Oxidative Stress Level in the Testes of Mice and Rats during Nickel Intoxication

The genotioxic and carcinogenic effect of nickel probably results from its capacity to produce reactive oxygen species (ROS) and disturb the redox balance. The aim of the study was to find out if rats lacking spermatic protamine 2 are less susceptible to Ni(II) than mice. Consequently, the levels of malondialdehyde + 4 hydroxynonenal (MDA+4HDA) − markers of lipid peroxidation, as well as the level of reduced glutathione (GSH) were measured within the rat and mouse testes. Our results showed that the levels of lipid peroxidation markers were elevated in testicular homogenates of intoxicated mice without any changes in rats. GSH level was lower in the group of intoxicated mice comparing to the control without statistically significant changes in rats’ homogenates. Moreover, the level of GSH in the testes of intoxicated mice was lower than in rats. On the basis of our results, it appears that Ni(II) can initiate oxidative stress in the testes of mice but not of rats and can reduce GSH level. Consequently, the antioxidative defense of the testes is reduced. Ni(II) that causes oxidative stress in the testes may also contribute to infertility.

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Ginkgo biloba extract (EGb 761) attenuates oxidative stress induction in erythrocytes of sickle cell disease patients

Brazilian Journal of Pharmaceutical Sciences ◽

10.1590/s1984-82502012000400009 ◽

2012 ◽

Vol 48 (4) ◽

pp. 659-665 ◽

Cited By ~ 2

Author(s):

Aline Emmer Ferreira Furman ◽

Railson Henneberg ◽

Priscila Bacarin Hermann ◽

Maria Suely Soares Leonart ◽

Aguinaldo José do Nascimento

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Lipid Peroxidation ◽

Sickle Cell ◽

Reduced Glutathione ◽

Reactive Oxygen ◽

Intracellular Reactive Oxygen Species ◽

Oxygen Species ◽

Egb 761 ◽

Cell Disease

Sickle cell disease promotes hemolytic anemia and occlusion of small blood vessels due to the presence of high concentrations of hemoglobin S, resulting in increased production of reactive oxygen species and decreased antioxidant defense capacity. The aim of this study was to evaluate the protective action of a standardized extract of Ginkgo biloba (EGb 761), selected due to its high content of flavonoids and terpenoids, in erythrocytes of patients with sickle cell anemia (HbSS, SS erythrocytes) subjected to oxidative stress using tert-butylhydroperoxide or 2,2-azobis-(amidinepropane)-dihydrochloride, in vitro. Hemolysis indexes, reduced glutathione, methemoglobin concentrations, lipid peroxidation, and intracellular reactive oxygen species were determined. SS erythrocytes displayed increased rates of oxidation of hemoglobin and membrane lipid peroxidation compared to normal erythrocytes (HbAA, AA erythrocytes), and the concentration of EGb 761 necessary to achieve the same antioxidant effect in SS erythrocytes was at least two times higher than in normal ones, inhibiting the formation of intracellular reactive oxygen species (IC50 of 13.6 µg/mL), partially preventing lipid peroxidation (IC50 of 242.5 µg/mL) and preventing hemolysis (IC50 of 10.5 µg/mL). Thus, EGb 761 has a beneficial effect on the oxidative status of SS erythrocytes. Moreover, EGb 761 failed to prevent oxidation of hemoglobin and reduced glutathione at the concentrations examined.

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Effects of Progesterone on Benzene Toxicity in Rats

Archives of Industrial Hygiene and Toxicology ◽

10.2478/10004-1254-59-2008-1835 ◽

2008 ◽

Vol 59 (1) ◽

pp. 1-9 ◽

Cited By ~ 8

Author(s):

Yeshvandra Verma ◽

Suresh Rana

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Lipid Peroxidation ◽

Cytochrome P450 ◽

Reduced Glutathione ◽

Female Rats ◽

Oxygen Species ◽

Cytochrome P450 2E1 ◽

Antioxidative Effect ◽

Cyp2e1 Activity

Effects of Progesterone on Benzene Toxicity in RatsBenzene is a frequently used industrial solvent. Its toxic manifestations could be modified by sex hormones, but mechanisms of their action are poorly understood. We have examined the influence of progesterone on lipid peroxidation (malondialdehyde), reduced glutathione (GSH), and cytochrome P450 2E1 (CYP2E1) in the liver and kidneys of female rats. Progesterone applied to benzene-treated rats inhibited the formation of reactive oxygen species (ROS), but in ovariectomised benzene-treated rats it significantly increased GSH in the liver. No improvement in CYP2E1 activity was observed in progesterone treated rats. Our results evidence that progesterone changes benzene toxicity (generation of ROS, oxidative stress). However, the probable antioxidative effect of progesterone needs to be confirmed by further studies.

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DHA reduces oxidative stress following hypoxia-ischemia in newborn piglets: a study of lipid peroxidation products in urine and plasma

Journal of Perinatal Medicine ◽

10.1515/jpm-2016-0334 ◽

2018 ◽

Vol 46 (2) ◽

pp. 209-217 ◽

Cited By ~ 9

Author(s):

Marianne Ullestad Huun ◽

Håvard T. Garberg ◽

Javier Escobar ◽

Consuelo Chafer ◽

Maximo Vento ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Lipid Peroxidation ◽

Oxygen Species ◽

Major Contributor ◽

Time Points ◽

Newborn Piglets ◽

Hypoxia Group ◽

Hypoxia Ischemia ◽

Anti Oxidant

AbstractBackground:Lipid peroxidation mediated by reactive oxygen species is a major contributor to oxidative stress. Docosahexaenoic acid (DHA) has anti-oxidant and neuroprotective properties. Our objective was to assess how oxidative stress measured by lipid peroxidation was modified by DHA in a newborn piglet model of hypoxia-ischemia (HI).Methods:Fifty-five piglets were randomized to (i) hypoxia, (ii) DHA, (iii) hypothermia, (iv) hypothermia+DHA or (v) sham. All groups but sham were subjected to hypoxia by breathing 8% O2. DHA was administered 210 min after end of hypoxia and the piglets were euthanized 9.5 h after end of hypoxia. Urine and blood were harvested at these two time points and analyzed for F4-neuroprostanes, F2-isoprostanes, neurofuranes and isofuranes using UPLC-MS/MS.Results:F4-neuroprostanes in urine were significantly reduced (P=0.006) in groups receiving DHA. Hypoxia (median, IQR 1652 nM, 610–4557) vs. DHA (440 nM, 367–738, P=0.016) and hypothermia (median, IQR 1338 nM, 744–3085) vs. hypothermia+DHA (356 nM, 264–1180, P=0.006). The isoprostane compound 8-iso-PGF2α was significantly lower (P=0.011) in the DHA group compared to the hypoxia group. No significant differences were found between the groups in blood.Conclusion:DHA significantly reduces oxidative stress by measures of lipid peroxidation following HI in both normothermic and hypothermic piglets.

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Research Strategies in the Study of the Pro-Oxidant Nature of Polyphenol Nutraceuticals

Journal of Toxicology ◽

10.1155/2011/467305 ◽

2011 ◽

Vol 2011 ◽

pp. 1-12 ◽

Cited By ~ 51

Author(s):

Harvey Babich ◽

Alyssa G. Schuck ◽

Jeffrey H. Weisburg ◽

Harriet L. Zuckerbraun

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Lipid Peroxidation ◽

Copper Ions ◽

Oxygen Species ◽

Research Strategies ◽

Dual Nature ◽

Intracellular Glutathione ◽

Divalent Cobalt ◽

Per Se

Polyphenols of phytochemicals are thought to exhibit chemopreventive effects against cancer. These plant-derived antioxidant polyphenols have a dual nature, also acting as pro-oxidants, generating reactive oxygen species (ROS), and causing oxidative stress. When studying the overall cytotoxicity of polyphenols, research strategies need to distinguish the cytotoxic component derived from the polyphenolper sefrom that derived from the generated ROS. Such strategies include (a) identifying hallmarks of oxidative damage, such as depletion of intracellular glutathione and lipid peroxidation, (b) classical manipulations, such as polyphenol exposures in the absence and presence of antioxidant enzymes (i.e., catalase and superoxide dismutase) and of antioxidants (e.g., glutathione andN-acetylcysteine) and cotreatments with glutathione depleters, and (c) more recent manipulations, such as divalent cobalt and pyruvate to scavenge ROS. Attention also must be directed to the influence of iron and copper ions and to the level of polyphenols, which mediate oxidative stress.

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Magnesium deficiency augments myocardial response to reactive oxygen species

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y06-017 ◽

2006 ◽

Vol 84 (6) ◽

pp. 617-624 ◽

Cited By ~ 5

Author(s):

L. Manju ◽

R. Renuka Nair

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Lipid Peroxidation ◽

Tissue Injury ◽

Ischemia Reperfusion ◽

Reactive Oxygen ◽

Oxygen Species ◽

Inotropic Response ◽

Mg Deficiency ◽

Negative Inotropic Response

Magnesium (Mg) deficiency and oxidative stress are independently implicated in the etiopathogenesis of various cardiovascular disorders. This study was undertaken to examine the hypothesis that Mg deficiency augments the myocardial response to oxidative stress. Electrically stimulated rat papillary muscle was used for recording the contractile variation. Biochemical variables of energy metabolism (adenosine triphosphate (ATP) and creatine phosphate) and markers of tissue injury (lactate dehydrogenase (LDH) release and lipidperoxidation), which can affect myocardial contractility, were assayed in Langendorff-perfused rat hearts. Hydrogen peroxide (100 µmol/L) was used as the source of reactive oxygen species. The negative inotropic response to H2O2 was significantly higher in Mg deficiency (0.48 mmol Mg/L) than in Mg sufficiency (1.2 mmol Mg/L). Low Mg levels did not affect ATP levels or tissue lipid peroxidation. However, H2O2 induced a decrease in ATP; enhanced lipid peroxidation and the release of LDH were augmented by Mg deficiency. Increased lipid peroxidation associated with a decrease in available energy might be responsible for the augmentation of the negative inotropic response to H2O2 in Mg deficiency. The observations from this study validate the hypothesis that myocardial response to oxidative stress is augmented by Mg deficiency. This observation has significance in ischemia–reperfusion injury, where Mg deficiency can have an additive effect on the debilitating consequences.

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Applications of nanomaterials for scavenging reactive oxygen species in the treatment of central nervous system diseases

Journal of Materials Chemistry B ◽

10.1039/d0tb01380c ◽

2020 ◽

Vol 8 (38) ◽

pp. 8748-8767

Author(s):

Zhen An ◽

Jincong Yan ◽

Ye Zhang ◽

Renjun Pei

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Central Nervous System ◽

Nervous System ◽

Redox Balance ◽

Oxygen Species ◽

Nervous System Diseases ◽

Central Nervous System Diseases ◽

Ros Scavenging ◽

Function Recovery

Nanomaterials with excellent ROS-scavenging ability and biodistribution are considered as promising candidates in alleviating oxidative stress and restoring redox balance in CNS diseases, further facilitating the function recovery of the CNS.

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Analysis of Malondialdehyde Level in Leprosy Patients

International Journal of Innovative Research in Medical Science ◽

10.23958/ijirms/vol03-i10/443 ◽

2018 ◽

Vol 3 (10) ◽

Cited By ~ 1

Author(s):

Ria S Pane ◽

Syahril R Lubis ◽

Mila Darmi

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Lipid Peroxidation ◽

Disease Process ◽

Mycobacterium Leprae ◽

Hplc Method ◽

Oxygen Species ◽

Leprosy Patients ◽

Laboratory Examinations ◽

The Mean

Background: Leprosy is a chronic disease caused by Mycobacterium leprae. Oxidative stress (OS) is a condition associated with an increased rate of celluler damage induced by the oxygen derived oxidants commonly known as reactive oxygen species (ROS). ROS are capable of damaging celluler constituen generated in excess during the chronic, inflammatory, and neurodegenerative disease process of leprosy. Malondialdehyde (MDA) is end product of lipid peroxidation by ROS and serves as marker of celluler damage. Aim: To analyse the diference of MDA level in Paucibacillary (PB) and Multibacillary (MB) leprosy. Methods: 17 new cases of leprosy patients that were diagnosed by clinical and laboratory examinations. We conducted blood samplings and measurements of plasma MDA level with HPLC method. Results: In this study, there was increased the mean of MDA level in MB compared with PB and significant statistically (p<0, 05). Conclusion: Tissue damage due to OS in leprosy patients is more severe in MB group than PB group

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Phototoxicity of Kava — Formation of Reactive Oxygen Species Leading to Lipid Peroxidation and DNA Damage

The American Journal of Chinese Medicine ◽

10.1142/s0192415x12500942 ◽

2012 ◽

Vol 40 (06) ◽

pp. 1271-1288 ◽

Cited By ~ 18

Author(s):

Qingsu Xia ◽

Hsiu-Mei Chiang ◽

Yu-Ting Zhou ◽

Jun-Jie Yin ◽

Fang Liu ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Lipid Peroxidation ◽

Singlet Oxygen ◽

The United States ◽

Oxygen Species ◽

Uva Irradiation ◽

Skin Keratinocytes ◽

Spin Resonance ◽

Dna Strand

Kava is one of the most widely sold herbal dietary supplements in the United States. It has been reported that, besides exhibiting hepatotoxicity, kava also possesses photosensitivity and induces dermopathy in humans. In this study, we determined that UVA irradiation of kava in the presence of a lipid, methyl linoleate, generated lipid peroxidation which was mediated by singlet oxygen generated during photoirradiation. The six major kavalactones(yangonin, 7,8-dihydrokawa in, kawain, 7,8-dihydromethysticin, methysticin, and 5,6-dehydrokawain) were also studied in parallel; only 5,6-dehydrokawain and yangonin-induced a low level of lipid peroxidation. UVA irradiation of kava in human HaCaT skin keratinocytes induced cytotoxicity which was mediated by oxidative stress, led to DNA strand cleavage, and produced 8-hydroxy-2′-deoxyguanosine (8-OHdG) adduct. Study by the electron spin resonance (ESR) method revealed that UVA irradiation of kava produced singlet oxygen and carbon-centered radicals. The overall results suggest that kava is photocytotoxic and photogenotoxic, both mediated by free radicals generated during photoirradiation.

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