Changes in the Activity and Concentration of Superoxide Dismutase Isoenzymes (Cu/Zn SOD, MnSOD) in the Blood of Healthy Subjects and Patients with Acute Pancreatitis

Abstract

This study was aimed at evaluating the changes in the concentration and activity of all superoxide dismutase isoenzymes (SOD1, SOD2, SOD3) in the blood of patients with acute pancreatitis (AP) and healthy subjects, taking into account the extracellular (plasma) and intracellular (erythrocyte lysate) compartment. The relationships between the activity/concentration of SODs, metal concentration and the markers of inflammation were evaluated. To assess the pro/antioxidative imbalance, the malonyldialdehyde (MDA) concentration and the value of total antioxidant capacity (TAC) were measured. The impact of single-nucleotide polymorphism (SNP) in the SOD1 gene (rs2070424) on the activity/concentration of SOD1 as the main isoenzyme of the SOD family was also analyzed in this study. The SOD2 activity in erythrocytes was increased compared to plasma: 10-fold in the AP patient group and 5-fold in healthy subjects. The plasma of AP patients showed an increased SOD1 concentration and decreased SOD2 and SOD3 concentrations compared to healthy subjects. The Cu/Zn SOD (SOD1 + SOD3) concentration in plasma of AP patients was elevated compared to healthy subjects, but changes in plasma Cu/Zn SOD (SOD1 + SOD3) activity in the examined groups were not observed. An influence of SNP rs2070424 in the SOD1 gene on the total activity of SOD in AP patients (with AG genotype), accompanied by an increased IL-6 concentration, was observed. In oxidative stress conditions induced by inflammation, the participation of individual forms of plasma SOD isoenzymes in total antioxidative activity of SOD changed. A significant increase in the intracellular SOD1 concentration in plasma of AP patients proves the important role of this isoenzyme in the neutralization of oxidative stress induced by impaired Cu and Zn homeostasis. The presence of increased concentration of SOD2 in erythrocytes of healthy subjects and AP patients confirms the important function of this isoenzyme in the antioxidative defense.

Importance of Genetic Polymorphisms in MT1 and MT2 Genes in Metals Homeostasis and Their Relationship with the Risk of Acute Pancreatitis Occurrence in Smokers—Preliminary Findings

“…Additionally, our results showed increased total activity of SODs in erythrocytes of AP patients compared to healthy subjects, which could be related to increased MT concentration. MT, as a donor of Zn2+ ions, can take part in antioxidative defense and can regulate the activity of superoxide dismutase, especially its SOD1 and SOD3 isoenzymes [ 41 ]. The activity of Cu/Zn SOD strictly depends on metals such as Zn and Cu, where MT participates in its metabolism [ 14 ].…”

“…The patients were classified into the AP group on the basis of personal interviews, epigastric pain with touch sensitivity and medical and laboratory blood tests. Specific criteria for the inclusion of the patients in the study were described in [ 41 ]. The severity of the disease was determined according to the Atlanta classification.…”

Associations of Habitual Mineral Intake with New-Onset Prediabetes/Diabetes after Acute Pancreatitis

“…The mechanistic link between manganese and HbA1c and FPG is not fully understood; however, there is a possible role of the involvement of superoxide dismutase (SOD) enzymes [45,52,53]. There are three forms of SOD in mammals and manganese is a crucial component of manganese SOD (MnSOD) (it is worth noting that two of the other studied minerals-copper and zinc-are structural components of copper/zinc and extracellular SOD) [54]. SODs contribute to metabolic processes and protect cells against oxidative damage [45,52].…”

“…This leads to elevated oxidant levels and, consequently, MnSOD may be upregulated to manage oxidative damage [60]. Ściskalska et al observed that patients with AP had a 3-fold increased MnSOD in erythrocytes compared with healthy controls and decreased plasma MnSOD, suggesting migration of MnSOD from other cells circulating in plasma (e.g., leukocytes and platelets) in the state of oxidative stress induced by AP [54]. Gut hormones (e.g., gastric inhibitory peptide and peptide YY) appear to increase circulating levels of pro-inflammatory cytokines, leading to persistent subclinical inflammation following an attack of AP [58,59].…”

Effect of Antioxidant Therapy on Oxidative Stress in Vivo

“…Sciskalska et al [14] assessed the impact of acute pancreatitis (AP) on changes in the concentrations and activities of all three superoxide dismutase (SOD) isoenzymes and the interrelationships between the different isoenzymes and the oxidative and inflammatory status. Finally, the effect of single-nucleotide polymorphism (SNP) in the SOD1 gene (rs2070424) was also taken into consideration.…”