In the mammalian central nervous system, reactive oxygen species (ROS) generation is counterbalanced by antioxidant defenses. When large amounts of ROS accumulate, antioxidant mechanisms become overwhelmed and oxidative cellular stress may occur. Therefore, ROS are typically characterized as toxic molecules, oxidizing membrane lipids, changing the conformation of proteins, damaging nucleic acids, and causing deficits in synaptic plasticity. High ROS concentrations are associated with a decline in cognitive functions, as observed in some neurodegenerative disorders and age-dependent decay of neuroplasticity. Nevertheless, controlled ROS production provides the optimal redox state for the activation of transductional pathways involved in synaptic changes. Since ROS may regulate neuronal activity and elicit negative effects at the same time, the distinction between beneficial and deleterious consequences is unclear. In this regard, this review assesses current research and describes the main sources of ROS in neurons, specifying their involvement in synaptic plasticity and distinguishing between physiological and pathological processes implicated.

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Purpose The aim of this study was to investigate the hemodynamic, oxidative stress (OS), and nitric oxide (NO−) responses to a submaximal isometric exercise session (IES) involving large muscle mass. Methods Fourteen hypertensive (HTG: age = 35.9 ± 8.1 yr, height = 1.73 ± 0.10 m, total body mass = 78.0 ± 15.8 kg) and 10 normotensive (NTG: age = 41.1 ± 9.4 yr, height = 1.71 ± 0.12 m, total body mass = 82.3 ± 22.4 kg) participants performed two experimental sessions in the leg press and bench press: (i) control session and (ii) 8 sets × 1 min contraction at 30% maximal voluntary isometric contraction with 2-min rest interval. Blood pressure (BP) was measured at rest and during 60 min postexercise. Blood samples were collected at rest, immediately after the session, and 60 min postexercise. NO− was obtained through the Griess reaction method. OS parameters were analyzed using commercial kits. A repeated-measures ANOVA with Bonferroni post hoc test was used to analyze all dependent variables. Results A significant decrease in systolic BP was observed only for HTG at 45 and 60 min postexercise (baseline vs 45 min: P = 0.03, Δ% = 4.44%; vs 60 min: P = 0.018, Δ% = 5.58%). NO− increased immediately postexercise only for HTG (P = 0.008, Δ% = 16.44%). Regarding OS parameters, thiobarbituric acid reactive substances presented a significant reduction 60 min after the IES for NTG and HTG; catalase increased in both groups. Conclusions The data showed that only 8 min of IES with a large muscle mass elicits an elevated pro-oxidant activity leading to a greater NO− bioavailability, increases antioxidant reaction, and consequently reduces BP in hypertensive patients.