scholarly journals Astaxanthin Protects PC12 Cells against Homocysteine- and Glutamate-Induced Neurotoxicity

Molecules ◽  
2020 ◽  
Vol 25 (1) ◽  
pp. 214 ◽  
Author(s):  
Chi-Huang Chang ◽  
Kuan-Chou Chen ◽  
Kuo-Chun Liaw ◽  
Chiung-Chi Peng ◽  
Robert Y. Peng
Keyword(s):  
Oxidative Stress ◽  
Pc12 Cells ◽  
Memory Impairment ◽  
Calcium Influx ◽  
Cell Model ◽  
Mechanisms Of Action ◽  
Ros Production ◽  
Oxygen Species ◽  
Huge Amount ◽  
And Oxidative Stress

Memory impairment has been shown to be associated with glutamate (Glu) excitotoxicity, homocysteine (Hcy) accumulation, and oxidative stress. We hypothesize that Glu and Hcy could damage neuronal cells, while astaxanthin (ATX) could be beneficial to alleviate the adverse effects. Using PC12 cell model, we showed that Glu and Hcy provoked a huge amount of reactive oxygen species (ROS) production, causing mitochondrial damage at EC50 20 and 10 mm, respectively. The mechanisms of action include: (1) increasing calcium influx; (2) producing ROS; (3) initiating lipid peroxidation; (4) causing imbalance of the Bcl-2/Bax homeostasis; and (5) activating cascade of caspases involving caspases 12 and 3. Conclusively, the damages caused by Glu and Hcy to PC12 cells can be alleviated by the potent antioxidant ATX.

scholarly journals Tremella fuciformis Polysaccharides Attenuate Oxidative Stress and Inflammation in Macrophages through miR-155

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yang Ruan ◽  
Hong Li ◽  
Lianmei Pu ◽  
Tao Shen ◽  
Zening Jin
Keyword(s):  
Oxidative Stress ◽  
Small Rnas ◽  
Nuclear Translocation ◽  
Raw264.7 Cells ◽  
Ros Production ◽  
Oxygen Species ◽  
Tremella Fuciformis ◽  
Mtt Assays ◽  
And Oxidative Stress ◽  
Inflammatory Effect

Aim. To investigate the function of Tremella fuciformis polysaccharides (TFPS) in LPS-induced inflammation and oxidative stress of macrophages. Methods. RAW264.7 cells were pretreated with TFPS and then stimulated with 0.1 μg/ml LPS. NFκB, Akt, p38MAPK, MCP-1, and SOD-1 were analyzed by Western blotting. Cell viability was measured using MTT assays. Reactive oxygen species (ROS) production, real-time PCR, ELISA, and immunofluorescence staining were performed on RAW264.7 cells that were treated with LPS and/or TFPS to investigate the anti-inflammatory effect of TFPS. Results. LPS induced inflammation and ROS production and promoted the secretion of cytokines such as TNF-α and IL-6. LPS also enhanced the nuclear translocation of NFκB, which promoted inflammation by oxidative stress. However, pretreatment with TFPS profoundly inhibited the activation of Akt, p38MAPK, and NFκB and attenuated the expression of MCP-1 in macrophages. Meanwhile, TFPS also decreased cytokine and ROS levels and attenuated cell inflammation after treatment with LPS. Moreover, miR-155, one of the key small RNAs which regulate NFκB and inflammation in macrophages, was significantly downregulated. Conclusion. TFPS inhibits LPS-induced oxidative stress and inflammation by inhibiting miR-155 expression and NFκB activation in macrophages, which suggests that TFPS may be a potential reagent for inhibiting the development of inflammation.

Oxidative Stress and Kidney Function: A Brief Update

2019 ◽  
Vol 24 (40) ◽  
pp. 4794-4799 ◽  
Author(s):  
Giuseppe Coppolino ◽  
Giuseppe Leonardi ◽  
Michele Andreucci ◽  
Davide Bolignano
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Single Cells ◽  
Biological Tissues ◽  
Ros Production ◽  
Oxygen Species ◽  
Ckd Progression ◽  
Biochemical Components ◽  
Oxidation Effect ◽  
And Oxidative Stress

In this review we summarized some information regarding the link between kidney and oxidative stress. Accruing evidences indicated the kidney as a fundamental organ in reactive oxygen species (ROS) production. ROS are highly reactive and cause in single cells: protein alteration, DNA damage, cellular senescence and apoptosis; while the effect of ROS in biological tissues leads to a harmful oxidation effect on all their biochemical components: lipids, proteins, carbohydrates, and nucleic acids. Oxidative stress plays a role in the pathophysiology of renal impairment and is a mediator of CKD progression; furthermore, during substitutive therapy with haemodialysis or peritoneal dialysis and in case of transplantation, organism continues to be exposed to oxidation causing the development of major systemic comorbidities in particular cardiovascular diseases.

scholarly journals Mitophagy and Oxidative Stress: The Role of Aging

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 794
Author(s):  
Anna De Gaetano ◽  
Lara Gibellini ◽  
Giada Zanini ◽  
Milena Nasi ◽  
Andrea Cossarizza ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Damage ◽  
Ros Production ◽  
Oxygen Species ◽  
Prime Mover ◽  
Age Related ◽  
Chronic Oxidative Stress ◽  
Parkinson’S Diseases ◽  
And Oxidative Stress

Mitochondrial dysfunction is a hallmark of aging. Dysfunctional mitochondria are recognized and degraded by a selective type of macroautophagy, named mitophagy. One of the main factors contributing to aging is oxidative stress, and one of the early responses to excessive reactive oxygen species (ROS) production is the induction of mitophagy to remove damaged mitochondria. However, mitochondrial damage caused at least in part by chronic oxidative stress can accumulate, and autophagic and mitophagic pathways can become overwhelmed. The imbalance of the delicate equilibrium among mitophagy, ROS production and mitochondrial damage can start, drive, or accelerate the aging process, either in physiological aging, or in pathological age-related conditions, such as Alzheimer’s and Parkinson’s diseases. It remains to be determined which is the prime mover of this imbalance, i.e., whether it is the mitochondrial damage caused by ROS that initiates the dysregulation of mitophagy, thus activating a vicious circle that leads to the reduced ability to remove damaged mitochondria, or an alteration in the regulation of mitophagy leading to the excessive production of ROS by damaged mitochondria.

scholarly journals Intracellular Sources of ROS/H2O2 in Health and Neurodegeneration: Spotlight on Endoplasmic Reticulum

Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 233
Author(s):  
Tasuku Konno ◽  
Eduardo Pinho Melo ◽  
Joseph E. Chambers ◽  
Edward Avezov
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Endoplasmic Reticulum ◽  
Neurodegenerative Diseases ◽  
Antioxidative Enzymes ◽  
Redox Reactions ◽  
Ros Production ◽  
Oxygen Species ◽  
Specific Target

Reactive oxygen species (ROS) are produced continuously throughout the cell as products of various redox reactions. Yet these products function as important signal messengers, acting through oxidation of specific target factors. Whilst excess ROS production has the potential to induce oxidative stress, physiological roles of ROS are supported by a spatiotemporal equilibrium between ROS producers and scavengers such as antioxidative enzymes. In the endoplasmic reticulum (ER), hydrogen peroxide (H2O2), a non-radical ROS, is produced through the process of oxidative folding. Utilisation and dysregulation of H2O2, in particular that generated in the ER, affects not only cellular homeostasis but also the longevity of organisms. ROS dysregulation has been implicated in various pathologies including dementia and other neurodegenerative diseases, sanctioning a field of research that strives to better understand cell-intrinsic ROS production. Here we review the organelle-specific ROS-generating and consuming pathways, providing evidence that the ER is a major contributing source of potentially pathologic ROS.

scholarly journals Vitamin E-Coated Dialyzer Inhibits Oxidative Stress

2017 ◽  
Vol 44 (4) ◽  
pp. 288-293 ◽  
Author(s):  
Shiho Yamadera ◽  
Yuya Nakamura ◽  
Masahiro Inagaki ◽  
Isao Ohsawa ◽  
Hiromichi Gotoh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Synthetic Polymer ◽  
Intracellular Reactive Oxygen Species ◽  
Ros Production ◽  
Oxygen Species ◽  
In Vitro Methods ◽  
Stress Effects ◽  
Intracellular Ros

Aim: To examine the effects of vitamin E-coated dialyzer on oxidative stress in vitro. Methods: A dialyzer with a synthetic polymer membrane (APS-11SA) and vitamin E-coated dialyzer (VPS-11SA) were connected to a blood tubing line, and U937 cells were circulated in the device. The circulating fluid was collected at 1, 2, 5, 10, 25, and 50 cycles, which are estimated numbers of passes through the dialyzer. Intracellular reactive oxygen species (ROS) production, malondialdehyde (MDA), and Cu/Zn-superoxide dismutase (SOD) were quantified. Results: Intracellular ROS production was increased in the first cycle by APS-11SA and was decreased throughout the experiment by VPS-11SA. Intracellular ROS production in the VPS-11SA device was lower, and MDA levels were decreased. MDA levels were lower during VPS-11SA processing than during APS-11SA processing. Cu/Zn-SOD levels remained unchanged. Conclusion: Our results highlight anti-oxidative-stress effects of a vitamin E-coated dialyzer.

Differential susceptibility of a few members of the nasuta–albomicans complex of Drosophila to paraquat-induced lethality and oxidative stress

Genome ◽  
2011 ◽  
Vol 54 (10) ◽  
pp. 829-835 ◽  
Author(s):  
Mysore S. Ranjini ◽  
Ravikumar Hosamani ◽  
Muralidhara ◽  
Nallur B. Ramachandra
Keyword(s):  
Oxidative Stress ◽  
Biochemical Analysis ◽  
Reduced Glutathione ◽  
Differential Susceptibility ◽  
Activity Levels ◽  
Oxygen Species ◽  
Stress Markers ◽  
The Status ◽  
Markers Of Oxidative Stress ◽  
And Oxidative Stress

The evolution of karyotypically stabilized short-lived (SL) and long-lived (LL) cytoraces in the laboratory have been established and validated through our previous lifespan studies. In the present investigation, we examined the possible reason(s) for the differential longevity among selected members of SL and LL cytoraces, employing the well known paraquat (PQ) resistance bioassay. Exposure of these races to varying concentrations of PQ revealed relatively higher resistance among LL cytoraces than SL cytoraces, as evident by the lower incidence of mortality. Biochemical analysis for endogenous markers of oxidative stress revealed that LL-2 cytorace exhibited lower reactive oxygen species (ROS) and lipid peroxidation (LPO) levels, higher activity levels of superoxide dismutase (SOD), and coupled with higher levels of reduced glutathione (GSH) compared with the levels found in SL-2 cytorace. These findings suggest that the higher susceptibility of SL cytoraces to PQ challenge may be, at least in part, related to the higher endogenous levels of oxidative stress markers. Although the precise mechanisms responsible for the longer longevity among LL cytoraces of the nasuta–albomicans complex of Drosophila merits further investigation, our data suggest that the relatively longer lifespan may be related to the status of endogenous markers that renders them more resistant towards oxidative-stress-mediated lethality, as evident in the PQ assay.

Hyperglycemia Induces Generation of Reactive Oxygen Species and Accelerates Apoptotic Cell Death in Salivary Gland Cells

Pathobiology ◽  
2021 ◽  
pp. 1-8
Author(s):  
Naoyuki Matsumoto ◽  
Daisuke Omagari ◽  
Ryoko Ushikoshi-Nakayama ◽  
Tomoe Yamazaki ◽  
Hiroko Inoue ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Salivary Gland ◽  
Tissue Injury ◽  
Ros Production ◽  
Oxygen Species ◽  
Saliva Secretion ◽  
Salivary Gland Tissue ◽  
Gland Tissue

<b><i>Introduction:</i></b> Type-2 diabetes mellitus (T2DM) is associated with several systemic vascular symptoms and xerostomia. It is considered that hyperglycemia-induced polyuria and dehydration cause decreased body-water volume, leading to decreased saliva secretion and, ultimately, xerostomia. In T2DM, increased production of reactive oxygen species (ROS) causes tissue damage to vascular endothelial cells as well as epithelial tissue, including pancreas and cornea. Hence, a similar phenomenon may occur in other tissues and glands in a hyperglycemic environment. <b><i>Methods:</i></b> Salivary gland tissue injury was examined, using T2DM model mouse (db/db). Transferase‐mediated dUTP nick‐end labeling (TUNEL) was conducted to evaluate tissue injury. The levels of malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine, Bax/Bcl-2 ratio were measured as indicator of oxidative stress. Moreover, in vitro ROS production and cell injury was evaluated by mouse salivary gland-derived normal cells under high-glucose condition culture. <b><i>Results:</i></b> In vivo and in vitro analysis showed a higher percentage of TUNEL-positive cells and higher levels of MDA and 8-hydroxy-2′-deoxyguanosine in salivary gland tissue of db/db mice. This suggests damage of saliva secretion-associated lipids and DNA by hyperglycemic-induced oxidative stress. To analyze the mechanism by which hyperglycemia promotes ROS production, mouse salivary gland-derived cells were isolated. The cell culture with high-glucose medium enhanced ROS production and promotes apoptotic and necrotic cell death. <b><i>Conclusion:</i></b> These findings suggest a novel mechanism whereby hyperglycemic-induced ROS production promotes salivary gland injury, resulting in hyposalivation.

A multifunctional compound ebselen reverses memory impairment, apoptosis and oxidative stress in a mouse model of sporadic Alzheimer's disease

2019 ◽  
Vol 109 ◽  
pp. 107-117 ◽  
Author(s):  
Franciele Martini ◽  
Suzan Gonçalves Rosa ◽  
Isabella Pregardier Klann ◽  
Bruna Cruz Weber Fulco ◽  
Fabiano Barbosa Carvalho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Memory Impairment ◽  
Sporadic Alzheimer’S Disease ◽  
And Oxidative Stress
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