The role of kallikrein-8 and its relationship to oxidative stress in patients with bipolar disorder and first-degree relatives

Bipolar disorder (BB) is a mood disorder characterized by two separate episodes of illness consisting of mania and depression. Although the pathophysiology of BB disease is not fully known, it is thought that it may be caused by a combination of factors such as chemical imbalance caused by neurotransmitters, genes or changes in genes affecting brain cells and producing faulty proteins, oxidative stress and psychological trigger elements. It is known that oxidative stress, which occurs as a result of the disruption of the balance between oxidant and antioxidant system, is associated with the development of psychiatric diseases. Expressed in the hippocampus, amygdala lateral nucleus, and limbic system regions of the brain associated with learning and memory, Kallikrein-8 (KLK-8) is an extracellular serine protease that modulates synaptic plasticity. It has been suggested that with the discovery of KLK-8, it may be an indicator for the diagnosis or prognosis of many diseases. In this study, it was aimed to evaluate the possible differences between the groups by investigating KLK-8 level, total oxidant capacity (TOS), total antioxidant capacity (TAS) and oxidative stress index (OSI) in serum obtained from blood samples taken from BB patient, first-degree relatives and healthy control groups. There was a significant difference in the levels of KLK-8, TAS, TOS and OSI between the BB diagnosed patient, first-degree patient' relatives and control groups (p=0.001, p=0.021, p<0.001 and p<0.001). It was found that serum KLK-8, TOS and OSI levels were higher in patients diagnosed with BB and first-degree patients' relatives compared to the control group, but serum TAS levels were lower. The findings of this study showed for the first time that there may be a relationship between serum KLK-8 level and the development of BB. The significant difference between the oxidative stress parameters of the BB patients and their relatives compared with the control group indicates that free radical-induced oxidative damage in the pathophysiology of the disease should also be considered as a contributing parameter to the process.