scholarly journals The Potential Use of Melatonin for Preventing Cisplatin Ototoxicity: An Insight for a Clinical Approach

2014 ◽  
Vol 2014 ◽  
pp. 1-8
Author(s):  
Juliana Gusmão de Araujo ◽  
André Luiz Lopes Sampaio ◽  
Alessandra Ramos Venosa ◽  
Carlos Augusto Costa Pires de Oliveira
Keyword(s):  
Noise Exposure ◽  
Therapeutic Option ◽  
Organ Of Corti ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Clinical Approach ◽  
Cumulative Number ◽  
Oxygen Species ◽  
History Of ◽  
Potential Use

Cisplatin, one of the most effective and potent anticancer drugs, is used in the treatment of a wide variety of both pediatric and adult malignancies. However, the chemotherapeutic use of cisplatin is limited by its serious side effects, such as nephrotoxicity and ototoxicity. Ototoxicity produced by cisplatin is usually persistent, depending on the age of the patient, the cumulative number of doses, the number of chemotherapy cycles, the history of noise exposure, and deteriorating renal function. The mechanism of the ototoxicity caused by cisplatin is based on the generation of reactive oxygen species, which interfere with the antioxidant protection of the organ of Corti. Thus, protecting the cochlea with antioxidants ameliorates ototoxicity from cisplatin. In this context, melatonin appears as a therapeutic option for preventing the ototoxic effects of cisplatin, since the research in the last decade has proven its ability to be both a direct free radical scavenger and indirect antioxidant. In this sense, some of the evidence suggesting that melatonin is efficient for combating cisplatin-induced ototoxicity is summarized and discussed in this paper.

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

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 943 ◽  
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.

scholarly journals Molecular Mechanisms of Curcumin in COVID-19 Treatment and Prevention: A Global Health Perspective

2020 ◽  
Vol 8 (10) ◽  
Author(s):  
Nathan Roberts ◽  
Robert Brown ◽  
L. Buja ◽  
Priya Weerasinghe
Keyword(s):  
Molecular Mechanisms ◽  
Curcuma Longa ◽  
Clinical Manifestations ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Respiratory Disorder ◽  
Therapeutic Effects ◽  
Electron Transfer Mechanism ◽  
Treatment And Prevention ◽  
History Of

Turmeric (Curcuma Longa) has a near 4000-year history of extensive medical use in South Asia. Its main physiologically active phytochemical is curcumin (diferuloylmethane), derived from the rhizome of turmeric. Curcumin is a hydrophobic polyphenol with a diketone moiety connecting two phenoxy rings. It is widely available, and exerts systemic and pleiotropic effects via several key mechanisms. Most famously, it is known to inhibit pro-inflammatory pathways such as PI3k/akt/NF-kB activation. It is also a potent antioxidant and free radical scavenger via a sequential proton loss electron transfer mechanism in ionizing solvents due to its extended conjugating ability across the entire molecule, and its ability to induce NRF-2. It has been implicated in the treatment of diseases ranging from asthma to various cancers, and is also a broad spectrum anti-microbial. COVID-19 is a novel beta-coronavirus that was declared a pandemic by the WHO in March, 2020. It is primarily a respiratory disorder, but it can spread hematogenously and effect many other organs such as the heart, nervous system, and kidneys. There is a significant intersection between the clinical manifestations of COVID-19 and curcumin’s therapeutic effects. In addition, curcumin has been shown to inhibit initial viral infectivity. Thus, there is potential for curcumin to safely both prevent and treat COVID-19 infection across the globe.

scholarly journals Use of Melatonin in Oxidative Stress Related Neonatal Diseases

Antioxidants ◽  
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.

Alpha-lipoic acid improves acute deltamethrin-induced toxicity in rats

2014 ◽  
Vol 92 (9) ◽  
pp. 773-779 ◽  
Author(s):  
Rania H. Abdou ◽  
Mohamed M. Abdel-Daim
Keyword(s):  
Lipoic Acid ◽  
Therapeutic Option ◽  
Antioxidant Properties ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Dependent Manner ◽  
Protective Effects ◽  
Alpha Lipoic Acid ◽  
Pre Treatment ◽  
Tissue Lipid Peroxidation

Alpha-lipoic acid (ALA) is a natural dithiol compound, with a free radical scavenger and biological antioxidant properties. The purpose of the current study was to investigate the protective effects of ALA on biochemical alteration and oxidative stress induced by acute deltamethrin intoxication in rats. Markers of liver and kidney injuries in serum of deltamethrin-intoxicated as well as ALA-pretreated rats were analyzed. Moreover, serum and (or) tissue lipid peroxidation, malondialdehyde and antioxidant markers, reduced glutathione, catalase, superoxide dismutase activity, and total antioxidant capacity were evaluated. The results showed that all parameters were altered in the intoxicated group, indicating hepatorenal oxidative damage of deltamethrin. Pre-treatment with ALA reversed the changes in most of the studied parameters in a dose-dependent manner. Histopathological and biochemical findings were parallel. It can be concluded that ALA may be a promising therapeutic option for prevention and (or) treatment of deltamethin toxicity.

scholarly journals Reactive oxygen species modulate growth of cerebral aneurysms: a study using the free radical scavenger edaravone and p47phox−/− mice

2009 ◽  
Vol 89 (7) ◽  
pp. 730-741 ◽  
Author(s):  
Tomohiro Aoki ◽  
Masaki Nishimura ◽  
Hiroharu Kataoka ◽  
Ryota Ishibashi ◽  
Kazuhiko Nozaki ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Free Radical ◽  
Cerebral Aneurysms ◽  
Reactive Oxygen ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Oxygen Species

Hypoxia and reoxygenation modulate the arrhythmogenic activity of the pulmonary vein and atrium

2011 ◽  
Vol 122 (3) ◽  
pp. 121-132 ◽  
Author(s):  
Yung-Kuo Lin ◽  
Mei-Shou Lai ◽  
Yao-Chang Chen ◽  
Chen-Chuan Cheng ◽  
Jen-Hung Huang ◽  
...  
Keyword(s):  
Spontaneous Activity ◽  
Action Potentials ◽  
Pulmonary Veins ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Oxygen Species ◽  
Potassium Channel Opener ◽  
Pharmacological Interventions ◽  
Electrophysiological Responses ◽  
Ischaemia And Reperfusion

Ischaemia and reperfusion contribute to the genesis of AF (atrial fibrillation). PVs (pulmonary veins) and the atria are important foci for AF initiation and maintenance. However, the effect of ischaemia and reperfusion on PVs and the atria has not yet been fully elucidated. In the present study, conventional microelectrodes were used to record the APs (action potentials) in isolated rabbit PV, LA (left atrium) and RA (right atrium) specimens during hypoxia and reoxygenation, and pharmacological interventions. Hypoxia reduced the PV beating rates from 1.8±0.1 to 1.3±0.2 and 0.8±0.1 Hz at 30 and 60 min respectively (n=8, P<0.005), and induced EAD (early after depolarization) in three (37.5%) of the PVs and DAD (delayed after depolarization) in one (12.5%) of the PVs. Reoxygenation increased the PV spontaneous rate to 1.4±0.2 Hz (P<0.05) and induced PV burst firings (3.5±0.1 Hz, P<0.001) in six (75%) of the PVs. Hypoxia shortened the AP duration in the LA and PVs, but not in the RA. Pretreatment with glibenclamide attenuated hypoxia-induced decreases in the PV spontaneous activity and the shortening of the LA and PV AP duration. Similar to those in hypoxia, the KATP (ATP-sensitive potassium) channel opener pinacidil (30 μM) decreased PV spontaneous activity and shortened the AP duration. Pretreatment with 5 mM N-MPG [N-(mercaptopropionyl)glycine; a hydroxyl (•OH) free-radical scavenger] or 300 μM chloramphenicol [a cytochrome P450 inhibitor that reduces ROS (reactive oxygen species)] attenuated the rate changes induced by hypoxia and reoxygenation, and also decreased the burst firing incidence. In conclusion, hypoxia and reoxygenation significantly increased PV arrhythmogenesis and induced different electrophysiological responses in the RA and LA, which may play a role in the pathophysiology of AF.

A new prospective on the role of melatonin in diabetes and its complications

2019 ◽  
Vol 40 (1) ◽  
Author(s):  
Jia Xin Mok ◽  
Jack Hau Ooi ◽  
Khuen Yen Ng ◽  
Rhun Yian Koh ◽  
Soi Moi Chye
Keyword(s):  
Oxidative Stress ◽  
Molecular Level ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Oxygen Species ◽  
The Past ◽  
Melatonin Administration ◽  
Cellular Apoptosis ◽  
Oxidative Species

Abstract Melatonin is a hormone secreted by the pineal gland under the control of the circadian rhythm, and is released in the dark and suppressed during the day. In the past decades, melatonin has been considered to be used in the treatment for diabetes mellitus (DM). This is due to a functional inter-relationship between melatonin and insulin. Elevated oxidative stress is a feature found in DM associated with diabetic neuropathy (DN), retinopathy (DR), nephropathy and cardiovascular disease. Reactive oxygen species (ROS) and nitrogen oxidative species (NOS) are usually produced in massive amounts via glucose and lipid peroxidation, and this leads to diabetic complications. At the molecular level, ROS causes damage to the biomolecules and triggers apoptosis. Melatonin, as an antioxidant and a free radical scavenger, ameliorates oxidative stress caused by ROS and NOS. Besides that, melatonin administration is proven to bring other anti-DM effects such as reducing cellular apoptosis and promoting the production of antioxidants.

scholarly journals Iron induced genotoxicity: attenuation by vitamin C and its optimization

2014 ◽  
Vol 7 (3) ◽  
pp. 154-158 ◽  
Author(s):  
Nuzhat Parveen ◽  
Shoeb Ahmad ◽  
G.G. Hammad A. Shadab
Keyword(s):  
Dna Damage ◽  
Free Radical ◽  
Vitamin C ◽  
Free Radical Scavenger ◽  
Iron Sulfate ◽  
Radical Scavenger ◽  
Optimum Level ◽  
Acute Administration ◽  
Oxygen Species ◽  
Indirect Action

ABSTRACT Vitamin C (VC) is a well-known antioxidant and strong free radical scavenger. Its antioxidant activity is useful for protection of cellular macromolecules, particularly DNA, from oxidative damage induced by different agents. This study was undertaken to evaluate the optimum level of VC in attenuating the chromosome aberrations (CAs) and DNA damage after iron sulfate (FeSO4) acute administration in Wistar rats. The results exhibited that the increase of CAs and DNA damage induced by FeSO4, 200 mg Fe/kg, could be reduced significantly by VC pretreatment at the dose of 500 mg/kg (p<0.001), but not in the 100 mg/kg group. The findings provide evidence that VC at the dose of 500 mg/kg exerted a possible protective effect against FeSO4 induced CAs and DNA damage. The possible mechanisms of VC may be attributed to its property as a free radical scavenger or to its indirect action in reducing the level of reactive oxygen species (ROS).

Melatonin reduces high levels of lipid peroxidation induced by potassium iodate in porcine thyroid

2019 ◽  
pp. 1-7 ◽  
Author(s):  
Paulina Iwan ◽  
Jan Stepniak ◽  
Malgorzata Karbownik-Lewinska
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Membrane Lipids ◽  
Chemical Properties ◽  
Iodine Concentration ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Protective Effects ◽  
Potassium Iodate ◽  
Hormone Synthesis

Abstract. Iodine is essential for thyroid hormone synthesis. Under normal iodine supply, calculated physiological iodine concentration in the thyroid is approx. 9 mM. Either potassium iodide (KI) or potassium iodate (KIO3) are used in iodine prophylaxis. KI is confirmed as absolutely safe. KIO3 possesses chemical properties suggesting its potential toxicity. Melatonin (N-acetyl-5-methoxytryptamine) is an effective antioxidant and free radical scavenger. Study aims: to evaluate potential protective effects of melatonin against oxidative damage to membrane lipids (lipid peroxidation, LPO) induced by KI or KIO3 in porcine thyroid. Homogenates of twenty four (24) thyroids were incubated in presence of either KI or KIO3 without/with melatonin (5 mM). As melatonin was not effective against KI-induced LPO, in the next step only KIO3 was used. Homogenates were incubated in presence of KIO3 (200; 100; 50; 25; 20; 15; 10; 7.5; 5.0; 2.5; 1.25 mM) without/with melatonin or 17ß-estradiol. Five experiments were performed with different concentrations of melatonin (5.0; 2.5; 1.25; 1.0; 0.625 mM) and one with 17ß-estradiol (1.0 mM). Malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) concentration (LPO index) was measured spectrophotometrically. KIO3 increased LPO with the strongest damaging effect (MDA + 4-HDA level: ≈1.28 nmol/mg protein, p < 0.05) revealed at concentrations of around 15 mM, thus corresponding to physiological iodine concentrations in the thyroid. Melatonin reduced LPO (MDA + 4-HDA levels: from ≈0.97 to ≈0,76 and from ≈0,64 to ≈0,49 nmol/mg protein, p < 0.05) induced by KIO3 at concentrations of 10 mM or 7.5 mM. Conclusion: Melatonin can reduce very strong oxidative damage to membrane lipids caused by KIO3 used in doses resulting in physiological iodine concentrations in the thyroid.

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