scholarly journals Ozone as integrative and complementary support for pharmacological therapy.

2021 ◽  
Vol 4 (5) ◽  
pp. 37
Author(s):  
Lamberto Re
Keyword(s):  
Oxidative Stress ◽  
Mononuclear Cells ◽  
Stress Component ◽  
Legal Regulation ◽  
Pharmacological Therapy ◽  
Ozone Exposure ◽  
Metabolic Effects ◽  
Peripheral Blood Mononuclear ◽  
New Concepts ◽  
And Training

Ozone is not nowadays used in a single medical branch, due to its immune and metabolic effects. This molecule is considered as a pro-drug which can induce at certain non-toxic doses a rearrangement of the biochemical pathways with the activation of a second messenger in a cascade with a multiple system action. Nonetheless, its difference from a drug consists in the fact that its action can’t be explained as a simple interaction between a molecule and a receptor, thus, it can’t be considered according to the classical pharmacological schemes and new concepts must be defined. Furthermore, ozone is able to activate Nfr2 protein. Our study reflects how the levels of Nrf2 in peripheral blood mononuclear cells were found to increase immediately after ozone exposure and when measured 30 minutes following reinfusion demonstrating that the oxidative stress was able to activate all the blood components. After a series of 3 systemic indirect endovenous applications, Nrf2 returned back to the basal level. At the end of the experiment the activities of superoxide dismutase and catalase were increased. This metabolic pathway is common to all cell lines. In light of the above, ozone could be very helpful as integrative and complementary support for pharmacological therapy modulating the oxidative stress component in many illnesses, elderly and rare diseases, according to not only a legal regulation but also a proper education and training of physicians.

scholarly journals Exercise-Induced Reductive Stress Is a Protective Mechanism against Oxidative Stress in Peripheral Blood Mononuclear Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Ypatios Spanidis ◽  
Aristidis S. Veskoukis ◽  
Christina Papanikolaou ◽  
Dimitrios Stagos ◽  
Alexandros Priftis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Eccentric Exercise ◽  
Mononuclear Cells ◽  
Reductive Group ◽  
Redox Status ◽  
Protective Mechanism ◽  
Peripheral Blood Mononuclear ◽  
Reductive Stress ◽  
Blood Mononuclear Cells ◽  
Baseline Values

Eccentric exercise is a well-studied modality that induces oxidative stress and muscle damage. Furthermore, it promotes inflammatory response in which peripheral blood mononuclear cells (PBMCs) are the major mediators. Although free radicals are necessary in a specific range of concentrations, yet unknown, it remains unclear whether reductive redox status (i.e., increased antioxidant defenses and impaired free radical generation) is beneficial or not. Thus, the aim of the present investigation was to examine the effects of reductive stress and the impact of reduced glutathione (GSH) baseline values on the ability of PBMCs to counteract oxidative stress induced by a potent oxidative agent. PBMCs were isolated from the blood of subjects who performed eccentric exercise and treated with t-BOOH for 24 h. The subjects were clustered in the reductive and the oxidative group on the basis of increased or decreased GSH concentration postexercise compared to preexercise values, respectively. According to our results in PBMCs, lipid peroxidation levels as depicted by thiobarbituric acid reactive substances (TBARS) remained unchanged in the reductive group contrary to the observed enhancement in the oxidative group. In addition, GSH concentration and catalase activity increased in the reductive group, whereas they were not affected in the oxidative group. In conclusion, the effects of an oxidizing agent on the redox status of PBMCs isolated from the blood of athletes after acute eccentric exercise are dependent on the baseline values of GSH in erythrocytes. Otherwise, reductive stress defined by increased GSH levels is a protective mechanism, at least when followed by an oxidative stimulus.

scholarly journals Nuclear Phospho-SOD1 Protects DNA from Oxidative Stress Damage in Amyotrophic Lateral Sclerosis

2019 ◽  
Vol 8 (5) ◽  
pp. 729 ◽  
Author(s):  
Matteo Bordoni ◽  
Orietta Pansarasa ◽  
Michela Dell’Orco ◽  
Valeria Crippa ◽  
Stella Gagliardi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Amyotrophic Lateral Sclerosis ◽  
Oxidative Damage ◽  
Motor Neurons ◽  
Mononuclear Cells ◽  
Sporadic Amyotrophic Lateral Sclerosis ◽  
Peripheral Blood Mononuclear ◽  
High Level ◽  
Lateral Sclerosis

We already demonstrated that in peripheral blood mononuclear cells (PBMCs) of sporadic amyotrophic lateral sclerosis (sALS) patients, superoxide dismutase 1 (SOD1) was present in an aggregated form in the cytoplasmic compartment. Here, we investigated the possible effect of soluble SOD1 decrease and its consequent aggregation. We found an increase in DNA damage in patients PBMCs characterized by a high level of aggregated SOD1, while we found no DNA damage in PBMCs with normal soluble SOD1. We found an activation of ataxia-telangiectasia-mutated (ATM)/Chk2 and ATM and Rad3-related (ATR)/Chk1 DNA damage response pathways, which lead to phosphorylation of SOD1. Moreover, data showed that phosphorylation allows SOD1 to shift from the cytoplasm to the nucleus, protecting DNA from oxidative damage. Such pathway was finally confirmed in our cellular model. Our data lead us to suppose that in a sub-group of patients this physiologic pathway is non-functional, leading to an accumulation of DNA damage that causes the death of particularly susceptible cells, like motor neurons. In conclusion, during oxidative stress SOD1 is phosphorylated by Chk2 leading to its translocation in the nuclear compartment, in which SOD1 protects DNA from oxidative damage. This pathway, inefficient in sALS patients, could represent an innovative therapeutic target.

scholarly journals Metabolic Syndrome Is Associated with Oxidative Stress and Proinflammatory State

Antioxidants ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 236 ◽  
Author(s):  
Margalida Monserrat-Mesquida ◽  
Magdalena Quetglas-Llabrés ◽  
Xavier Capó ◽  
Cristina Bouzas ◽  
David Mateos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Vascular Function ◽  
Mononuclear Cells ◽  
Antioxidant Defenses ◽  
Peripheral Blood Mononuclear ◽  
Protein Levels ◽  
Inflammatory Parameters ◽  
Increased Risk ◽  
Factor Α

Metabolic syndrome (MetS) is associated with increased risk of developing diabetes and cardiovascular diseases. MetS is also characterized by an increase of oxidative stress which contributes to impaired inflammation, vascular function, and atherosclerosis. The aim was to assess the oxidative stress and inflammatory markers in plasma and PBMCs in adults with or without MetS. Antioxidant and inflammatory parameters were measured in peripheral blood mononuclear cells (PBMCs) of 80 men and 80 women over 55 to 80-years-old residing in the Balearic Islands without previously documented cardiovascular disease. Circulating leukocytes, neutrophils, lymphocytes, basophils, and monocytes were higher in MetS subjects with respect to those without MetS. Plasma levels of malondialdehyde, tumor necrosis factor α (TNFα), and interleukin 6 (IL-6) levels were higher in MetS subjects in both genders, but the superoxide dismutase activity was lower. The myeloperoxidase plasma activity was higher in the MetS male subjects. Higher activities and protein levels of catalase and glutathione reductase in PBMCs were observed in MetS subjects in both genders. Obtained data show that MetS is associated with oxidative stress and a proinflammatory state and with high antioxidant defenses in PBMCs probably derived from a pre-activation state of immune cells.

scholarly journals Postnatal episodic ozone results in persistent attenuation of pulmonary and peripheral blood responses to LPS challenge

2011 ◽  
Vol 300 (3) ◽  
pp. L462-L471 ◽  
Author(s):  
Kinjal Maniar-Hew ◽  
Edward M. Postlethwait ◽  
Michelle V. Fanucchi ◽  
Carol A. Ballinger ◽  
Michael J. Evans ◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Peripheral Blood Leukocyte ◽  
Innate Immune ◽  
Ozone Exposure ◽  
Prior History ◽  
Peripheral Blood Mononuclear ◽  
Lps Challenge ◽  
Exposed Infant

Early life is a dynamic period of growth for the lung and immune system. We hypothesized that ambient ozone exposure during postnatal development can affect the innate immune response to other environmental challenges in a persistent fashion. To test this hypothesis, we exposed infant rhesus macaque monkeys to a regimen of 11 ozone cycles between 30 days and 6 mo of age; each cycle consisted of ozone for 5 days (0.5 parts per million at 8 h/day) followed by 9 days of filtered air. Animals were subsequently housed in filtered air conditions and challenged with a single dose of inhaled LPS at 1 yr of age. After completion of the ozone exposure regimen at 6 mo of age, total peripheral blood leukocyte and polymorphonuclear leukocyte (PMN) numbers were reduced, whereas eosinophil counts increased. In lavage, total cell numbers at 6 mo were not affected by ozone, however, there was a significant reduction in lymphocytes and increased eosinophils. Following an additional 6 mo of filtered air housing, only monocytes were increased in blood and lavage in previously exposed animals. In response to LPS challenge, animals with a prior history of ozone showed an attenuated peripheral blood and lavage PMN response compared with controls. In vitro stimulation of peripheral blood mononuclear cells with LPS resulted in reduced secretion of IL-6 and IL-8 protein in association with prior ozone exposure. Collectively, our findings suggest that ozone exposure during infancy can result in a persistent effect on both pulmonary and systemic innate immune responses later in life.

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