The prevalence of psychiatric disorders has increased in recent years. Among existing mental disorders, major depressive disorder (MDD) has emerged as one of the leading causes of disability worldwide, affecting individuals throughout their lives. Currently, MDD affects 15% of adults in the Americas. Over the past 50 years, pharmacotherapy, psychotherapy, and brain stimulation have been used to treat MDD. The most common approach is still pharmacotherapy; however, studies show that about 40% of patients are refractory to existing treatments. Although the monoamine hypothesis has been widely accepted as a molecular mechanism to explain the etiology of depression, its relationship with other biochemical phenomena remains only partially understood. This is the case of the link between MDD and inflammation, mitochondrial dysfunction, and oxidative stress. Studies have found that depressive patients usually exhibit altered inflammatory markers, mitochondrial membrane depolarization, oxidized mitochondrial DNA, and thus high levels of both central and peripheral reactive oxygen species (ROS). The effect of antidepressants on these events remains unclear. Nevertheless, the effects of ROS on the brain are well known, including lipid peroxidation of neuronal membranes, accumulation of peroxidation products in neurons, protein and DNA damage, reduced antioxidant defenses, apoptosis induction, and neuroinflammation. Antioxidants such as ascorbic acid, tocopherols, and coenzyme Q have shown promise in some depressive patients, but without consensus on their efficacy. Hence, this paper provides a review of MDD and its association with inflammation, mitochondrial dysfunction, and oxidative stress and is aimed at thoroughly discussing the putative links between these events, which may contribute to the design and development of new therapeutic approaches for patients.

Oxidative stress is implicated in several human illnesses, including neurological disorders such as Parkinson's and Alzheimer's diseases. Acai is largely consumed in Brazil and contains high levels of antioxidant compounds. This work aims to study the antioxidant activity of acai frozen fruit pulp in the cerebral cortex, hippocampus, and cerebellum of rats treated with the oxidizing agent hydrogen peroxide (H₂O₂). Pretreatment of tissue with acai decreased H₂O₂-induced damage of both lipids and proteins in all tissues tested. This fruit was also able to reduce the activities of the antioxidant enzymes superoxide dismutase and catalase to basal levels. We observed a negative correlation between the polyphenol content of acai and the levels of lipid (r = −0.689; P ≤ .05) and protein damage (r = −0.569; P ≤ .05), suggesting the participation of polyphenols in the observed antioxidant activity. These data suggest that acai has a positive contribution in the development of age-related neurodegenerative diseases.

Paints are complex mixtures of solvents and metals that can induce health damages in workers exposed to them. The aim of the present work was to evaluate possible oxidative and genotoxic effects in workers exposed to paints. Peripheral blood and buccal cell samples were collected from 33 workers exposed to paints and 29 non-exposed workers (controls) during an ordinary working week (Monday morning and Friday evening). Oxidative markers were assessed using thiobarbituric acid assay, carbonylated proteins, superoxide dismutase and catalase activities. Hippuric acid and delta-aminolevulinic acid were determined as biomarkers of toluene and lead exposure, respectively. Genotoxicity was measured through comet assay and micronucleus (MN) frequencies. The exposed group showed higher hippuric acid and delta-aminolevulinic acid levels (Friday samples) and lower superoxide dismutase activity (Monday samples) in relation to control group. DNA damage index (comet assay) was higher in the exposed group, both in Monday and Friday samples, compared to the control group. No differences were observed in frequency of micronuclei (MN) between the groups, either in lymphocytes or buccal cells. However, the exposed group presented an increase (Monday samples) in nuclear buds frequency in lymphocytes — a marker of gene amplification — as well as an increase in condensed chromatin in the buccal cells (Monday and Friday samples), suggesting induction of apoptosis. Furthermore, a decrease in the nuclear division index (Friday samples) was observed in the exposed group, indicating that paint exposure induces cytostatic effects in lymphocytes. The results suggest that individuals exposed to paints have increased levels of DNA damage.

Background: Amiodarone (AMD) and its metabolite N‐desethylamiodarone can cause some adverse effects, which include pulmonary toxicity. Some studies suggest that mitochondrial dysfunction and oxidative stress may play a role in these adverse effects. Catechin and epicatechin are recognized as important phenolic compounds with the ability to decrease oxidative stress. Therefore, the aim of this study was to evaluate the potential of catechin and epicatechin to modulate mitochondrial dysfunction and oxidative damage caused by AMD in human lung fibroblast cells (MRC‐5).Methods: Mitochondrial dysfunction was assessed through the activity of mitochondrial complex I and ATP biosynthesis. Cell viability was evaluated using the 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay. Superoxide dismutase and catalase activity were measured spectrophotometrically at 480 and 240 nm, respectively. Lipid and protein oxidative levels were determined by thiobarbituric reactive substances and protein carbonyl assays, respectively. Nitric oxide (NO) levels were evaluated using the Griess reaction method.Results: AMD was able to inhibit the activity of mitochondrial complex I and ATP biosynthesis in MRC‐5 cells. Lipid and protein oxidative markers increased along with cell death, while superoxide dismutase and catalase activities and NO production decreased with AMD treatment. Both catechin and epicatechin circumvented mitochondrial dysfunction, thereby restoring the activity of mitochondrial complex I and ATP biosynthesis. Furthermore, the phenolic compounds were able to restore the imbalance in superoxide dismutase and catalase activities as well as the decrease in NO levels induced by AMD. Protein and lipid oxidative damage and cell death were reduced by catechin and epicatechin in AMD‐treated cells.Conclusions: Catechin and epicatechin reduced mitochondrial dysfunction and oxidative stress caused by AMD in MRC‐5 cells.

The present work aimed to analyze the alkaloid content of the ethanolic extract of Tabernaemontana catharinensis (Apocynaceae family) and its fractions as well as to evaluate their antioxidant and anticholinesterasic activities. The analyses of the ethanolic extract of T. catharinensis by mass spectrometry allowed identifying the presence of the alkaloids 16‐epi‐affinine, coronaridine‐hydroxyindolenine, voachalotine, voacristine‐hydroxyindolenine, and 12‐methoxy‐n‐methyl‐voachalotine, as well as an alkaloid with m/z 385.21 whose spectrum suggests a derivative of voacristine or voacangine. The extract and its alkaloid rich fractions showed antioxidant activity, especially those that contain the alkaloid m/z 385.21 or 16‐epi‐affinine with DPPH scavenging activity (IC₅₀) between 37.18 and 74.69 μg/mL. Moreover, the extract and its fractions exhibited anticholinesterasic activity, particularly the fractions characterized by the presence of 12‐methoxy‐n‐methyl‐voachalotine, with IC₅₀ = 2.1 to 2.5 μg/mL. Fractions with 16‐epi‐affinine combined good antioxidant (IC₅₀ = 65.59 to 74.69 μg/mL) and anticholinesterasic (IC₅₀ = 7.7 to 8.3 μg/mL) activities, representing an option for further studies aimed at treating neurodegenerative diseases.