Administration Dependent Antioxidant Effect ofCarica papayaSeeds Water Extract

Carica papayais widely used in folk medicine as herbal remedy to prevent, protect against, and cure several diseases. These curative properties are based on the presence in different parts of the plant of phytochemical nutrients with antioxidant effect. Seeds are the less exploited part; thus this study is aimed at assessing the antioxidant activities of theC. papayaseeds water extract against hydrogen peroxide (H2O2) oxidative stress in human skin Detroit 550 fibroblasts.C. papayaseeds water extract is not toxic and acts as a potent free radical scavenger, providing protection to Detroit 550 fibroblasts that underwent H2O2oxidative stress. Data show that (i) the maximum protective effect is achieved by the simultaneous administration of the extract with 1 mM H2O2; (ii) the extract in presence of an oxidative stress does not increase catalase activity and prevents the release of cytochrome C and the inner mitochondrial transmembrane potential(Δψm)loss; (iii) the extract is more efficient than vitamin C to hamper the oxidative damage; (iv) the purified subfractions of the seeds water extract exert the same antioxidant effect of whole extract. In conclusion,C. papayaseeds water extract is potentially useful for protection against oxidative stress.

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Antioxidant defense responses to sleep loss and sleep recovery

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00565.2004 ◽

2005 ◽

Vol 288 (2) ◽

pp. R374-R383 ◽

Cited By ~ 86

Author(s):

Carol A. Everson ◽

Christa D. Laatsch ◽

Neil Hogg

Keyword(s):

Oxidative Stress ◽

Sleep Deprivation ◽

Cell Injury ◽

Antioxidant Activities ◽

Defense Responses ◽

Free Radical Scavenger ◽

Pentose Phosphate ◽

Radical Scavenger ◽

Enzymatic Antioxidants ◽

Recovery Sleep

Sleep deprivation in humans is widely believed to impair health, and sleep is thought to have powerful restorative properties. The specific physical and biochemical factors and processes mediating these outcomes, however, are poorly elucidated. Sleep deprivation in the animal model produces a condition that eventually becomes highly lethal, lacks specific localization, and is reversible with sleep, implying mediation by a biochemical abnormality. Metabolic and immunological consequences of sleep deprivation point to a high potential for antioxidant imbalance. The objective, therefore, was to study glutathione content in the liver, heart, and lung, because glutathione is considered a major free radical scavenger that reflects the degree to which a tissue has been oxidatively challenged. We also investigated major enzymatic antioxidants, including catalase and glutathione peroxidase, as well as indexes of glutathione recycling. Catalase activity and glutathione content, which normally are tightly regulated, were both decreased in liver by 23–36% by 5 and 10 days of sleep deprivation. Such levels are associated with impaired health in other animal models of oxidative stress-associated disease. The decreases were accompanied by markers of generalized cell injury and absence of responses by the other enzymatic antioxidants under study. Enzymatic activities in the heart indicated an increased rate of oxidative pentose phosphate pathway activity during sleep deprivation. Recovery sleep normalized antioxidant content in liver and enhanced enzymatic antioxidant activities in both the liver and the heart. The present results link uncompensated oxidative stress to health effects induced by sleep deprivation and provide evidence that restoration of antioxidant balance is a property of recovery sleep.

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Traumatic Brain Injury: Oxidative Stress and Novel Anti-Oxidants Such as Mitoquinone and Edaravone

Antioxidants ◽

10.3390/antiox9100943 ◽

2020 ◽

Vol 9 (10) ◽

pp. 943 ◽

Cited By ~ 1

Author(s):

Helene Ismail ◽

Zaynab Shakkour ◽

Maha Tabet ◽

Samar Abdelhady ◽

Abir Kobaisi ◽

...

Keyword(s):

Oxidative Stress ◽

Traumatic Brain Injury ◽

Brain Injury ◽

Neuroprotective Effect ◽

Treatment Options ◽

Free Radical Scavenger ◽

Health Concern ◽

Radical Scavenger ◽

History Of ◽

Ionic Imbalance

Traumatic brain injury (TBI) is a major health concern worldwide and is classified based on severity into mild, moderate, and severe. The mechanical injury in TBI leads to a metabolic and ionic imbalance, which eventually leads to excessive production of reactive oxygen species (ROS) and a state of oxidative stress. To date, no drug has been approved by the food and drug administration (FDA) for the treatment of TBI. Nevertheless, it is thought that targeting the pathology mechanisms would alleviate the consequences of TBI. For that purpose, antioxidants have been considered as treatment options in TBI and were shown to have a neuroprotective effect. In this review, we will discuss oxidative stress in TBI, the history of antioxidant utilization in the treatment of TBI, and we will focus on two novel antioxidants, mitoquinone (MitoQ) and edaravone. MitoQ can cross the blood brain barrier and cellular membranes to accumulate in the mitochondria and is thought to activate the Nrf2/ARE pathway leading to an increase in the expression of antioxidant enzymes. Edaravone is a free radical scavenger that leads to the mitigation of damage resulting from oxidative stress with a possible association to the activation of the Nrf2/ARE pathway as well.

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Cellular Cysteine Network and Neurodegeneration

Quality Control of Cellular Protein in Neurodegenerative Disorders - Advances in Medical Diagnosis, Treatment, and Care ◽

10.4018/978-1-7998-1317-0.ch012 ◽

2020 ◽

pp. 303-325

Author(s):

Shubhangi H. Pawar ◽

Vishal S. Gulecha ◽

Manoj S. Mahajan ◽

Aman B Upaganiawar ◽

Chandrashekhar D. Upasani

Keyword(s):

Oxidative Stress ◽

Defense Mechanism ◽

Free Radical Scavenger ◽

Cellular Damage ◽

Radical Scavenger ◽

Post Translational Modifications ◽

Cellular Defense ◽

Brain Antioxidants ◽

The Brain ◽

Oxidative Species

Oxidative stress is strongly linked to neurodegeneration and oxidative species can modify many amino acids and proteins in the brain. Cysteine amino acid is most susceptible to oxidative post-translational modifications (PTMs). Reversible or irreversible cysteine PTMs can cause dyshomeostasis, which further continued to cellular damage. Many cysteine dependent proteins and many non-proteins using cysteine as their structural components are affected by oxidative stress. Several cysteine dependent enzymes are acting as antioxidants. Cysteine is a major contributor to glutathione (GSH) and superoxide dismutase (SOD) synthesis. Cysteine precursor N-acetylcysteine (NAC) supplementation is proven as a potent free radical scavenger and increase brain antioxidants and subsequently potentiates the natural antioxidant cellular defense mechanism. Thus, in this chapter, the authors explore the linkage of cellular cysteine networks and neurodegenerative disorders.

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Therapeutic Time Window for Edaravone Treatment of Traumatic Brain Injury in Mice

BioMed Research International ◽

10.1155/2013/379206 ◽

2013 ◽

Vol 2013 ◽

pp. 1-13 ◽

Cited By ~ 11

Author(s):

Kazuyuki Miyamoto ◽

Hirokazu Ohtaki ◽

Kenji Dohi ◽

Tomomi Tsumuraya ◽

Dandan Song ◽

...

Keyword(s):

Oxidative Stress ◽

Traumatic Brain Injury ◽

Brain Injury ◽

Neuronal Death ◽

Time Window ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Free Radical Scavenger ◽

Radical Scavenger ◽

Therapeutic Time Window

Traumatic brain injury (TBI) is a major cause of death and disability in young people. No effective therapy is available to ameliorate its damaging effects. Our aim was to investigate the optimal therapeutic time window of edaravone, a free radical scavenger which is currently used in Japan. We also determined the temporal profile of reactive oxygen species (ROS) production, oxidative stress, and neuronal death. Male C57Bl/6 mice were subjected to a controlled cortical impact (CCI). Edaravone (3.0 mg/kg), or vehicle, was administered intravenously at 0, 3, or 6 hours following CCI. The production of superoxide radicals (O2∙-) as a marker of ROS, of nitrotyrosine (NT) as an indicator of oxidative stress, and neuronal death were measured for 24 hours following CCI. Superoxide radical production was clearly evident 3 hours after CCI, with oxidative stress and neuronal cell death becoming apparent after 6 hours. Edaravone administration after CCI resulted in a significant reduction in the injury volume and oxidative stress, particularly at the 3-hour time point. Moreover, the greatest decrease inO2∙-levels was observed when edaravone was administered 3 hours following CCI. These findings suggest that edaravone could prove clinically useful to ameliorate the devastating effects of TBI.

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Day and Night GSH and MDA Levels in Healthy Adults and Effects of Different Doses of Melatonin on These Parameters

International Journal of Cell Biology ◽

10.1155/2011/404591 ◽

2011 ◽

Vol 2011 ◽

pp. 1-5 ◽

Cited By ~ 15

Author(s):

Shilpa Chakravarty ◽

Syed Ibrahim Rizvi

Keyword(s):

Oxidative Stress ◽

Membrane Lipid ◽

Free Radical Scavenger ◽

Radical Scavenger ◽

Secretory Product ◽

Therapeutic Implications ◽

Antioxidative Function ◽

Reliable Marker

The pineal secretory product melatonin (chemically, N-acetyl-5-methoxytryptamine) acts as an effective antioxidant and free-radical scavenger and plays an important role in several physiological functions such as sleep induction, immunomodulation, cardiovascular protection, thermoregulation, neuroprotection, tumor-suppression and oncostasis. Membrane lipid-peroxidation in terms of malondialdehyde (MDA) and intracellular glutathione (GSH) is considered to be a reliable marker of oxidative stress. The present work was undertaken to study the modulating effect of melatonin on MDA and GSH in human erythrocytes during day and night. Our observation shows the modulation of these two biomarkers by melatonin, and this may have important therapeutic implications.In vitrodose-dependent effect of melatonin also showed variation during day and night. We explain our observations on the basis of melatonin's antioxidative function and its effect on the fluidity of plasma membrane of red blood cells. Rhythmic modulation of MDA and GSH contents emphasized the role of melatonin as an antioxidant and its function against oxidative stress.

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Antioxidant and Anti Aging Assays of Oryza sativa Extracts, Vanillin and Coumaric Acid

Journal of Natural Remedies ◽

10.18311/jnr/2016/7220 ◽

2016 ◽

Vol 16 (3) ◽

pp. 88 ◽

Cited By ~ 8

Author(s):

Wahyu Widowati ◽

Nurul Fauziah ◽

Heddy Herdiman ◽

Merry Afni ◽

Ervi Afifah ◽

...

Keyword(s):

Oryza Sativa ◽

Antioxidant Activities ◽

Free Radical Scavenger ◽

Radical Scavenger ◽

Phytochemical Analysis ◽

Coumaric Acid ◽

Antioxidant Power ◽

Modified Method ◽

Reducing Activity ◽

High Level

Aging is a natural process in humans as accumulation of oxygen-derived free radicals which leads to the activation of hyaluronidase, collagenase and elastase, that can further contribute to cellular and tissue damage. Bioactive compounds from plants have been used as antioxidant that might inhibit aging processes as well. This study aimed to determine antioxidant and anti aging properties of Oryza sativa Extract (OSE), and its compounds, vanillin and coumaric acid. The phytochemical analysis of OSE was performed with Farnsworth modified method. Antioxidant activities were performed by measurement of 2,2-diphenyl 1-pichylhydazyl (DPPH) free radical scavenger, Ferric Reducing Antioxidant Power (FRAP), and 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulphonic acid) (ABTS) reducing activity, while anti aging assay were observed through inhibitory of elastase, collagenase, and hyaluronidase activities. Phytochemical analysis showed the presence of terpenoids and saponins in high level. OSE showed lowest DPPH activity (IC50 = 314.51 μg/mL) compared to vanillin (IC50 = 283 μg/mL) and coumaric acid (IC50 = 255.69 μg/mL). In ABTS assay, OSE resulted lowest activity(IC50 = 145.67 μg/mL), compared to vanillin (IC50 = 4.96 μg/mL) and coumaric acid (IC50 = 1.67 μg/mL). OSE also showed the lowest FRAP-reducing activity (21.26 μM Fe(II)/μg), compared to vanillin (35.05 μM Fe(II)/μg) and coumaric acid (48.52μM Fe(II)/μg). OSE showed the lowest collagenase, elastase, and hyaluronidase inhibitory activity (IC50 = 816.78,107.51, and 203.13 μg/mL), compared to vanillin (IC50 = 16.27, 14.46, 45.23 μg/mL respectively) and coumaric acid (IC50 = 146.89, 25.38, 8.21 μg/mL respectively). In summary, OSE possess the lowest antioxidant and anti aging activities compared to vanillin and coumaric acid.

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Melatonin protects the mouse testis against heat-induced damage

MHR Basic science of reproductive medicine ◽

10.1093/molehr/gaaa002 ◽

2020 ◽

Vol 26 (2) ◽

pp. 65-79 ◽

Cited By ~ 7

Author(s):

Pengfei Zhang ◽

Yi Zheng ◽

Yinghua Lv ◽

Fuyuan Li ◽

Lihong Su ◽

...

Keyword(s):

Oxidative Stress ◽

Heat Stress ◽

Male Fertility ◽

Reactive Oxygen Species Generation ◽

Free Radical Scavenger ◽

Testicular Atrophy ◽

Therapeutic Drug ◽

Radical Scavenger ◽

Induced Apoptosis ◽

And Oxidative Stress

Abstract Spermatogenesis, an intricate process occurring in the testis, is responsible for ongoing production of spermatozoa and thus the cornerstone of lifelong male fertility. In the testis, spermatogenesis occurs optimally at a temperature 2–4°C lower than that of the core body. Increased scrotal temperature generates testicular heat stress and later causes testicular atrophy and spermatogenic arrest, resulting in a lower sperm yield and therefore impaired male fertility. Melatonin (N-acetyl-5-methoxytryptamine), a small neuro-hormone synthesized and secreted by the pineal gland and the testis, is widely known as a potent free-radical scavenger; it has been reported that melatonin protects the testis against inflammation and reactive oxygen species generation thereby playing anti-inflammatory, -oxidative and -apoptotic roles in the testis. Nevertheless, the role of melatonin in the testicular response to heat stress has not been studied. Here, by employing a mouse model of testicular hyperthermia, we systematically investigated the testicular response to heat stress as well as the occurrence of autophagy, apoptosis and oxidative stress in the testis. Importantly, we found that pre-treatment with melatonin attenuated heat-induced apoptosis and oxidative stress in the testis. Also, post-treatment with melatonin promoted recovery of the testes from heat-induced damage, probably by maintaining the integrity of the Sertoli cell tight-junction. Thus, we for the first time provide the proof of concept that melatonin can protect the testis against heat-induced damage, supporting the potential future use of melatonin as a therapeutic drug in men for sub/infertility incurred by various testicular hyperthermia factors.

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Use of Melatonin in Oxidative Stress Related Neonatal Diseases

Antioxidants ◽

10.3390/antiox9060477 ◽

2020 ◽

Vol 9 (6) ◽

pp. 477

Author(s):

Gabriella D’Angelo ◽

Roberto Chimenz ◽

Russel J. Reiter ◽

Eloisa Gitto

Keyword(s):

Oxidative Stress ◽

Antioxidant Defense ◽

Perinatal Period ◽

Oxygen Radical ◽

Free Radical Scavenger ◽

Radical Scavenger ◽

Oxygen Species ◽

Perinatal Brain Injury ◽

Radical Generation ◽

Prophylactic Use

Reactive oxygen species have a crucial role in the pathogenesis of perinatal diseases. Exposure to inflammation, infections, or high oxygen concentrations is frequent in preterm infants, who have high free iron levels that enhance toxic radical generation and diminish antioxidant defense. The peculiar susceptibility of newborns to oxidative stress supports the prophylactic use of melatonin in preventing or decreasing oxidative stress-mediated diseases. Melatonin, an effective direct free-radical scavenger, easily diffuses through biological membranes and exerts pleiotropic activity everywhere. Multiple investigations have assessed the effectiveness of melatonin to reduce the “oxygen radical diseases of newborn” including perinatal brain injury, sepsis, chronic lung disease (CLD), and necrotizing enterocolitis (NEC). Further studies are still awaited to test melatonin activity during perinatal period.

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Pleiotropic roles of melatonin against oxidative stress mediated tissue injury in the gastrointestinal tract: An overview

Melatonin Research ◽

10.32794/mr11250027 ◽

2019 ◽

Vol 2 (2) ◽

pp. 158-184 ◽

Cited By ~ 4

Author(s):

Palash K Pal ◽

Bharati Bhattacharjee ◽

Aindrila Chattopadhyay ◽

Debasish Bandyopadhyay

Keyword(s):

Oxidative Stress ◽

Molecular Mechanisms ◽

Clinical Symptoms ◽

Tissue Injury ◽

Ischemia Reperfusion ◽

Antioxidant Properties ◽

Free Radical Scavenger ◽

Radical Scavenger ◽

Gi Tract ◽

Pathological Conditions

The excessive production of free radicals and/or reactive oxygen species (ROS) in gastrointestinal (GI) tract leads to oxidative damages in GI tissues with development of varied pathological conditions and clinical symptoms. Many endogenous as well as exogenous factors are involved in such pathogenesis, herein, focus was given to the factors of metal toxicity, non-steroidal anti-inflammatory drugs (NSAIDs), ischemia-reperfusion, consumption of high fat diet and alcohol, and different pathological conditions and diseases. Since ROS is more or less involved in the GI damages caused by these factors, therefore attempts have been made to develop appropriate therapeutic agents that possess antioxidant properties. Being a potent antioxidant and free radical scavenger, melatonin was suggested as a potent therapeutic answer to these GI damages. The discovery of different binding sites and receptors of melatonin in the GI tissues further proves its local actions to protect these tissues from oxidative stress. In the review, we attempt to try our best to summarize the current developments regarding the GI injuries caused by oxidative stress and the potential beneficial effects of melatonin on these injuries. The important molecular mechanisms associated with these changes were also highlighted in the discussion. We hope that this review will provide valuable information to consider melatonin as a suitable molecule used for GI tract protection.

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Ceria-Zirconia Antioxidant Nanoparticles Attenuate Hypoxia-Induced Acute Kidney Injury by Restoring Autophagy Flux and Alleviating Mitochondrial Damage

Journal of Biomedical Nanotechnology ◽

10.1166/jbn.2020.2948 ◽

2020 ◽

Vol 16 (7) ◽

pp. 1144-1159

Author(s):

Sang-Eun Hong ◽

Jong Hun An ◽

Seong-Lan Yu ◽

Jaeku Kang ◽

Chang Gyo Park ◽

...

Keyword(s):

Acute Kidney Injury ◽

Free Radical ◽

Antioxidant Activities ◽

Kidney Injury ◽

Mitochondrial Damage ◽

Free Radical Scavenger ◽

Radical Scavenger ◽

Autophagy Flux ◽

Novel Approach

Oxidative stress is one of the principal causes of hypoxia-induced kidney injury. The ceria nanoparticle (CNP) is known to exhibit free radical scavenger and catalytic activities. When zirconia is attached to CNPs (CZNPs), the ceria atom tends to remain in a Ce3+ form and its efficacy as a free radical scavenger thus increases. We determined the effectiveness of CNP and CZNP antioxidant activities against hypoxia-induced acute kidney injury (AKI) and observed that these nanoparticles suppress the apoptosis of hypoxic HK-2 cells by restoring autophagy flux and alleviating mitochondrial damage. In vivo experiments revealed that CZNPs effectively attenuate hypoxia-induced AKI by preserving renal structures and glomerulus function. These nanoparticles can successfully diffuse into HK-2 cells and effectively counteract reactive oxygen species (ROS) to block hypoxia-induced AKI. This suggests that these particles represent a novel approach to controlling this condition.

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