In a state of oxidative stress, there is an increase of reactive species, which induce an altered intracellular signaling, leading to dysregulation of the inflammatory response. The inability of the antioxidant defense systems to modulate the proinflammatory response is key to the onset and progression of neurodegenerative diseases. The aim of this work is to review the effect of the state of oxidative stress on the loss of regulation of the inflammatory response on the microglia and astrocytes, the induction of different CD4⁺T cell populations in neuroinflammation, as well as its role in some neurodegenerative diseases. For this purpose, an intentional search of original articles, short communications, and reviews, was carried out in the following databases: PubMed, Scopus, and Google Scholar. The articles reviewed included the period from 1997 to 2017. With the evidence obtained, we conclude that the loss of redox balance induces alterations in the differentiation and number of CD4⁺T cell subpopulations, leading to an increase in Th1 and Th17 response. This contributes to the development of neuroinflammation as well as loss of the regulation of the inflammatory response in neurodegenerative diseases such as Alzheimer's (AD), Parkinson's (PD), and Multiple Sclerosis (MS). In contrast, regulatory T cells (Tregs) and Th2 modulate the inflammatory response of effect of T cells, microglia, and astrocytes. In this respect, it has been found that the mobilization of T cells with anti-inflammatory characteristics toward damaged regions of the CNS can provide neuroprotection and become a therapeutic strategy to control inflammatory processes in neurodegeneration.

Ever since Linus Pauling published his studies, the effects of vitamin C have been surrounded by contradictory results. This may be because its effects depend on a number of factors such as the redox state of the body, the dose used, and also on the tissue metabolism. This review deals with vitamin C pharmacokinetics and its participation in neurophysiological processes, as well as its role in the maintenance of redox balance. The distribution and the concentration of vitamin C in the organs depend on the ascorbate requirements of each and on the tissue distribution of sodium-dependent vitamin C transporter 1 and 2 (SVCT1 and SVCT2). This determines the specific distribution pattern of vitamin C in the body. Vitamin C is involved in the physiology of the nervous system, including the support and the structure of the neurons, the processes of differentiation, maturation and neuronal survival; the synthesis of catecholamine, and the modulation of neurotransmission. This antioxidant interacts with self-recycling mechanisms, including its participation in the endogenous antioxidant system. We conclude that the pharmacokinetic properties of ascorbate are related to the redox state and its functions and effects in tissues.

Oxidative stress is involved in many neurodegenerative diseases. Chronic ozone exposure causes a secondary increase of reactive oxygen species, which cause an oxidative stress state in the organism. Ozone is one of the main components of photochemical pollution. Our purpose was to test that oxidative stress caused by chronic low doses of ozone, by itself, alters adult neurogenesis and causes progressive neurodegeneration in the hippocampus, which actions lead to the loss of brain plasticity in the mature central nervous system of rats. Animals were exposed to an ozone-free air stream and for 15, 30, 60, and 90 days to low doses of ozone to cause oxidative stress. Each group was then tested by (1) a spectrophotometer test to quantify lipid peroxidation (LPO) levels; (2) immunohistochemistry testing against doublecortin, Neu-N, p53, microglia, and glial fibrillary acidic protein; (3) Western blot tests for doublecortin and Neu-N; and (4) a one-trial passive avoidance test. Our results indicated that ozone causes an increase of LPO levels, morphological changes in the nucleus and the cytoplasm, and cell swelling in neurons. The Western blot shows a decrease for Neu-N and doublecortin. Activated and later phagocytic microglia and an increased number of astrocytes were found. There was a memory deficiency positively related to the amount of ozone exposure. These alterations suggest that oxidative stress caused by low doses of ozone causes dysregulation of inflammatory processes, progressive neurodegeneration, chronic loss of brain repair in the hippocampus, and brain plasticity changes in the rat analogous to those seen in Alzheimer’s disease.

Ozone is one of the main atmospheric pollutants. Its inhalation causes an increase in free radicals, when these free radicals are not compensated by antioxidants, it leads to an oxidative stress state. This oxidative stress state has been implicated in neurodegenerative processes. To determine the effects of oxidative stress caused by exposure to ozone on memory and motor activity, we used 120 male Wistar rats exposed to one of the following ozone doses, (0.0, 0.1, 0.4, 0.7, 1.1 and 1.5 ppm), for four hours. After ozone exposure, short and long term memory of a one trial passive avoidance test were measured, and motor activity was registered for five minutes, in 10 rats of each group. In 16 rats exposed to 0.0, 0.4, 0.7 or 1.1 ppm lipid peroxidation levels from frontal cortex, hippocampus, striatum and cerebellum, were measured. Results show that ozone, causes memory impairment from doses of 0.7 ppm, decrease in motor activity from doses of 1.1 ppm, and increase in lipid peroxidation levels from doses of 0.4 ppm, that increase with the dose.

Purpose: The purpose of this review is to consider the state of oxidative stress, failure of the antioxidant systems and mitochondrial failure as the main physiopathological mechanisms leading to multiple organ dysfunction during sepsis. Principal findings: Sepsis is a clinical syndrome caused by a severe infection that triggers an exaggerated inflammatory response. Involved in the pathogenesis of sepsis are the activation of inflammatory, immune, hormonal, metabolic and bioenergetic responses. One of the pivotal factors in these processes is the increase of reactive species accompanied by the failure of the antioxidant systems, leading to a state of irreversible oxidative stress and mitochondrial failure. In a physiological state, reactive species and antioxidant systems are in redox balance. The loss of this balance during both chronic and infectious diseases leads to a state of oxidative stress, which is considered to be the greatest promoter of a systemic inflammatory response. The loss of the redox balance, together with a systemic inflammatory response during sepsis, can lead to progressive and irreversible mitochondrial failure, energy depletion, hypoxia, septic shock, severe sepsis, multiple organ dysfunction and death of the patient. Conclusion: Knowledge of the molecular processes associated with the development of oxidative stress should facilitate the development of effective therapies and better prognosis for patients with sepsis and organ dysfunction.