Sulfhydrylated albumin mitigates Acetaminophen-induced liver injury by restoring the integrated H₂S-albumin thiol antioxidant network.

ABSTRACT: Acetaminophen (APAP) overdose is the leading cause of acute liver failure and a major global health issue. APAP hepatotoxicity is primarily driven by oxidative stress resulting from the depletion of hepatic glutathione (GSH). Given that hydrogen sulfide (H₂S) and albumin are crucial components of the thiol antioxidant system, we hypothesized they play a critical role in the body's defense against APAP-induced liver injury (AILI). This study aimed to test this hypothesis and explore novel therapeutic approach. Administration of APAP to mice induced significant hepatic damage, associated with marked local and systemic oxidative stress, evidenced by elevated serum transaminases and oxidative injury markers. Furthermore, APAP exposure disrupted the hepatic H₂S-generating

SUBMITTER: Wang X 

PROVIDER: S-EPMC12304942 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature