen; Garg, B. K.; Reddy, Sridhar; Patel, Paryus

doi:10.7759/cureus.40364

Cited by 1 publication

(2 citation statements)

References 12 publications

(13 reference statements)

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“…ACM generated progressive heart failure, cardiac dysfunction, and abnormal electrocardiogram. 19 Longterm alcohol consumption caused damage to the heart, which manifested as impaired systolic function, enlarged heart chambers, and eventually heart failure. 20 The present data showed that alcohol significantly impaired cardiac function and structure as determined by ECG and histological examination.…”

Section: Discussionmentioning

confidence: 99%

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Role of Ferroptosis Regulation by Nrf2/NQO1 Pathway in Alcohol-Induced Cardiotoxicity In Vitro and In Vivo

Song,

Li,

Huang

et al. 2024

Chem. Res. Toxicol.

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The aim of the present study was to evaluate the cardiotoxic effects of alcohol and its potential toxic mechanism on ferroptosis in mice and H9c2 cells. Mice were intragastrically treated with three different concentrations of alcohol, 7, 14, and 28%, each day for 14 days. Body weight and electrocardiography (ECG) were recorded over the 14 day period. Serum creatine kinase (CK), lactic dehydrogenase (LDH), MDA, tissue iron, and GSH levels were measured. Cardiac tissues were examined histologically, and ferroptosis was assessed. In H9c2 cardiomyocytes, cell viability, reactive oxygen species (ROS), labile iron pool (LIP), and mitochondrial membrane potential (MMP) were measured. The proteins of ferroptosis were evaluated by the western blot technique in vivo and in vitro. The results showed that serum CK, LDH, MDA, and tissue iron levels significantly increased in the alcohol treatment group in a dose-dependent manner. The content of GSH decreased after alcohol treatment. ECG and histological examinations showed that alcohol impaired cardiac function and structure. In addition, the levels of ROS and LIP increased, and MMP levels decreased after alcohol treatment. Ferrostatin-1 (Fer-1) protected cells from lipid peroxidation. Western blotting analysis showed that alcohol downregulated the expression of Nrf2, NQO1, HO-1, and GPX4. The expressions of P53 and TfR were upregulated in vivo and in vitro. Fer-1 significantly alleviated alcohol-induced ferroptosis. In conclusion, the study showed that Nrf2/NQO1-dependent ferroptosis played a vital role in the cardiotoxicity induced by alcohol.

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Section: Discussionmentioning

confidence: 99%

“…Long-term alcohol consumption induces alcoholic cardiomyopathy (ACM). ACM generated progressive heart failure, cardiac dysfunction, and abnormal electrocardiogram . Long-term alcohol consumption caused damage to the heart, which manifested as impaired systolic function, enlarged heart chambers, and eventually heart failure .…”

Section: Discussionmentioning

confidence: 99%