scholarly journals Enhanced Oxidative Stress and Physiological Damage inDaphnia magnaby Copper in the Presence of Nano-TiO2

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
W. H. Fan ◽  
M. M. Cui ◽  
Z. W. Shi ◽  
C. Tan ◽  
X. P. Yang
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species Generation ◽  
Aquatic Organisms ◽  
Potential Hazard ◽  
Oxygen Species ◽  
Nano Tio2 ◽  
Physiological Regulation ◽  
Toxic Injury ◽  
Transfer Channel ◽  
Atpase Inhibition

This study examines the potential hazard of an individual nanomaterial on the Cu biotoxicity to aquatic organisms.Daphnia magnain the absence or presence of nano-TiO2was exposed to Cu. Maintaining nano-TiO2at a safe concentration cannot eliminate its potential hazard. The biomarkers superoxide dismutase, catalase, and Na+/K+-ATPase inD. magnawere measured. Cu in the presence of nano-TiO2induced higher levels of oxidative stress and physiological damage because of the sorption of Cu. Nano-TiO2also caused Na+/K+-ATPase inhibition possibly by impeding the Na+/K+transfer channel. The correlations among the biomarkers, mortality, and accumulation further showed that the overloading reactive oxygen species generation caused by nano-TiO2contributed to deeper oxidative stress and physiological regulation, thereby causing greater toxic injury.

Toxicity assessment of metallic nickel nanoparticles in various biological models: An interplay of reactive oxygen species, oxidative stress, and apoptosis

2021 ◽  
pp. 074823372110110
Author(s):  
Shabnoor Iqbal ◽  
Farhat Jabeen ◽  
Abdul Shakoor Chaudhry ◽  
Muhammad Ajmal Shah ◽  
Gaber El-Saber Batiha
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nickel Nanoparticles ◽  
Hypoxia Inducible Factor ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Volume Ratio ◽  
Nuclear Factor Κb ◽  
Metallic Nickel ◽  
Oxygen Species

Nickel nanoparticles (Ni-NPs) are widely used for multiple purposes in industries. Ni-NPs exposure is detrimental to ecosystems owing to widespread use, and so their toxicity is important to consider for real-world applications. This review mainly focuses on the notable pathophysiological activities of Ni-NPs in various research models. Ni-NPs are stated to be more toxic than bulk forms because of their larger surface area to volume ratio and are reported to provoke toxicity through reactive oxygen species generation, which leads to the upregulation of nuclear factor-κB and promotes further signaling cascades. Ni-NPs may contribute to provoking oxidative stress and apoptosis. Hypoxia-inducible factor 1α and mitogen-activated protein kinases pathways are involved in Ni-NPs associated toxicity. Ni-NPs trigger the transcription factors p-p38, p-JNK, p-ERK1/2, interleukin (IL)-3, TNF-α, IL-13, Fas, Cyt c, Bax, Bid protein, caspase-3, caspase-8, and caspase-9. Moreover, Ni-NPs have an occupational vulnerability and were reported to induce lung-related disorders owing to inhalation. Ni-NPs may cause serious effects on reproduction as Ni-NPs induced deleterious effects on reproductive cells (sperm and eggs) in animal models and provoked hormonal alteration. However, recent studies have provided limited knowledge regarding the important checkpoints of signaling pathways and less focused on the toxic limitation of Ni-NPs in humans, which therefore needs to be further investigated.

scholarly journals Comparison of Efficacies of Different Jakyakgamcho-tang Extracts on H2O2-Induced C2C12 Cell Viability

2020 ◽  
Author(s):  
Young Sook Kim ◽  
Heung Joo Yuk ◽  
Dong-Seon Kim
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Viability ◽  
Muscle Pain ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Ethanol Extract ◽  
Oxygen Species ◽  
Water Extracts ◽  
Ethanol Extracts

Oxidative stress is a major contributor to muscle aging and loss of muscle tissue. Jakyakgamcho-tang has been used in traditional Eastern medicine to treat muscle pain. Here, we compared various solvent-based Jakyakgamcho-tang extracts in terms of their effects against hydrogen peroxide-induced oxidative stress in murine C2C12 skeletal muscle cells. Total phenolic content and total flavonoid content in 30% ethanol extracts of Jakyakgamcho-tang were higher than those of water extracts of Jakyakgamcho-tang. Ethanol extracts of Jakyakgamcho-tang had stronger antioxidant and 2,2-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid and 2,2´-diphenyl-1-picrylhydrazyl-scavenging activity than water extracts of Jakyakgamcho-tang. The ethanol extract of Jakyakgamcho-tang inhibited peroxide-induced cell viability and intracellular reactive oxygen species generation more effectively than the water extract of Jakyakgamcho-tang in a dose-dependent manner. These results suggest that the ethanol extract of Jakyakgamcho-tang is relatively more efficacious at protecting against oxidative stress-induced muscle cell death because it prevents reactive oxygen species generation in C2C12 cells. Moreover, the current study indicated that the effective dose of the ethanol extract of Jakyakgamcho-tang required to alleviate muscle pain might be lower than that required for Jakyakgamcho-tang.

scholarly journals Oxidative Stress and the Microbiota-Gut-Brain Axis

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Laura Dumitrescu ◽  
Iulia Popescu-Olaru ◽  
Liviu Cozma ◽  
Delia Tulbă ◽  
Mihail Eugen Hinescu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurological Diseases ◽  
Brain Lesions ◽  
Brain Inflammation ◽  
Oxygen Species ◽  
Mutual Relationship ◽  
Therapeutic Approaches ◽  
Physiological Regulation ◽  
New Therapeutic Approaches ◽  
Important Pathway

The gut-brain axis is increasingly recognized as an important pathway of communication and of physiological regulation, and gut microbiota seems to play a significant role in this mutual relationship. Oxidative stress is one of the most important pathogenic mechanisms for both neurodegenerative diseases, such as Alzheimer’s or Parkinson’s, and acute conditions, such as stroke or traumatic brain injury. A peculiar microbiota type might increase brain inflammation and reactive oxygen species levels and might favor abnormal aggregation of proteins. Reversely, brain lesions of various etiologies result in alteration of gut properties and microbiota. These recent hypotheses could open a door for new therapeutic approaches in various neurological diseases.

scholarly journals LPS from P. gingivalis Negatively Alters Gingival Cell Mitochondrial Bioenergetics

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Kiran Napa ◽  
Andrea C. Baeder ◽  
Jeffrey E. Witt ◽  
Sarah T. Rayburn ◽  
Madison G. Miller ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Mitochondrial Function ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Human Gingival Fibroblast ◽  
Gingival Fibroblast ◽  
Oxygen Species ◽  
Atp Production ◽  
Lps Treatment

Objective. Oral inflammatory pathologies are linked to increased oxidative stress, thereby partly explaining their relevance in the etiology of systemic disorders. The purpose of this work was to determine the degree to which LPS from Porphyromonas gingivalis, the primary pathogen related to oral inflammation, altered gingival mitochondrial function and reactive oxygen species generation. Methods. Human gingival fibroblast (HGF-1) cells were treated with lipopolysaccharide of P. gingivalis. Mitochondrial function was determined via high-resolution respirometry. Results. LPS-treated HGF-1 cells had significantly higher mitochondrial complex IV and higher rates of mitochondrial respiration. However, this failed to translate into greater ATP production, as ATP production was paradoxically diminished with LPS treatment. Nevertheless, production of the reactive H2O2 was elevated with LPS treatment. Conclusions. LPS elicits an increase in gingival cell mitochondria content, with a subsequent increase in reactive oxygen species production (i.e., H2O2), despite a paradoxical reduction in ATP generation. These findings provide an insight into the nature of oxidative stress in oral inflammatory pathologies.

HO-2 provides endogenous protection against oxidative stress and apoptosis caused by TNF-α in cerebral vascular endothelial cells

2006 ◽  
Vol 291 (5) ◽  
pp. C897-C908 ◽  
Author(s):  
Shyamali Basuroy ◽  
Sujoy Bhattacharya ◽  
Dilyara Tcheranova ◽  
Yan Qu ◽  
Raymond F. Regan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Serum Deprivation ◽  
Oxygen Species ◽  
Tnf Α ◽  
Endogenous Protection ◽  
Cerebral Vascular

Tumor necrosis factor-α (TNF-α) causes oxidative stress and apoptosis in a variety of cell types. Heme oxygenase (HO) degrades heme to bilirubin, an antioxidant, and carbon monoxide (CO), a cell cycle modulator, and a vasodilator. Newborn pig cerebral microvascular endothelial cells (CMVEC) highly express constitutive HO-2. We investigated the role of HO-2 in protection against TNF-α-induced apoptosis in cerebral vascular endothelium. In CMVEC from mice and newborn pigs, 15 ng/ml TNF-α alone, or with 10 μg/ml cycloheximide (CHX) caused apoptosis detected by nuclear translocation of p65 NF-κB, caspase-3 activation, DNA fragmentation, cell-cell contact destabilization, and cell detachment. TNF-α did not induce HO-1 expression in CMVEC. CMVEC from HO-2 knockout mice showed greater sensitivity to apoptosis caused by serum deprivation and TNF-α than did wild-type mice. TNF-α increased reactive oxygen species generation, including hydrogen peroxide and superoxide radicals, as detected by dihydrorhodamine-123 and dihydroethidium. The TNF-α response was inhibited by superoxide dismutase and catalase suggesting apoptosis is oxidative stress related. Inhibition of endogenous HO-2 in newborn pig CMVEC increased oxidative stress and exaggerated apoptosis caused by serum deprivation and TNF-α. In HO-1-overexpressing CMVEC (HO-1 selective induction by cobalt portophyrin), TNF-α did not cause apoptosis. A CO-releasing compound, CORM-A1, and bilirubin blocked TNF-α-induced reactive oxygen species accumulation and apoptosis consistent with the antioxidant and antiapoptotic roles of the end products of HO activity. We conclude that HO-2 is critical for protection of cerebrovascular endothelium against apoptotic changes induced by oxidative stress and cytokine-mediated inflammation.

scholarly journals The effect of acrylamide on sperm oxidative stress, total antioxidant levels, tyrosine phosphorylation, and carboxymethyl-lysine expression: A laboratory study

2021 ◽  
Author(s):  
Mojdeh Hosseinpoor Kashani ◽  
Mina Ramezani ◽  
Zeinab Piravar
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Tyrosine Phosphorylation ◽  
Laboratory Study ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Total Antioxidant ◽  
Carboxymethyl Lysine

Background: Acrylamide (AA) is a reactive molecule produced during food processing at temperatures above 120°C. Objective: To evaluate the impact of different concentrations of AA on human sperm parameters, oxidative stress and total antioxidant capacity (TAC). Materials and Methods: In this laboratory study, semen samples were obtained from healthy donors referred to the Taleghani Hospital, Tehran, Iran between June and July 2019. Samples were divided into four groups (n = 10/each): one control and three treatment groups (0.5, 1, and 2 mM of AA). After 2 hr of exposure to AA, the superoxide dismutase and malondialdehyde levels were measured based on colorimetric methods. The TAC was determined by the ferric-reducing antioxidant power assay. Flow cytometry was performed to measure the intracellular reactive oxygen species generation. Also, immunohistochemistry was done to determine the effect of AA on tyrosine phosphorylation and carboxymethyl-lysine expression. Results: Results of the study demonstrated that the motility and viability of spermatozoa were significantly decreased after AA exposure (p < 0.001). This decrease was also seen in the TAC and superoxide dismutase activity as well as in the phosphotyrosine percentage compared with the control (p < 0.01). However, the carboxymethyllysine and prooxidant activity including reactive oxygen species generation and lipid peroxidation level increased (p < 0.001). Conclusion: Overall, the results confirmed the detrimental effect of AA on human spermatozoa which may be due to oxidative stress and decreased total antioxidant levels. AA may reduce fertility by reducing sperm capacitation and motility. Key words: Acrylamide, Oxidative stress, Antioxidant, Spermatozoa, Infertility.

scholarly journals Effects of Aging on Cardiac Oxidative Stress and Transcriptional Changes in Pathways of Reactive Oxygen Species Generation and Clearance

2021 ◽  
Author(s):  
Farhan Rizvi ◽  
Claudia C. Preston ◽  
Larisa Emelyanova ◽  
Mohammed Yousufuddin ◽  
Maria Viqar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Complex I ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Functional Enrichment ◽  
Pathway Enrichment Analysis ◽  
Oxygen Species ◽  
Age Related ◽  
Ros Homeostasis

Background Age‐related heart diseases are significant contributors to increased morbidity and mortality. Emerging evidence indicates that mitochondria within cardiomyocytes contribute to age‐related increased reactive oxygen species (ROS) generation that plays an essential role in aging‐associated cardiac diseases. Methods and Results The present study investigated differences between ROS production in cardiomyocytes isolated from adult (6 months) and aged (24 months) Fischer 344 rats, and in cardiac tissue of adult (18–65 years) and elderly (>65 years) patients with preserved cardiac function. Superoxide dismutase inhibitable ferricytochrome c reduction assay (1.32±0.63 versus 0.76±0.31 nMol/mg per minute; P =0.001) superoxide and H 2 O 2 production, measured as dichlorofluorescein diacetate fluorescence (1646±428 versus 699±329, P =0.04), were significantly higher in the aged versus adult cardiomyocytes. Similarity in age‐related alteration between rats and humans was identified in mitochondrial‐electron transport chain‐complex‐I‐associated increased oxidative‐stress by MitoSOX fluorescence (53.66±18.58 versus 22.81±12.60; P =0.03) and in 4‐HNE adduct levels (187.54±54.8 versus 47.83±16.7 ng/mg protein, P =0.0063), indicative of increased peroxidation in the elderly. These differences correlated with changes in functional enrichment of genes regulating ROS homeostasis pathways in aged human and rat hearts. Functional merged collective network and pathway enrichment analysis revealed common genes prioritized in human and rat aging‐associated networks that underlay enriched functional terms of mitochondrial complex I and common pathways in the aging human and rat heart. Conclusions Aging sensitizes mitochondrial and extramitochondrial mechanisms of ROS buildup within the heart. Network analysis of the transcriptome highlights the critical elements involved with aging‐related ROS homeostasis pathways common in rat and human hearts as targets.

scholarly journals Role of Polyphenols as Antioxidant Supplementation in Ischemic Stroke

2021 ◽  
Vol 2021 ◽  
pp. 1-19
Author(s):  
Yuan Zhou ◽  
Shanshan Zhang ◽  
Xiang Fan
Keyword(s):  
Oxidative Stress ◽  
Ischemic Stroke ◽  
Cause Of Death ◽  
Experimental Studies ◽  
Reactive Oxygen Species Generation ◽  
Oxygen Species ◽  
Potential Therapeutic Target ◽  
Antioxidant Effects ◽  
And Oxidative Stress

Stroke is the second most common cause of death globally and the leading cause of death in China. The pathogenesis of cerebral ischemia injury is complex, and oxidative stress plays an important role in the fundamental pathologic progression of cerebral damage in ischemic stroke. Previous studies have preliminarily confirmed that oxidative stress should be a potential therapeutic target and antioxidant as a treatment strategy for ischemic stroke. Emerging experimental studies have demonstrated that polyphenols exert the antioxidant potential to play the neuroprotection role after ischemic stroke. This comprehensive review summarizes antioxidant effects of some polyphenols, which have the most inhibition effects on reactive oxygen species generation and oxidative stress after ischemic stroke.

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