Disrupted H₂S Signaling by Cigarette Smoking and Alcohol Drinking: Evidence from Cellular, Animal, and Clinical Studies

• Main Authors: Ethan Read (Author), Jiechun Zhu (Author), Guangdong Yang (Author)
• Format: Book
• Published: MDPI AG, 2021-01-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.
• Notes: 10.3390/antiox10010049; 2076-3921
• Keywords: H₂S; cigarette smoking; alcohol drinking; oxidative stress; inflammation; Therapeutics. Pharmacology; RM1-950
• Source: Antioxidants, Vol 10, Iss 1, p 49 (2021)

The role of endogenous hydrogen sulfide (H₂S) as an antioxidant regulator has sparked interest in its function within inflammatory diseases. Cigarette and alcohol use are major causes of premature death, resulting from chronic oxidative stress and subsequent tissue damage. The activation of the Nrf2 antioxidant response by H₂S suggests that this novel gasotransmitter may function to prevent or potentially reverse disease progression caused by cigarette smoking or alcohol use. The purpose of this study is to review the interrelationship between H₂S signaling and cigarette smoking or alcohol drinking. Based on the databases of cellular, animal, and clinical studies from Pubmed using the keywords of H₂S, smoking, and/or alcohol, this review article provides a comprehensive insight into disrupted H₂S signaling by alcohol drinking and cigarette smoking-caused disorders. Major signaling and metabolic pathways involved in H₂S-derived antioxidant and anti-inflammatory responses are further reviewed. H₂S supplementation may prove to be an invaluable asset in treating or preventing diseases in those suffering from cigarette or alcohol addiction.