Prevention of cognitive deficits and brain oxidative stress with superoxide dismutase/catalase mimetics in aged mice

Administration of streptozotocin (STZ) through intracerebroventricular (ICV) route manifests AD symptoms in rats. STZ deregulates the control over GSK-3 and eNOS activities through disruption of phosphoinositides mediated signaling. We attempted to elucidate the functions of GSK-3 and eNOS in memory enhancing activity of ellagic acid (EGA) in STZ (ICV) triggered AD type dementia. A 3 mg/kg dose of STZ was injected gently in lateral cerebral ventricles of rats on day 1 and 3. The rats were given EGA (35 mg/kg b.w.) through oral route for four weeks daily. LiCl (GSK-3 inhibitor) and L-Arginine (NO precursor) were administered for four weeks to explore the modulation of GSK-3 and eNOS respectively by EGA in STZ (ICV) injected rats. MWM and EPM paradigms were utilized for evaluation of memory of rats. The rats were sacrificed on day 28 to determine markers of oxidative stress (TBARS, GSH, SOD, CAT), nitrite, AChE, LDH, TNF-α and eNOS in brain. STZ (ICV) initiated cognitive deficits through enhancement of brain oxidative stress, nitrite, TNF-α, AChE, LDH activity and reduction in eNOS levels. EGA attenuated the rise in oxidative stress, inflammation and LDH activity in STZ (ICV) treated rats. Decrease in nitrite content, AChE activity and resurrection of eNOS activity by EGA averted STZ (ICV) induced memory dysfunction in rats. Chronic inhibition of GSK-3 by LiCl (100 mg/kg, i.p.) enhanced these effects of EGA in STZ (ICV) injected rats which thereby exhibited marked cognitive improvement. L-Arginine group manifested inflation in brain oxidative stress, TNF-α content, AChE and LDH activities. L-Arginine (200 mg/kg, i.p.) surged the nitrite content even though eNOS expression was diminished in brain of EGA and STZ (ICV) administered rats resulting in profound loss of memory. It can be concluded that GSK-3 and eNOS are involved in memory enhancing activity of EGA in STZ (ICV) injected rats.

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State of the enzyme link of antioxidant protection in boys with hypoandrogenism

Problems of Uninterrupted Medical Training and Science ◽

10.31071/promedosvity2020.04.032 ◽

2020 ◽

Vol 40 (4) ◽

pp. 32-36

Author(s):

L. K. Parkhomenko ◽

◽

L. A. Strashok ◽

S. I. Turchina ◽

G. V. Kosovtsova ◽

...

Keyword(s):

Oxidative Stress ◽

Superoxide Dismutase ◽

Free Radical ◽

Glutathione Peroxidase ◽

Free Radical Oxidation ◽

Conjugated Dienes ◽

Delayed Puberty ◽

Control Group ◽

Antioxidant Protection ◽

Radical Oxidation

Recently, interest in the problem of free radical oxidation in biological membranes, which is directly related to both the normal functioning of cells and the occurrence, course and outcome of many pathological conditions, has increased again in clinical medicine. The aim was to determine the role and impact of antioxidant defense in boys with hypoandrogenism. The study involved 75 adolescents with hypoandrogenism aged 13–18 years, who underwent a complex of clinical and laboratory examinations. All patients were conducted complex of anthropometric research and determination of the degree of delayed puberty, laboratory and instrumental examination. Free radical oxidation was determined by the levels of malondialdehyde, conjugated dienes, carbonated proteins, superoxide dismutase and catalase in the serum, and restored glutathione and glutathione peroxidase in whole blood. Based on their determination, the coefficient of oxidative stress was calculated. Statistical processing of results was performed using parametric and nonparametric methods. The study of indicators of the free radical oxidation process found that adolescents with hypoandrogenism have multidirectional changes in the oxidation of proteins and lipids, namely: the level of conjugated dienes increases, the concentration of malondialdehyde remains at the level of the control group, and the level of carbonated proteins tends to decrease. As for the activity of antioxidant protection enzymes, a significant decrease in the level of glutathione peroxidase was detected, while the level of superoxide dismutase and catalase remained at the level of normative indicators. Oxidative stress accompanies and is one of the pathogenetic links in the formation or maintenance of the state of hypoandrogenism in boys. This requires the use of antioxidants, the complex of which must be selected individually.

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Faculty Opinions recommendation of Posttranscriptional induction of two Cu/Zn superoxide dismutase genes in Arabidopsis is mediated by downregulation of miR398 and important for oxidative stress tolerance.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1033617.387847 ◽

2006 ◽

Author(s):

Eric Lam

Keyword(s):

Oxidative Stress ◽

Superoxide Dismutase ◽

Stress Tolerance ◽

Oxidative Stress Tolerance

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Assessment of Superoxide Dismutase and Catalase Evolution in Different Stages of an Experimental Endometriosis

Revista de Chimie ◽

10.37358/rc.17.6.5678 ◽

2017 ◽

Vol 68 (6) ◽

pp. 1381-1383

Author(s):

Allia Sindilar ◽

Carmen Lacramioara Zamfir ◽

Eusebiu Viorel Sindilar ◽

Alin Constantin Pinzariu ◽

Eduard Crauciuc ◽

...

Keyword(s):

Oxidative Stress ◽

Superoxide Dismutase ◽

Antioxidant Enzymes ◽

Reproductive Function ◽

Female Rats ◽

Oxygen Species ◽

Efficient Treatment ◽

Endometrial Cells ◽

Gynecological Disorder ◽

The Impact

Endometriosis is described as a gynecological disorder characterized by the presence of endometrial tissue outside the uterus; extensively explored because of its increasing incidency, with an indubitable diagnostic only after invasive surgery, with no efficient treatment, it has still many aspects to be elucidated. A growing body of facts sustain oxidative stress as a crucial factor between the numerous incriminated factors implicated in endometriosis ethiopathogeny. Reactive oxygen species(ROS) act to decline reproductive function. Our study intends to determine if an experimental model of endometriosis may be useful to assess the impact of oxidative stress on endometrial cells; we have used a murine model of 18 adult Wistar female rats. A fragment from their left uterine horn was implanted in the abdominal wall. After 4 weeks, a laparatomy was performed, 5 endometrial implants were removed, followed by biochemical tissue assay of superoxide dismutase(SOD) and catalase(CAT). At the end of the experiment, the rats were sacrificed, the implants were removed for histopathological exam and biochemical assay of antioxidant enzymes. The results revealed decreased levels of antioxidant enzymes, pointing on significant oxidative stress involvement.

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PROTECTIVE EFFECT OF CAPSAICIN AGAINST BRAIN OXIDATIVE STRESS INDUCED BY HEAT STRESS IN APRI RABBITS

Egyptian Journal of Rabbit Science ◽

10.21608/ejrs.2018.40419 ◽

2018 ◽

Vol 0 (0) ◽

pp. 1-22

Keyword(s):

Oxidative Stress ◽

Heat Stress ◽

Protective Effect ◽

Brain Oxidative Stress

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Effect of Fluoxetine on Brain Oxidative Stress, Neuronal Damage and Behavioural Induced in the Olfactory Bulbectomy Model of Depression

Letters in Drug Design & Discovery ◽

10.2174/157018007784620013 ◽

2007 ◽

Vol 4 (4) ◽

pp. 305-310 ◽

Cited By ~ 6

Author(s):

Isaac Tunez ◽

Francisco Medina ◽

Ignacio Jimena ◽

María del Munoz

Keyword(s):

Oxidative Stress ◽

Neuronal Damage ◽

Olfactory Bulbectomy ◽

Brain Oxidative Stress

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Diazoxide Modulates Cardiac Hypertrophy by Targeting H2O2 Generation and Mitochondrial Superoxide Dismutase Activity

Current Molecular Pharmacology ◽

10.2174/1874467212666190723144006 ◽

2020 ◽

Vol 13 (1) ◽

pp. 76-83

Author(s):

Aline Maria Brito Lucas ◽

Joana Varlla de Lacerda Alexandre ◽

Maria Thalyne Silva Araújo ◽

Cicera Edna Barbosa David ◽

Yuana Ivia Ponte Viana ◽

...

Keyword(s):

Oxidative Stress ◽

Superoxide Dismutase ◽

Cardiac Hypertrophy ◽

Superoxide Dismutase Activity ◽

Heart Weight ◽

Pharmacological Intervention ◽

Wall Thickening ◽

H2o2 Production ◽

Mitochondrial Superoxide ◽

Mitochondrial Superoxide Dismutase

Background: Cardiac hypertrophy involves marked wall thickening or chamber enlargement. If sustained, this condition will lead to dysfunctional mitochondria and oxidative stress. Mitochondria have ATP-sensitive K+ channels (mitoKATP) in the inner membrane that modulate the redox status of the cell. Objective: We investigated the in vivo effects of mitoKATP opening on oxidative stress in isoproterenol- induced cardiac hypertrophy. Methods: Cardiac hypertrophy was induced in Swiss mice treated intraperitoneally with isoproterenol (ISO - 30 mg/kg/day) for 8 days. From day 4, diazoxide (DZX - 5 mg/kg/day) was used in order to open mitoKATP (a clinically relevant therapy scheme) and 5-hydroxydecanoate (5HD - 5 mg/kg/day) or glibenclamide (GLI - 3 mg/kg/day) were used as mitoKATP blockers. Results: Isoproterenol-treated mice had elevated heart weight/tibia length ratios (HW/TL). Additionally, hypertrophic hearts had elevated levels of carbonylated proteins and Thiobarbituric Acid Reactive Substances (TBARS), markers of protein and lipid oxidation. In contrast, mitoKATP opening with DZX avoided ISO effects on gross hypertrophic markers (HW/TL), carbonylated proteins and TBARS, in a manner reversed by 5HD and GLI. Moreover, DZX improved mitochondrial superoxide dismutase activity. This effect was also blocked by 5HD and GLI. Additionally, ex vivo treatment of isoproterenol- induced hypertrophic cardiac tissue with DZX decreased H2O2 production in a manner sensitive to 5HD, indicating that this drug also acutely avoids oxidative stress. Conclusion: Our results suggest that diazoxide blocks oxidative stress and reverses cardiac hypertrophy. This pharmacological intervention could be a potential therapeutic strategy to prevent oxidative stress associated with cardiac hypertrophy.

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