[In Process Citation]

Area of Science:

• Hepatology
• Toxicology
• Biochemistry

Background:

• Fulminant hepatic failure (FHF) is a rare clinical syndrome characterized by sudden, severe liver dysfunction.
• Thioacetamide (TAA) is a hepatotoxin that induces centrilobular necrosis, oxidative stress, and lipid peroxidation in rat livers.
• Glutamine, a precursor for glutathione synthesis, may offer protective benefits against liver injury.

Purpose of the Study:

• To evaluate the antioxidant effects of glutamine in a rat model of TAA-induced FHF.
• To assess the impact of glutamine supplementation on biochemical, histological, and inflammatory markers of liver damage.

Main Methods:

• Wistar rats were divided into control, glutamine, thioacetamide (TAA), and TAA + glutamine groups.
• Animals were evaluated at 24, 36, and 48 hours post-treatment.
• Blood and liver samples were analyzed for liver enzymes (AST, ALT, AP), bilirubin, creatinine, lipid peroxidation (TBARS), antioxidant enzyme activities (SOD, GPx, CAT, GST), and inflammatory markers (NF-κB, TNF-α, iNOS).

Main Results:

• TAA administration caused significant biochemical and histological alterations, along with increased inflammatory markers.
• Glutamine treatment significantly reduced TBARS levels and modulated antioxidant enzyme activities (SOD, GST, CAT, GPx) compared to TAA-induced injury.
• Glutamine significantly decreased liver tissue damage and the expression of NF-κB, TNF-α, and iNOS.

Conclusions:

• Glutamine exhibits significant protective effects against thioacetamide-induced liver injury in a rat model of fulminant hepatic failure.
• These protective effects are attributed to glutamine's ability to mitigate oxidative stress and inflammatory responses.
• Glutamine represents a potential therapeutic agent for managing acute liver damage.