Abstract
Background. Numerous studies have demonstrated the leading role of oxidative stress in the pathogenesis of necrotic changes in the pancreas and the development of organ failure in acute pancreatitis. Reduced glutathione is a key component of antioxidant protection in tissues; N-acetylcysteine promotes the synthesis of reduced glutathione. Its use has the potential to reduce tissue damage and eliminate the manifestations of organ failure in acute pancreatitis.
The study aimed to identify changes in glutathione metabolism, oxidative stress activity, the state of antioxidant protection, and the potential for correction by N-acetylcysteine infusion.
Materials and methods. In an experiment on 60 white Wistar rats, acute necrotic pancreatitis was modelled by retrograde infusion of taurocholic acid into the biliopancreatic duct. The animals were removed from the experiment 6–48 hours after the induction of acute pancreatitis.
Results. The development of acute pancreatitis in all periods of the study resulted in a deficiency of reduced glutathione in the pancreas, small intestine mucosa, liver, and blood, which is attributed to the neutralization of lipoperoxides and active forms of oxygen. The administration of N-acetylcysteine 70 mg/kg significantly (p <0,05) increased the content of reduced glutathione in the tissues of internal organs and venous blood plasma, which improved the course of the inflammatory process in the pancreas and reduced morphological changes in internal organs.
Conclusions. The development of acute pancreatitis is accompanied by a deficiency of glutathione, which is consumed to neutralize the components of oxidative stress. Infusion of N-acetylcysteine at a dose of 70 mg/kg/day effectively restores glutathione content and reduces morphological signs of damage to internal organ tissues caused by oxidative stress.
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