scholarly journals Cytoplasmic superoxide dismutase activity is a sensitive indicator of the antioxidant status of the rat liver and brain

2014 ◽  
Vol 60 (1) ◽  
pp. 63-71 ◽  
Author(s):  
T.V. Sirota ◽  
M.V. Zakharchenko ◽  
M.N. Kondrashova

Several parameters of the cytoplasmic enzymatic antioxidant system of the liver and brain of the rat have been investigated under conditions of immobilization stress and of an antioxidant preparation in the diet of animals. These included superoxide dismutase (SOD) and glutathione reductase (GR) activities and nonspecific NADPH oxidation. Only changes in the activity of SOD both in the liver and brain were revealed. In the liver of animals that receive no preparation, a decrease in the activity of SOD after 30-min immobilization and its restoration after a 360-min immobilization were observed. In the brain, the activity of SOD decreased only in preconditioned animals after 30 and 360 min of exposure to stress. In addition, the activity of SOD in the brain of preconditioned animals, both stressed and unstressed, was lower than in the corresponding groups of control animals. It is probable that, under the conditions of immobilization stress, the level of reactive oxygen species (ROS) and as a consequence the activity of SOD decrease. The intake of an antioxidant preparation under these conditions seems to be not correct.

Author(s):  
Abderrakib Zahid

Reactive oxygen species (ROS) production causes damage, and to better deal with the toxic effects of ROS, the seeds have developed detoxification mechanisms, among which the enzymes of the antioxidant system (catalase, superoxide dismutase, ascorbate peroxidase). Another result supports the link between ROS and redox regulation catalyzed by redoxin family in the seed. Among which, thioredoxins (Trxs) and peroxiredoxins (Prxs), particularly 1-Cys-Prx, expressed during maturation and germination steps.


2001 ◽  
Vol 47 (11) ◽  
pp. 987-993 ◽  
Author(s):  
Varinder K Randhawa ◽  
Fengzhen Zhou ◽  
Xiaolei Jin ◽  
Czesia Nalewajko ◽  
Donn J Kushner

Treatment with Ni(NO3)2 leads to the formation of reactive oxygen species (ROS) in the green alga Scenedesmus acutus f. alternans, causing lipid peroxidation. This effect was stronger in a Ni-sensitive strain, UTEX72, than in a Ni-resistant strain, B4. In the resistant strain, Ni induced an increased ratio of reduced to oxidized glutathione (GSH:GSSG), whereas it caused a lowered ratio in the sensitive strain. Enzymes involved in the control of ROS were studied in these strains as well as two others that have shown different degrees of nickel resistance. The resistant strain, B4, which grows while containing large amounts of internal Ni, had much higher levels of glutathione reductase and catalase than the other strains. The sensitive strain, UTEX72, had higher levels of glutathione peroxidase, superoxide dismutase, and glucose-6-phosphate dehydrogenase than did strain B4. The resistant strains, Ni-Tol and Cu-Tol, derived from strain UTEX72, which are partly able to exclude Ni, had enzyme profiles that resembled that of UTEX72 more closely than that of B4. Treatment with 10 and 100 µM Ni for 4 or 22 h had complex effects on enzyme levels in all four strains. Ni decreased glutathione reductase in B4, slightly increased it in Ni-Tol and Cu-Tol, and did not affect the low levels of this enzyme in UTEX72. Ni lowered glutathione peroxidase in B4 and either did not affect it or slightly raised it in the other strains. Ni lowered catalase in B4 and did not affect the other strains. Superoxide dismutase was raised in B4 and Ni-Tol and lowered in Cu-Tol and UTEX72, and glucose-6-phosphate dehydrogenase was lowered in all four strains. These results suggest that one major mechanism of Ni resistance, especially in strain B4, may be the ability to combat the formation of ROS when exposed to this metal, likely by maintaining a high GSH:GSSG ratio.Key words: Scenedesmus acutus f. alternans, glutathione reductase, glutathione peroxidase, catalase, superoxide dismutase, glucose-6-phosphate dehydrogenase, lipid peroxidation, nickel, reactive oxygen species.


2013 ◽  
Vol 641-642 ◽  
pp. 18-21
Author(s):  
Jiang Yan Gao ◽  
Sheng Xu ◽  
Wei Chen ◽  
Xing Yuan He

Changes of oxidative stress and antioxidant system were studied in leaves of Ginkgo biloba exposed to elevated CO2 and O3 fumigation (2006-2008), and released the gases fumigation for the natural recovery in open-top chambers (OTCs) during the growing season in 2009. Elevated CO2 had no significant effect on hydrogen peroxide (H2O2) and malondialdehyde (MDA) contents, and the activities of antioxidant enzymes in leaves of G. biloba during the gas fumigation in 2008. Elevated O3 increased significantly H2O2 and MDA contents, especially after 90 days of gas fumigation. The adverse effect or damage of elevated O3 on trees during the gas fumigation was also alleviated by the released-O3 exposure during the natural recovery. The antioxidative enzyme including superoxide dismutase (SOD), catalase (CAT) and ascorbate peroxidase (APX) activities showed higher levels under the natural recovery than under the gas fumigation, which may be a helpful response to scavenging reactive oxygen species (ROS). The results also indicated that future alleviating the emissions of CO2 and O3 would differentially affect the antioxidant system in plants.


2021 ◽  
Vol 12 ◽  
Author(s):  
Qian Zhang ◽  
Jinwei Dai ◽  
Zhibing Song ◽  
Yuchen Guo ◽  
Shanshan Deng ◽  
...  

MQ (l-methionyl-l-glutamic acid), anti-inflammatory dipeptide, is one of the metabolites of monocyte locomotion inhibitory factor, a thermostable pentapeptide secreted by Entamoeba histolytica. Monocyte locomotion inhibitory factor injection has been approved as an investigational drug for the potential neural protection in acute ischemic stroke. This study further investigated the neuroprotective effect of MQ in ischemic brain damage. Ischemia-reperfusion injury of the brain was induced in the rat model by middle cerebral artery occlusion. 2,3,5-triphenyltetrazolium chloride staining assay was used to measure cerebral infarction areas in rats. Laser Doppler measurement instrument was used to detect blood flow changes in the rat model. Nissl staining and NeuN staining were utilized to observe the numbers and structures of neuron cells, and the pathological changes in the brain tissues were examined by hematoxylin–eosin staining. Terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling (TUNEL) staining was used to assess cell apoptosis. The changes in oxidative stress indexes, superoxide dismutase and malondialdehyde (MDA), were measured in serum. Methyl thiazolyl tetrazolium was used to measure the survival rates of PC12 cells. Flow cytometry assessed the apoptosis rates and the levels of reactive oxygen species. Real-time PCR was used to evaluate the mRNA expression levels, and Western blotting was used to analyze the changes in protein levels of p-JNK, Bax, cleaved Caspase3. We revealed that MQ improved neurobehavior, decreased cerebral infarction areas, altered blood flow volume, and the morphology of the cortex and hippocampus. On the other hand, it decreased the apoptosis of cortical neurons and the levels of MDA, and increased the levels of superoxide dismutase. In vitro studies demonstrated that MQ enhanced the cell survival rates and decreased the levels of reactive oxygen species. Compared to the oxygen-glucose deprivation/reperfusion group, the protein and mRNA expressions of p-JNK, Bax, cleaved Caspase3 was decreased significantly. These findings suggested that MQ exerts a neuroprotective effect in cerebral ischemia by blocking apoptosis via the p-JNK/Bax pathway.


2021 ◽  
Vol 46 (1) ◽  
pp. 77-87
Author(s):  
Arnaud Tauffenberger ◽  
Pierre J. Magistretti

AbstractCellular homeostasis plays a critical role in how an organism will develop and age. Disruption of this fragile equilibrium is often associated with health degradation and ultimately, death. Reactive oxygen species (ROS) have been closely associated with health decline and neurological disorders, such as Alzheimer’s disease or Parkinson’s disease. ROS were first identified as by-products of the cellular activity, mainly mitochondrial respiration, and their high reactivity is linked to a disruption of macromolecules such as proteins, lipids and DNA. More recent research suggests more complex function of ROS, reaching far beyond the cellular dysfunction. ROS are active actors in most of the signaling cascades involved in cell development, proliferation and survival, constituting important second messengers. In the brain, their impact on neurons and astrocytes has been associated with synaptic plasticity and neuron survival. This review provides an overview of ROS function in cell signaling in the context of aging and degeneration in the brain and guarding the fragile balance between health and disease.


2010 ◽  
Vol 110 (6) ◽  
pp. 633-637 ◽  
Author(s):  
Chartchalerm Isarankura-Na-Ayudhya ◽  
Sakda Yainoy ◽  
Tanawut Tantimongcolwat ◽  
Leif Bülow ◽  
Virapong Prachayasittikul

1997 ◽  
Vol 6 (5-6) ◽  
pp. 369-374
Author(s):  
Y. Oyanagui

Anti-inflammatory actions of two anti-allergic drugs, alone or with dexamethasone (Dex) were examined in two models, because inflammation is claimed to be important for allergic events, especially for asthma. Cromoglycate and nedocromil were tested in ischaemic- and histamineinduced paw oedema models of mice. These antiallergic drugs (1–100 mg/kg, i.p.) failed to suppress these oedemata, but enhanced the suppressions by a low dose of dexamethasone (0.1 mg/kg, s.c.) at 3–8 h after Dex injection. The mode of effects by anti-allergic drugs resembled that of a natural antioxidant (α-tocopherol, β-carotene etc.), and was different from that of an immunosuppressant like FK506. The enhancing potencies of the two anti-allergic drugs were similar at 6 h after Dex in both oedemata, and were diminished by superoxide dismutase (SOD) or catalase (i.p.). Cycloheximide completely abolished suppressions. Nedocromil, but not cromoglycate, inhibits inflammatory events. Therefore, there are common unknown actions by which the two anti-allergics enhance suppression by Dex. A possible mechanism of this action was supposed to enhance the superoxide and/or hydrogen peroxide-dependent glucocorticoid receptor (GR) signalling in the target cells.


2021 ◽  
Vol 86 (7) ◽  
pp. 878-886
Author(s):  
Vitaly D. Samuilov ◽  
Dmitry B. Kiselevsky ◽  
Elena V. Dzyubinskaya ◽  
Olga Yu. Frolova

Open Biology ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 210013
Author(s):  
Vyshnavy Balendra ◽  
Sandeep Kumar Singh

Oxidative stress, the imbalance of the antioxidant system, results in an accumulation of neurotoxic proteins in Alzheimer's disease (AD). The antioxidant system is composed of exogenous and endogenous antioxidants to maintain homeostasis. Superoxide dismutase (SOD) is an endogenous enzymatic antioxidant that converts superoxide ions to hydrogen peroxide in cells. SOD supplementation in mice prevented cognitive decline in stress-induced cells by reducing lipid peroxidation and maintaining neurogenesis in the hippocampus. Furthermore, SOD decreased expression of BACE1 while reducing plaque burden in the brain. Additionally, Astaxanthin (AST), a potent exogenous carotenoid, scavenges superoxide anion radicals. Mice treated with AST showed slower memory decline and decreased depositions of amyloid-beta (A β ) and tau protein. Currently, the neuroprotective potential of these supplements has only been examined separately in studies. However, a single antioxidant cannot sufficiently resist oxidative damage to the brain, therefore, a combinatory approach is proposed as a relevant therapy for ameliorating pathological changes in AD.


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