Bipolar disorder (BD) is associated with systemic toxicity, represented by changes in biomarkers associated with mood episodes, leading to neurological damage, which may reflect cognitive functions and functionality and the progression of the disease. We aimed to analyze the effect of four biomarkers, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and thiobarbituric acid reactive substances (TBA-RS), related to oxidative stress in BD and to correlate them with cognitive functions and functionality. We studied 50 bipolar types I/II patients in the euthymic phase, which was divided into two subgroups with 25 patients each (≤ 3 years and ≥ 10 years of diagnosis, from the first episode of mania) and 25 control patients. To analyze frontal cognitive functions and functionality, we used the Frontal Assessment Battery (FAB) and Functioning Assessment Short Test (FAST) tests, respectively. The scores of the FAST and FAB tests showed an increase and decrease respectively, in both bipolar groups, when compared to the control group, demonstrating impairment in cognitive functions and functionality since the disease onset. In addition, changes occurred in all six domains of the FAST test, and in four domains of the FAB test in bipolar patients when compared to the control group. Regarding oxidative stress biomarkers, we did not find changes in SOD and GSH-Px activities; however, a significant increase in CAT activity and lipid peroxidation was observed in both groups, although the patients were euthymic and medicated. These results allow us to raise the hypothesis that since the beginning of the disease, the euthymic bipolar patient has presented a level of oxidative stress, which gets worse with the evolution of the disease, promoting impairments in the frontal cognitive functions and functionality gradually.
Depression is one of the disorders involving mental health that most affects the population worldwide. Considering the available pharmacological therapies for the treatment of depression are ineffective in most patients, the search for new alternatives is crucial. In line with this, we investigated the phenolic profile, antidepressant-like, and antioxidant effects triggered by the administration of aqueous extracts from Psidium guajava L. (GUA), Psidium cattleianum Sw. (CAT), and Psidium guineense Sabine (GUI) leaves in mice. Our results show that quercetin is the major compound of GUA and GUI, and o-coumaric acid in CAT extracts. The acute and subchronic administrations of the three plant extracts exerted an antidepressant-like effect in mice exposed to the tail suspension test, without changes on locomotor performance evaluated by the open field test. Furthermore, the GUI and CAT decreased oxidative stress markers, mainly lipid peroxidation and nitrites in the hippocampus, prefrontal cortex, liver, and plasma. Notably, GUA and CAT increased non-protein thiols in all tissues. Therefore, the Psidium extracts demonstrated an antidepressant-like effect in mice, and the antioxidant capacity of the extracts seems to underlie the behavioral effect.
Bipolar disorder (BD) is associated with changes in biomarkers and mood episodes, leading to neurological damage, which may reflect alterations in cognitive functions and functionality. We analyzed the effect of four biomarkers related to metabolic energy in leukocytes. Two enzymes are related to the tricarboxylic acid (TCA) cycle (citrate synthase and succinate dehydrogenase), and two proteins are related to electron transport chain (ETC) (complexes I and II). We studied 50 euthymic patients divided into two subgroups with 25 patients (≤ 3 years and ≥ 10 years of diagnosis, from the first episode of mania) and 25 control patients. All the patients were using mood stabilizers. There were no changes in the levels of TCA cycle enzymes in the leukocytes in any subgroup. However, complex I activity showed a significant increase in patients ≤ 3 years (461.80±162.76) and ≥ 10 years (561.21±328.13) since disease onset compared to the control group (335.39±167.64) (p<0.01). Complex II activity was significantly increased in the ≥ 10 years (3.42±1.38) group compared to the ≤ 3 years (2.66±1.17) group and the control group (2.43±0.95) (p<0.01). These results suggest that stabilizing medications improve the activity of ETC complexes and stabilize TCA cycle enzymes.
Bipolar Disorder (BD) is associated with systemic toxicity, represented by changes in the biomarkers, associated with mood episodes, leading to neurological damage, which may reflect on cognitive functions and functionality, and the progression of the disease. We aimed to analyze the effect of four biomarkers superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzymes, and thiobarbituric acid reactive substances (TBA-RS) related to oxidative stress in BD and to correlate them with cognitive functions and functionality. We studied 50 bipolar patients type I/II, in the euthymic phase, which was divided into two subgroups with 25 patients, (≤3 years and ≥10 years of diagnosis, from the first episode of mania), and 25 control patients. To analyze frontal cognitive functions and functionality, we used the tests: Frontal Assessment Battery (FAB) and Functioning Assessment Short Test (FAST), respectively. The FAST test scores results were ≤3 years (20.63±8.21), ≥10 years (27.80±12.50), and control group (9.80±5.94), p<0.001. Changes occurred in all domains. The FAB test scores were ≤3 years (14.64±2.48), ≥10 years (12.44±2.78), and control group (15.84±1.55), p<0.001, and showed lower scores in four domains. The oxidative stress showed an increase in TBA-RS levels: ≤3 years (3.18±1.17), ≥10 years (3.01±1.03) compared to the control group (1.62±0.28), p<0.0001; and in the CAT enzyme activity we found, ≤3 years (8.10±4.18), ≥10 years (9.41±4.95), compared to the control group (3.47±0.77), p<0.0001. Even during the euthymic phase, bipolar patients showed and maintained an increase in CAT activity and lipid peroxidation with significant changes in the FAB and FAST tests in different groups of patients, demonstrating impairment in cognitive functions and functionality since disease onset.
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