Differences between antioxidant defense parameters and specific trace element concentrations in healthy, benign, and malignant brain tissues

There are only a few reports examining the impact of oxidative stress in patients with benign andmalignant brain tumors. In this study we investigated whether there are changes in antioxidantsystem (AOS) parameters and key trace elements between control, benign and malignant braintissues. The study also aimed to examine correlations between the analyzed parameters. The studyenrolled both types of brain tumors, benign tumors (BT) and malignant tumors (MT). The resultswere compared with control tissue (CT) without tumor infiltration collected from patients with BT.The following antioxidant parameters were determined: activities of total, manganese‑containing,and copper/zinc‑containing superoxide dismutase (TotSOD, MnSOD and CuZnSOD), activities ofcatalase, glutathione peroxidase, glutathione S‑transferase, glutathione reductase and acetylcholineesterase (AChE), the concentrations of glutathione and sulfhydryl groups and of manganese (Mn),copper (Cu), zinc (Zn), and selenium (Se). BT and MT had altered activities/levels of multiple AOSparameters as compared to CT, indicating that tumor cells had an altered cell metabolism and changesin AOS represent adaptive response to increased oxidative stress. Low MnSOD and AChE and highGST activities were significant for distinguishing between MT and CT. Malignant tissue was alsocharacterized by lower Mn and Cu concentrations relative to CT and BT. Principal Component Analysisclearly discriminated BT from CT and MT (PC1, 66.97%), while PC2 clearly discriminated CT from BTand MT (33.03%). Most correlative relationships were associated with Se in the BT group and Cu in theMT group. The results of this study reveal differences between the AOS parameters and the essentialtrace elements between the analyzed groups. The observed dysregulations show that oxidative stresscould have an important role in disrupting brain homeostasis and its presence in the pathogenesis ofbenign and malignant brain tumors