Oxidative Stress and Mitochondrial Functions in the Intestinal Caco-2/15 Cell Line

We tested the effects of swimming training and insulin therapy, either alone or in combination, on the intracellular calcium ([Ca2+]i) homeostasis, oxidative stress, and mitochondrial functions in diabetic rat hearts. Male Wistar rats were separated into control, diabetic, or diabetic plus insulin groups. Type 1 diabetes mellitus was induced by streptozotocin (STZ). Insulin-treated groups received 1 to 4 UI of insulin daily for 8 wk. Each group was divided into sedentary or exercised rats. Trained groups were submitted to swimming (90 min/day, 5 days/wk, 8 wk). [Ca2+]i transient in left ventricular myocytes (LVM), oxidative stress in LV tissue, and mitochondrial functions in the heart were assessed. Diabetes reduced the amplitude and prolonged the times to peak and to half decay of the [Ca2+]i transient in LVM, increased NADPH oxidase-4 (Nox-4) expression, decreased superoxide dismutase (SOD), and increased carbonyl protein contents in LV tissue. In isolated mitochondria, diabetes increased Ca2+ uptake, susceptibility to permeability transition pore (MPTP) opening, uncoupling protein-2 (UCP-2) expression, and oxygen consumption but reduced H2O2 release. Swimming training corrected the time course of the [Ca2+]i transient, UCP-2 expression, and mitochondrial Ca2+ uptake. Insulin replacement further normalized [Ca2+]i transient amplitude, Nox-4 expression, and carbonyl content. Alongside these benefits, the combination of both therapies restored the LV tissue SOD and mitochondrial O2 consumption, H2O2 release, and MPTP opening. In conclusion, the combination of swimming training with insulin replacement was more effective in attenuating intracellular Ca2+ disruptions, oxidative stress, and mitochondrial dysfunctions in STZ-induced diabetic rat hearts.

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Developmental Neurotoxicity of Arsenic: Involvement of Oxidative Stress and Mitochondrial Functions

Biological Trace Element Research ◽

10.1007/s12011-018-1286-1 ◽

2018 ◽

Vol 186 (1) ◽

pp. 185-198 ◽

Cited By ~ 19

Author(s):

Lalit P. Chandravanshi ◽

Richa Gupta ◽

Rajendra K. Shukla

Keyword(s):

Oxidative Stress ◽

Developmental Neurotoxicity ◽

Mitochondrial Functions ◽

And Mitochondrial Functions

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Protective Effect of Perilla frutescens Extract against Oxidative Stress-Induced Cell Death in a Staurosporine-Differentiated Retinal Ganglion Cell Line

Journal of the Korean Society of Food Science and Nutrition ◽

10.3746/jkfn.2017.46.2.161 ◽

2017 ◽

Vol 46 (2) ◽

pp. 161-168

Author(s):

Bo Kyung Lee ◽

Lira Choe ◽

Ji In Lee ◽

Doo Yi Lee ◽

Sun-Young Chang ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Protective Effect ◽

Ganglion Cell ◽

Cell Line ◽

Retinal Ganglion Cell ◽

Perilla Frutescens ◽

Retinal Ganglion

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Characterizing effects of excess copper levels in a human astrocytic cell line with focus on oxidative stress markers

Journal of Trace Elements in Medicine and Biology ◽

10.1016/j.jtemb.2021.126711 ◽

2021 ◽

Vol 65 ◽

pp. 126711

Author(s):

Barbara Witt ◽

Michael Stiboller ◽

Stefanie Raschke ◽

Sharleen Friese ◽

Franziska Ebert ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Line ◽

Oxidative Stress Markers ◽

Stress Markers ◽

Excess Copper

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Dibenzoylthiamine Has Powerful Antioxidant and Anti-Inflammatory Properties in Cultured Cells and in Mouse Models of Stress and Neurodegeneration

Biomedicines ◽

10.3390/biomedicines8090361 ◽

2020 ◽

Vol 8 (9) ◽

pp. 361

Author(s):

Margaux Sambon ◽

Anna Gorlova ◽

Alice Demelenne ◽

Judit Alhama-Riba ◽

Bernard Coumans ◽

...

Keyword(s):

Oxidative Stress ◽

Neurodegenerative Diseases ◽

Cell Line ◽

Mouse Models ◽

Cultured Cells ◽

Therapeutic Potential ◽

Motor Dysfunction ◽

Oxidative Stress Marker ◽

Bv2 Cells ◽

Anti Inflammatory

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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Glycine alleviates fluoride‐induced oxidative stress, apoptosis and senescence in a porcine testicular Sertoli cell line

Reproduction in Domestic Animals ◽

10.1111/rda.13930 ◽

2021 ◽

Author(s):

Ying Liu ◽

Boxing Sun ◽

Shaoxuan Zhang ◽

Jing Li ◽

Jiajia Qi ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Line ◽

Sertoli Cell ◽

Sertoli Cell Line

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Genomic Adaption and Mutational Patterns in a HaCaT Subline Resistant to Alkylating Agents and Ionizing Radiation

International Journal of Molecular Sciences ◽

10.3390/ijms22031146 ◽

2021 ◽

Vol 22 (3) ◽

pp. 1146

Author(s):

Reinhard Ullmann ◽

Benjamin Valentin Becker ◽

Simone Rothmiller ◽

Annette Schmidt ◽

Horst Thiermann ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Line ◽

Copy Number ◽

Resistant Cell ◽

Resistant Cell Line ◽

Chromosomal Translocations ◽

Dna Copy Number ◽

Mutational Signatures ◽

Copy Number Changes ◽

And Oxidative Stress

Sulfur mustard (SM) is a chemical warfare agent that can damage DNA via alkylation and oxidative stress. Because of its genotoxicity, SM is cancerogenic and the progenitor of many chemotherapeutics. Previously, we developed an SM-resistant cell line via chronic exposure of the popular keratinocyte cell line HaCaT to increasing doses of SM over a period of 40 months. In this study, we compared the genomic landscape of the SM-resistant cell line HaCaT/SM to its sensitive parental line HaCaT in order to gain insights into genetic changes associated with continuous alkylation and oxidative stress. We established chromosome numbers by cytogenetics, analyzed DNA copy number changes by means of array Comparative Genomic Hybridization (array CGH), employed the genome-wide chromosome conformation capture technique Hi-C to detect chromosomal translocations, and derived mutational signatures by whole-genome sequencing. We observed that chronic SM exposure eliminated the initially prevailing hypotetraploid cell population in favor of a hyperdiploid one, which contrasts with previous observations that link polyploidization to increased tolerance and adaptability toward genotoxic stress. Furthermore, we observed an accumulation of chromosomal translocations, frequently flanked by DNA copy number changes, which indicates a high rate of DNA double-strand breaks and their misrepair. HaCaT/SM-specific single-nucleotide variants showed enrichment of C > A and T > A transversions and a lower rate of deaminated cytosines in the CpG dinucleotide context. Given the frequent use of HaCaT in toxicology, this study provides a valuable data source with respect to the original genotype of HaCaT and the mutational signatures associated with chronic alkylation and oxidative stress.

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Power Failure of Mitochondria and Oxidative Stress in Neurodegeneration and Its Computational Models

Antioxidants ◽

10.3390/antiox10020229 ◽

2021 ◽

Vol 10 (2) ◽

pp. 229

Author(s):

JunHyuk Woo ◽

Hyesun Cho ◽

YunHee Seol ◽

Soon Ho Kim ◽

Chanhyeok Park ◽

...

Keyword(s):

Oxidative Stress ◽

Mitochondrial Dysfunction ◽

Computational Models ◽

Neuronal Damage ◽

Living Organism ◽

The Body ◽

Mitochondrial Functions ◽

A Cell ◽

The Brain ◽

And Oxidative Stress

The brain needs more energy than other organs in the body. Mitochondria are the generator of vital power in the living organism. Not only do mitochondria sense signals from the outside of a cell, but they also orchestrate the cascade of subcellular events by supplying adenosine-5′-triphosphate (ATP), the biochemical energy. It is known that impaired mitochondrial function and oxidative stress contribute or lead to neuronal damage and degeneration of the brain. This mini-review focuses on addressing how mitochondrial dysfunction and oxidative stress are associated with the pathogenesis of neurodegenerative disorders including Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Parkinson’s disease. In addition, we discuss state-of-the-art computational models of mitochondrial functions in relation to oxidative stress and neurodegeneration. Together, a better understanding of brain disease-specific mitochondrial dysfunction and oxidative stress can pave the way to developing antioxidant therapeutic strategies to ameliorate neuronal activity and prevent neurodegeneration.

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