scholarly journals Radioprotective and Radiomitigative Effects of Melatonin in Tissues with Different Proliferative Activity

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1885
Author(s):  
Serazhutdin A. Abdullaev ◽  
Sergey I. Glukhov ◽  
Azhub I. Gaziev
Keyword(s):  
Oxidative Stress ◽  
Cerebral Cortex ◽  
Proliferative Activity ◽  
Nuclear Dna ◽  
Significant Proportion ◽  
Spleen Tissue ◽  
X Ray ◽  
Mouse Tissues ◽  
Baseline Values ◽  
Cerebral Cortex Tissue

We used various markers to analyze damage to mouse tissues (spleen and cerebral cortex) which have different proliferative activity and sensitivity to ionizing radiation (IR). We also assessed the degree of modulation of damages that occurs when melatonin is administered to mice prior to and after their X-ray irradiation. The data from this study showed that lesions in nuclear DNA (nDNA) were repaired more actively in the spleen than in the cerebral cortex of mice irradiated and treated with melatonin (N-acetyl-5-methoxytryptamine). Mitochondrial biogenesis involving mitochondrial DNA (mtDNA) synthesis was activated in both tissues of irradiated mice. A significant proportion of the newly synthesized mtDNA molecules were mutant copies that increase oxidative stress. Melatonin reduced the number of mutant mtDNA copies and the level of H2O2 in both tissues of the irradiated mice. Melatonin promoted the restoration of ATP levels in the tissues of irradiated mice. In the mouse tissues after exposure to X-ray, the level of malondialdehyde (MDA) increased and melatonin was able to reduce it. The MDA concentration was higher in the cerebral cortex tissue than that in the spleen tissue of the mouse. In mouse tissues following irradiation, the glutathione (GSH) level was low. The spleen GSH content was more than twice as low as that in the cerebral cortex. Melatonin helped restore the GSH levels in the mouse tissues. Although the spleen and cerebral cortex tissues of mice differ in the baseline values of the analyzed markers, the radioprotective and radiomitigative potential of melatonin was observed in both tissues.

scholarly journals Effect of astaxanthin on malondialdehyde level in damaged cerebral cortex tissue in male rat (Rattus norvegicus) induced by formaldehyde orally

2021 ◽  
Vol 129 (s2) ◽  
Author(s):  
Erik Ahmad Hasyim ◽  
Virhan Novianry ◽  
Mistika Zakiah ◽  
Andriani ◽  
Dyan Roshinta Laksmi Dewi
Keyword(s):  
Oxidative Stress ◽  
Cerebral Cortex ◽  
Human Body ◽  
Rattus Norvegicus ◽  
Male Rat ◽  
Cerebral Cortex Tissue

Background: Malondialdehyde (MDA) is a dialdehyde substance that is the final product of lipids peroxidation in the human body, and it can be used as a biomarker of oxidative stress. One of the most potent antioxidants known nowadays is astaxanthin. This study aims to investigate the effect of astaxanthin on the MDA level in cerebral cortex tissue of Rattus norvegicus, which was given oral formaldehyde.

scholarly journals Hydrothermal Synthesis of Iridium-Substituted NaTaO3 Perovskites

Nanomaterials ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1537
Author(s):  
David L. Burnett ◽  
Christopher D. Vincent ◽  
Jasmine A. Clayton ◽  
Reza J. Kashtiban ◽  
Richard I. Walton
Keyword(s):  
Significant Proportion ◽  
Edge Length ◽  
Perovskite Oxide ◽  
Hydrogen Yield ◽  
Orthorhombic Space Group ◽  
X Ray ◽  
Profile Fitting ◽  
Transmission Electron ◽  
Scanning Transmission ◽  
One Step

Iridium-containing NaTaO3 is produced using a one-step hydrothermal crystallisation from Ta2O5 and IrCl3 in an aqueous solution of 10 M NaOH in 40 vol% H2O2 heated at 240 °C. Although a nominal replacement of 50% of Ta by Ir was attempted, the amount of Ir included in the perovskite oxide was only up to 15 mol%. The materials are formed as crystalline powders comprising cube-shaped crystallites around 100 nm in edge length, as seen by scanning transmission electron microscopy. Energy dispersive X-ray mapping shows an even dispersion of Ir through the crystallites. Profile fitting of powder X-ray diffraction (XRD) shows expanded unit cell volumes (orthorhombic space group Pbnm) compared to the parent NaTaO3, while XANES spectroscopy at the Ir LIII-edge reveals that the highest Ir-content materials contain Ir4+. The inclusion of Ir4+ into the perovskite by replacement of Ta5+ implies the presence of charge-balancing defects and upon heat treatment the iridium is extruded from the perovskite at around 600 C in air, with the presence of metallic iridium seen by in situ powder XRD. The highest Ir-content material was loaded with Pt and examined for photocatalytic evolution of H2 from aqueous methanol. Compared to the parent NaTaO3, the Ir-substituted material shows a more than ten-fold enhancement of hydrogen yield with a significant proportion ascribed to visible light absorption.

scholarly journals NME3 Regulates Mitochondria to Reduce ROS-Mediated Genome Instability

2020 ◽  
Vol 21 (14) ◽  
pp. 5048
Author(s):  
Chih-Wei Chen ◽  
Ning Tsao ◽  
Wei Zhang ◽  
Zee-Fen Chang
Keyword(s):  
Oxidative Stress ◽  
Dna Repair ◽  
Genome Stability ◽  
Nuclear Dna ◽  
Genome Instability ◽  
Mitochondrial Fission ◽  
Nucleoside Diphosphate Kinase ◽  
Mitochondrial Fusion ◽  
Mitochondrial Outer Membrane ◽  
Mitochondrial Oxidative Stress

NME3 is a member of the nucleoside diphosphate kinase (NDPK) family that binds to the mitochondrial outer membrane to stimulate mitochondrial fusion. In this study, we showed that NME3 knockdown delayed DNA repair without reducing the cellular levels of nucleotide triphosphates. Further analyses revealed that NME3 knockdown increased fragmentation of mitochondria, which in turn led to mitochondrial oxidative stress-mediated DNA single-strand breaks (SSBs) in nuclear DNA. Re-expression of wild-type NME3 or inhibition of mitochondrial fission markedly reduced SSBs and facilitated DNA repair in NME3 knockdown cells, while expression of N-terminal deleted mutant defective in mitochondrial binding had no rescue effect. We further showed that disruption of mitochondrial fusion by knockdown of NME4 or MFN1 also caused mitochondrial oxidative stress-mediated genome instability. In conclusion, the contribution of NME3 to redox-regulated genome stability lies in its function in mitochondrial fusion.

Effect of Acute Administration of 3-Butyl-1-Phenyl-2-(Phenyltelluro)Oct-En-1-One on Oxidative Stress in Cerebral Cortex, Hippocampus, and Cerebellum of Rats

2010 ◽  
Vol 30 (7) ◽  
pp. 1135-1142 ◽  
Author(s):  
Cláudia Funchal ◽  
Carlos Augusto Souza Carvalho ◽  
Tanise Gemelli ◽  
Andressa S. Centeno ◽  
Robson Brum Guerra ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Cortex ◽  
Acute Administration

scholarly journals Histopathological Assessment of the Effect of Pregabalin Toxicity on Cerebrum and Cerebellum of Adult Albino Rats

2021 ◽  
Author(s):  
Wael Abdou Hassan ◽  
Shaimaa Shehata ◽  
Ahmad ElBana
Keyword(s):  
Cerebral Cortex ◽  
Acute Toxicity ◽  
Chronic Toxicity ◽  
Control Group ◽  
Albino Rats ◽  
Histopathological Study ◽  
Addictive Behaviors ◽  
Group 3 ◽  
Group 2 ◽  
Cerebral Cortex Tissue

Abstract Background: Pregabalin (PGB) used as analgesic in treatment of neurogenic pains of chronic diseases, is considered as one of the most abused anti-epileptic drugs worldwide and it has been proved that it induces addictive behaviors. The present histopathological study aimed to identify the effect of PGB administration on cerebral cortex and cerebellar cortex, in both acute and chronic toxicity. Seventy-two male and non-pregnant female adult albino rats’ 6- to 8-week-old divided into 3 main groups of 24 rats each were studied. Group 1 represented the control group and group 2 represented the acute toxicity group, in which rats were given a single dose of PGB (5000 mg/kg) orally by gavage and after 24 hours, rats were sacrificed and examined. Group 3 represented the chronic toxicity group; were given PGB 500 mg/kg orally by gavage for 12 weeks, after which rats were sacrificed and examined. Result: Cerebral cortex tissue of acute toxicity group displayed astrocytosis and dystrophic changes, while in chronic group showed degeneration, necrosis and cellular infiltrates. The cerebellum of chronic groups showed degeneration and shrunken of Purkinje cells. Conclusion: Acute and chronic intoxication with pregabalin adversely altered the structure of cerebral cortex and cerebellum.

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