PATHOGENETIC PARALLELS OF GENERAL PROTEOLISIS AND OXIDANT-ANTIOXIDANT STATUS AT CHRONIC PANCREATITIS
DOI:
https://doi.org/10.11603/1811-2471.2023.v.i3.14080Keywords:
chronic pancreatitis, general proteolysis, oxidative stress, antioxidant defense systemAbstract
SUMMARY. In the development and progression of CP, the role of violations in the antioxidant defense system (ADS), activation of peroxidation processes, and systemic kallikrein-kinin system has been proven. The presence and depth of disorders in ADS and systemic proteolysis largely determine the severity of the course of CP.
The aim – to investigate the relationships between indicators of oxidative stress, ADS, and systemic proteolysis in patients with CP.
Material and Methods. 117 patients with CP were examined. The state of lipids was assessed by the level of malonaldehyde (MA), the state of ADS enzyme composition was estimated by the levels of superoxide dismutase (SOD) and catalase, the non-enzymatic composition of ADS was determined by the levels of SH-groups and ceruloplasmin. Evaluation of indicators of general and specific proteolysis (α1-inhibitor of proteinases (α1-IP); α2-macroglobulin (α2-MG); kallikrein (KK); kininase II activity; prekallikrein (PKK); proteolytic activity of plasma (PAP).
Results. The presence of statistically significant moderate correlations was revealed for most indicators, and for the level of α2-MG and catalase, the level of KK and SOD – a significant correlation, which proves the relationship in the imbalance between these two systems in CP. A statistically significant direct correlation between these indicators was revealed, which indicates a statistically significant relationship between the phenomena of oxidative stress and the activation of general proteolysis.
Conclusion. A statistically significant relationship was established between the activation of general proteolysis processes, the deepening of oxidative stress phenomena, and the weakening of enzymatic and non-enzymatic ADS, which indicates the mutually aggravating influence of the studied pathogenetic links of CP on the progression of the disease.
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