Sites and Mechanisms of Low-Level Oxidative Stress in Cultured Cells

Thiamine precursors, the most studied being benfotiamine (BFT), have protective effects in mouse models of neurodegenerative diseases. BFT decreased oxidative stress and inflammation, two major characteristics of neurodegenerative diseases, in a neuroblastoma cell line (Neuro2a) and an immortalized brain microglial cell line (BV2). Here, we tested the potential antioxidant and anti-inflammatory effects of the hitherto unexplored derivative O,S-dibenzoylthiamine (DBT) in these two cell lines. We show that DBT protects Neuro2a cells against paraquat (PQ) toxicity by counteracting oxidative stress at low concentrations and increases the synthesis of reduced glutathione and NADPH in a Nrf2-independent manner. In BV2 cells activated by lipopolysaccharides (LPS), DBT significantly decreased inflammation by suppressing translocation of NF-κB to the nucleus. Our results also demonstrate the superiority of DBT over thiamine and other thiamine precursors, including BFT, in all of the in vitro models. Finally, we show that the chronic administration of DBT arrested motor dysfunction in FUS transgenic mice, a model of amyotrophic lateral sclerosis, and it reduced depressive-like behavior in a mouse model of ultrasound-induced stress in which it normalized oxidative stress marker levels in the brain. Together, our data suggest that DBT may have therapeutic potential for brain pathology associated with oxidative stress and inflammation by novel, coenzyme-independent mechanisms.

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Photobiomodulation with Red and Near-Infrared Light Improves Viability and Modulates Expression of Mesenchymal and Apoptotic-Related Markers in Human Gingival Fibroblasts

Materials ◽

10.3390/ma14123427 ◽

2021 ◽

Vol 14 (12) ◽

pp. 3427

Author(s):

Ievgeniia Kocherova ◽

Artur Bryja ◽

Katarzyna Błochowiak ◽

Mariusz Kaczmarek ◽

Katarzyna Stefańska ◽

...

Keyword(s):

Oxidative Stress ◽

Energy Density ◽

Near Infrared ◽

Infrared Light ◽

Specific Gene ◽

Gingival Fibroblasts ◽

Inflammation Markers ◽

Low Level ◽

Low Level Laser ◽

Level Laser

Photobiomodulation (PBM), also called low-level laser treatment (LLLT), has been considered a promising tool in periodontal treatment due to its anti-inflammatory and wound healing properties. However, photobiomodulation’s effectiveness depends on a combination of parameters, such as energy density, the duration and frequency of the irradiation sessions, and wavelength, which has been shown to play a key role in laser-tissue interaction. The objective of the study was to compare the in vitro effects of two different wavelengths—635 nm and 808 nm—on the human primary gingival fibroblasts in terms of viability, oxidative stress, inflammation markers, and specific gene expression during the four treatment sessions at power and energy density widely used in dental practice (100 mW, 4 J/cm2). PBM with both 635 and 808 nm at 4 J/cm2 increased the cell number, modulated extracellular oxidative stress and inflammation markers and decreased the susceptibility of human primary gingival fibroblasts to apoptosis through the downregulation of apoptotic-related genes (P53, CASP9, BAX). Moreover, modulation of mesenchymal markers expression (CD90, CD105) can reflect the possible changes in the differentiation status of irradiated fibroblasts. The most pronounced results were observed following the third irradiation session. They should be considered for the possible optimization of existing low-level laser irradiation protocols used in periodontal therapies.

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Low level laser therapy reduces oxidative stress in cortical neurons in vitro

10.1117/12.912948 ◽

2012 ◽

Author(s):

Ying-Ying Huang ◽

Clark E. Tedford ◽

Thomas McCarthy ◽

Michael R. Hamblin

Keyword(s):

Oxidative Stress ◽

Laser Therapy ◽

Cortical Neurons ◽

Low Level Laser Therapy ◽

Low Level ◽

Low Level Laser ◽

Level Laser

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RNA Interference-Mediated Inhibition of Wild-Type Torsin A Expression Increases Apoptosis Caused by Oxidative Stress in Cultured Cells

Neurochemical Research ◽

10.1007/s11064-010-0177-4 ◽

2010 ◽

Vol 35 (8) ◽

pp. 1214-1223 ◽

Cited By ~ 5

Author(s):

Xue-Ping Chen ◽

Xiao-Hui Hu ◽

Shu-Hui Wu ◽

Yang-Wei Zhang ◽

Bo Xiao ◽

...

Keyword(s):

Oxidative Stress ◽

Rna Interference ◽

Cultured Cells ◽

Wild Type

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Oxidative Stress, hogg1 Expression and NF‐κB Activity in Cells Exposed to Low Level Chromium

Journal of Occupational Health ◽

10.1539/joh.45.271 ◽

2003 ◽

Vol 45 (5) ◽

pp. 271-277 ◽

Cited By ~ 12

Author(s):

Yong‐Dae Kim ◽

Sung‐Chul An ◽

Tsunehiro Oyama ◽

Toshihiro Kawamoto ◽

Heon Kim

Keyword(s):

Oxidative Stress ◽

Low Level ◽

In Cells

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Protective effects of hydrogen against irradiation

Current Pharmaceutical Design ◽

10.2174/1381612827666210119103545 ◽

2021 ◽

Vol 27 ◽

Author(s):

Yasuhiro Terasaki ◽

Mika Terasaki ◽

Akira Shimizu

Keyword(s):

Oxidative Stress ◽

Lung Injury ◽

Cultured Cells ◽

Animal Experiments ◽

Lung Epithelial Cells ◽

Lung Damage ◽

Protective Effects ◽

Chronic Radiation ◽

Radiation Induced ◽

Reactive Oxidants

: Radiation-induced lung injury is characterized by an acute pneumonia phase followed by a fibrotic phase. At the time of irradiation, a rapid, short-lived burst of reactive oxygen species (ROS) such as hydroxyl radicals (•OH) occurs, but chronic radiation-induced lung injury may occur due to excess ROS such as H2O2 , O2•− , ONOO− , and •OH. Molecular hydrogen (H2 ) is an efficient antioxidant that quickly diffuses cell membranes, reduces ROS such as •OH and ONOO− , and suppresses damage caused by oxidative stress in various organs. In 2011, through the evaluation of electron-spin resonance and fluorescent indicator signals, we had reported that H2 can eliminate •OH and can protect against oxidative stress-related apoptotic damage induced by irradiation of cultured lung epithelial cells. We had explored for the first time the radioprotective effects of H2 treatment on acute and chronic radiation-induced lung damage in mice by inhaled H2 gas (for acute) and imbibed H2 -enriched water (for chronic). Thus, we had proposed that H2 be considered a potential radioprotective agent. Recent publications have shown that H2 directly neutralizes highly reactive oxidants and indirectly reduces oxidative stress by regulating the expression of various genes. By regulating gene expression, H2 functions as an anti-inflammatory and anti-apoptotic molecule and promotes energy metabolism. The increased evidence obtained from cultured cells or animal experiments reveal a putative place for H2 treatment and its radioprotective effect clinically. This review focuses on major scientific advances of in the treatment of H2 as a new class of radioprotective agents.

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Effects of low Level Laser Therapy on Oxidative Stress in Rats

Journal of High Institute of Public Health ◽

10.21608/jhiph.2006.155198 ◽

2006 ◽

Vol 36 (3) ◽

pp. 667-676

Author(s):

Hoda Hamdy ◽

Mamdouh El-Yamany ◽

Mohamed Shetewy ◽

Afaf El-Faras ◽

Aziza Ibrahim

Keyword(s):

Oxidative Stress ◽

Laser Therapy ◽

Low Level Laser Therapy ◽

Low Level ◽

Low Level Laser ◽

Level Laser

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Molecular adaptation of vascular endothelial cells to oxidative stress

AJP Cell Physiology ◽

10.1152/ajpcell.1993.264.3.c715 ◽

1993 ◽

Vol 264 (3) ◽

pp. C715-C722 ◽

Cited By ~ 128

Author(s):

D. Lu ◽

N. Maulik ◽

I. I. Moraru ◽

D. L. Kreutzer ◽

D. K. Das

Keyword(s):

Oxidative Stress ◽

Endothelial Cells ◽

Cultured Cells ◽

Vascular Endothelial Cells ◽

Molecular Adaptation ◽

Vascular Endothelial ◽

Trypan Blue Exclusion ◽

Two Dimensional Gel Electrophoresis ◽

H2o2 Treatment ◽

Trypan Blue Exclusion Test

Cellular organisms respond at the cellular and molecular level when confronted with sudden changes in environment, and molecular adaptation represents the ability of the cells to acclimate themselves to their new environment. In this study we examined the response of bovine vascular endothelial cells (VEC) to the oxidative stress by exposing the cultured cells to two different concentrations of H2O2, 0.04 or 0.08 mM, for 18-24 h. H2O2-exposed VEC displayed good viability (85-90% for 0.04 mM H2O2; 75-80% for 0.08 mM H2O2) and exhibited normal morphology. H2O2 treatment of the VEC was associated with the expression of a number of new proteins, as demonstrated by two-dimensional gel electrophoresis of total cell lysate. Cells exposed to 0.04 mM H2O2 expressed 25 new proteins, whereas 19 newly expressed proteins were detected when the cells were exposed to 0.08 mM H2O2. Western blot analysis of H2O2-treated VEC using specific antibodies to heat-shock proteins (HSP) identified one of these proteins as a member of the HSP 70 family. In addition, H2O2 induced an increase in antioxidative enzyme activities in the VEC, including superoxide dismutase, catalase, and glutathione peroxidase. Moreover, these changes were a truly adaptive phenomenon because challenging the VEC with brief exposure to toxic levels of H2O2 (1 mM for 30 min) showed increased viability (by Trypan blue exclusion test) and decreased injury (by lactate dehydrogenase supernatant-to-cellular ratio determination) in adapted cells (preexposed to 0.04 or 0.08 mM H2O2) compared with control cells.(ABSTRACT TRUNCATED AT 250 WORDS)

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