scholarly journals Hypoxic preconditioning modifies the activity of prond antioxidant systems in rat hippocampus

2013 ◽  
Vol 59 (6) ◽  
pp. 673-681 ◽  
Author(s):  
M.S. Kislin ◽  
S.A. Stroev ◽  
T.S. Gluschenko ◽  
E.I. Tulkova ◽  
M. Pelto-Huikko ◽  
...  

The effects of repetitive mild hypobaric hypoxic preconditioning upon pro- and antioxidant systems in rat hippocampus were studied. It was found that three-trial preconditioning by mild hypobaric hypoxia (360 mm Hg, 2 h) induced moderate oxidative stress immediately after the last preconditioning trial. In addition, it down-regualted the levels of peptide antioxidants (Trx-1, Trx-2, Cu,Zn-SOD) and several lipid peroxidation products 24 h later.

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Christina D’Agrosa ◽  
Charles L. Cai ◽  
Faisal Siddiqui ◽  
Karen Deslouches ◽  
Stephen Wadowski ◽  
...  

Abstract Background Neonatal intermittent hypoxia (IH) results in oxidative distress in preterm infants with immature antioxidant systems, contributing to lung injury. Coenzyme Q10 (CoQ10) and fish oil protect against oxidative injury. We tested the hypothesis that CoQ10 is more effective than fish oil for prevention of IH-induced lung injury in neonatal rats. Methods Newborn rats were exposed to two clinically relevant IH paradigms at birth (P0): (1) 50% O2 with brief hypoxia (12% O2); or (2) room air (RA) with brief hypoxia (12% O2), until P14 during which they were supplemented with daily oral CoQ10, fish oil, or olive oil from P0 to P14. Pups were studied at P14 or placed in RA until P21 with no further treatment. Lungs were assessed for histopathology and morphometry; biomarkers of oxidative stress and lipid peroxidation; and antioxidants. Results Of the two neonatal IH paradigms 21%/12% O2 IH resulted in the most severe outcomes, evidenced by histopathology and morphometry. CoQ10 was effective for preserving lung architecture and reduction of IH-induced oxidative stress biomarkers. In contrast, fish oil resulted in significant adverse outcomes including oversimplified alveoli, hemorrhage, reduced secondary crest formation and thickened septae. This was associated with elevated oxidants and antioxidants activities. Conclusions Data suggest that higher FiO2 may be needed between IH episodes to curtail the damaging effects of IH, and to provide the lungs with necessary respite. The negative outcomes with fish oil supplementation suggest oxidative stress-induced lipid peroxidation.


2021 ◽  
Vol 22 (10) ◽  
pp. 5272
Author(s):  
Débora Coimbra-Costa ◽  
Fernando Garzón ◽  
Norma Alva ◽  
Tiago C. C. Pinto ◽  
Fernando Aguado ◽  
...  

Background: Exposure to intermittent hypoxia has been demonstrated to be an efficient tool for hypoxic preconditioning, preventing damage to cells and demonstrating therapeutic benefits. We aimed to evaluate the effects of respiratory intermittent hypobaric hypoxia (IHH) to avoid brain injury caused by exposure to acute severe hypoxia (ASH). Methods: biomarkers of oxidative damage, mitochondrial apoptosis, and transcriptional factors in response to hypoxia were assessed by Western blot and immunohistochemistry in brain tissue. Four groups of rats were used: (1) normoxic (NOR), (2) exposed to ASH (FiO2 7% for 6 h), (3) exposed to IHH for 3 h per day over 8 days at 460 mmHg, and (4) ASH preconditioned after IHH. Results: ASH animals underwent increased oxidative-stress-related parameters, an upregulation in apoptotic proteins and had astrocytes with phenotype forms compatible with severe diffuse reactive astrogliosis. These effects were attenuated and even prevented when the animals were preconditioned with IHH. These changes paralleled the inhibition of NF-κB expression and the increase of erythropoietin (EPO) levels in the brain. Conclusions: IHH exerted neuroprotection against ASH-induced oxidative injury by preventing oxidative stress and inhibiting the apoptotic cascade, which was associated with NF-κB downregulation and EPO upregulation.


2021 ◽  
Vol 18 ◽  
Author(s):  
Sobia Manzoor ◽  
Ayesha Khan ◽  
Beena Hasan ◽  
Shamim Mushtaq ◽  
Nikhat Ahmed

Background: Oxidative damage contributes to the pathophysiology of schizophrenia (SZ). Redox imbalance may lead to increased lipid peroxidation, which produces toxic aldehydes like 4-hydroxynonenal (4-HNE) ultimately leading to oxidative stress. Conversely, implications of oxidative stress points towards an alteration in HNE-protein adducts and activities of enzymatic and antioxidant systems in schizophrenia. Objectives: Present study focuses on identification of HNE-protein adducts and its related molecular consequences in schizophrenia pathology due to oxidative stress, particularly lipid peroxidation. Material and Methods: Oxyblotting was performed on seven autopsied brain samples each from cortex and hippocampus region of schizophrenia patients and their respective normal healthy controls. Additionally, thiobarbituric acid substances (TBARS), reduced glutathione (GSH) levels and catalase (CAT) activities associated with oxidative stress, were also estimated. Results: Obtained results indicates substantially higher levels of oxidative stress in schizophrenia patients than healthy control group represented by elevated expression of HNE-protein adducts. Interestingly, hippocampus region of schizophrenia brain shows increased HNE protein adducts compared to cortex. An increase in catalase activity (4.8876 ± 1.7123) whereas decrease in antioxidant GSH levels (0.213 ± 0.015µmol/ml) have been observed in SZ brain. Elevated TBARS level (0.3801 ± 0.0532ug/ml) were obtained in brain regions SZ patients compared with their controls that reflects an increased lipid peroxidation (LPO). Conclusion: Conclusion: We propose the role of HNE modified proteins possibly associated with the pathology of schizophrenia. Our data revealed increase lipid peroxidation as a consequence of increased TBARS production. Furthermore, altered cellular antioxidants pathways related to GSH and CAT also highlight the involvement of oxidative stress in schizophrenia pathology.


Author(s):  
Fasna K. A. ◽  
Geetha N. ◽  
Jean Maliekkal

Background: Ageing is characterized by a gradual decline in body functions and decreased ability to maintain homeostasis. The free radical theory of ageing proposed by Harman D states that ageing is a result of cumulative damage incurred by free radical reactions. Free radicals are highly reactive molecular species with unpaired electrons; generated in the body by several physiological processes. Prime target to free radical attack are the polyunsaturated fatty acids of cell membranes causing lipid peroxidation. The free radicals are neutralized by the exogenous and endogenous antioxidant systems. Oxidative stress occurs when large number of free radicals are produced or the antioxidant activity is impaired. The present study is focused to find out the role of oxidative stress in ageing.Methods: A cross sectional observational study was undertaken to assess the oxidative stress in ageing; by determining the levels of lipid peroxidation product- malondialdehyde (MDA), the antioxidants- superoxide dismutase (SOD) and ceruloplasmin in various age groups. 150 healthy subjects were selected randomly and categorised into three different age groups of 20-30 years, 40-59 years and 60-90 years; with 50 subjects in each group. Results were expressed as mean ± standard deviation.Results: a significant elevation in serum MDA level and a decline in SOD were observed in 40-59 years and 60-90 years age groups. However, an elevated ceruloplasmin level was found in the above age groups.Conclusions: Aforementioned observations are suggestive of an association between oxidative stress and the progression of ageing process.


2021 ◽  
pp. 148-156
Author(s):  
I. D. Dubinets ◽  
M. Yu. Korkmazov ◽  
A. I. Sinitskii ◽  
E. I. Danshova ◽  
I. N. Skirpichnikov ◽  
...  

Introduction. According to the literature, oxidative stress is described as one of the main factors in the pathogenesis of chronic suppurative otitis media, supporting the inflammatory process at the local level. The transition of inflammatory mediators to the systemic level is associated with the risk of developing ear purulent-destructive complications. The study of the products of lipid peroxidation in comparison with morphological changes in the structures of the temporal bone will justify the tactics of the operation.Aim. Comparison of the levels of lipid peroxidation products at the local and systemic levels in chronic suppurative otitis media, depending on the nature of pathomorphological changes in the structures of the temporal bone.Materials and methods. A prospective study of 130 patients with chronic suppurative otitis media at the age of 20-62 years with a verified diagnosis of chronic suppurative otitis media, admitted for surgical treatment, was carried out. To study the indicators of oxidative stress at the systemic level, the blood serum of patients was used; at the local level, the bone biomaterial obtained from patients during the surgical treatment of chronic suppurative otitis media was used. The quantitative determination of the primary, secondary and final products of peroxidation was carried out in the groups of patients with separate registration of lipoperoxides in the heptane and isopropanol phases of the lipid extract by spectrophotometry.Results and discussion. In the observation of patients with morphological signs of purulent destruction of the temporal bone, not only a local level of inflammation activity, but also a systemic level of an unfavorable outcome was revealed in two variants: osteoproliferation or osteonecrosis of the bone tissue of the temporal bone in chronic purulent otitis media with a constant threat to the patient's life due to intracranial purulent complications.Conclusion. The appearance in low concentrations of lipid peroxidation products in serum in patients with chronic purulent otitis media substantiates the need for a behind-the-ear approach in reconstructive-sanitizing otosurgery even with minimal clinical manifestations and CT scan data, since at the preclinical level it confirms the osteonecrotic type of bone remodeling with the risk of delayed death.


2012 ◽  
Vol 6 (4) ◽  
pp. 333-337 ◽  
Author(s):  
M. S. Kislin ◽  
S. A. Stroev ◽  
T. S. Gluschenko ◽  
E. I. Tyulkova ◽  
M. Pelto-Huikko ◽  
...  

Crustaceana ◽  
2011 ◽  
Vol 84 (10) ◽  
pp. 1197-1210 ◽  

AbstractThe objective of this study was to determine the effect of sublethal copper concentrations on certain antioxidant enzymes and lipid peroxidation products in the postlarvae (PL) of Penaeus indicus when subjected to short- and long-term exposure in the laboratory. The PL of P. indicus were exposed to 0.1641 ppm (sublethal) copper for a period of 30 days along with a parallel control. Sampling was carried out at six different time intervals, i.e., 24, 48, and 96 hrs (shortterm), and 10, 20, and 30 days (long-term). Variations in the activity of the antioxidant enzymes, namely, catalase (CAT) and superoxide dismutase (SOD), as well as lipid peroxidation products (LPP) were measured as biomarkers of metal toxicity. Our results showed a significant (P < 0.05) increase in LPP (indicating oxidative stress) and CAT activity (indicating an adaptive response of the PL for protection against oxidative stress) in the exposed PL for all periods of exposure. However, SOD activity significantly (P < 0.05) decreased on 20 and 30 days exposure, indicating susceptibility of the PL to oxidative stress upon long-term exposure. Therefore, CAT can serve as a better biomarker of oxidative stress than SOD to long-term copper toxicity. Our results indicate that copper contamination causes oxidative stress even at sublethal doses in Penaeus indicus PL, which can thus be used as a potential biomarker of copper toxicity for long-term monitoring of coastal marine ecosystems.


1999 ◽  
Vol 7 (1) ◽  
pp. 31-51 ◽  
Author(s):  
Klara D Vichnevetskaia ◽  
D N Roy

Increased levels of active oxygen species or free radicals can create an oxidative stress. Concentration of free radicals in living cells increases as a result of exposure to environmental stresses that lead to aging, carcinogenesis, and immunodeficiencies in animals, and membrane leakage, senescence, chlorophyll destruction, and decreased photosynthesis in plants. The antioxidative system of higher plants consists of enzymes, low molecular weight compounds (among them peptides, vitamins, flavonoids, phenolic acids, alkaloids, etc.), and integrated detoxification chains. Enzymatic defense in plants include enzymes capable of removing, neutralizing, or scavenging oxy-intermediates. Catalases and superoxide dismutases are the most efficient antioxidant enzymes. Free radicals cause cell damage by a lipid peroxidation mechanism, which results in a blockade of natural antioxidant systems. Application of synthetic antioxidants can assist in coping with oxidative stress. There are very few publications on effects of synthetic antioxidants on plant growth and physiology. One of the examples of such synthetic antioxidant is 2-methyl-4-dimethylaminomethyl-5-hydroxybenzimidazole (Ambiol), which substantially promoted growth of agricultural and forestry plant species. Ambiol also demonstrated antitranspirant properties, increasing drought tolerance of conifers and agricultural species. The response of plants to Ambiol is under high genetic control. The identification of genes responsible for the reaction of plants to Ambiol may lead to attempts in genetic engineering of organisms with increased tolerance to oxidative stress. It seems impossible to find a universal scavenger trapping all free radicals active in the organism. However, analysis of the structure–activity relationships in antioxidants can contribute to the search for effective antioxidants.Key words: oxidative stress, lipid peroxidation, free radicals, natural and synthetic antioxidants, Ambiol.


2015 ◽  
Vol 238 (3) ◽  
pp. 53-59 ◽  
Author(s):  
Marieke Teppner ◽  
Franziska Böss ◽  
Beat Ernst ◽  
Axel Pähler

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