scholarly journals Oxidative stress, reactive oxygen species, antioxidants: a review

2018 ◽  
Vol 29 (1) ◽  
pp. 52-55
Author(s):  
Y. S. Voronkova ◽  
O. S. Voronkova ◽  
V. A. Gorban ◽  
K. K. Holoborodko
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Treatment Options ◽  
Reactive Oxygen ◽  
Natural Aging ◽  
Dietary Factors ◽  
Enzymatic System ◽  
Enzymatic Antioxidants ◽  
Oxygen Species ◽  
Small Molecular Weight

Oxidative stress is a disturbance of the balance between the production of reactive oxygen species (ROS) and antioxidants. Oxidative stress is caused by the presence of any of a number of reactive oxygen species, which the cell is unable to counterbalance. The result is damage to one or more biomolecules including DNA, RNA, proteins and lipids. Oxidative stress has been implicated in the natural aging process as well as a variety of disease states, such as neoplastic, metabolic, neurological etc., accompanied by different complications. Risk factors of generation of oxidative stress are oxidizing species, induced by pathologies include alcohol consumption, cigarette smoking, diet, gender, geographic location specifically at high altitude and occupation. ROS are composed of superoxide, hydroxyl, peroxyl, hydroperoxyl and alkoxyl radicals, hydrogen peroxide and singlet oxygen and ozone. These compounds produced endogenous in reaction of autooxidation in respiratory chaine of bioobjects. Among exogenous sources of ROS can be listed exposure of pollutants, toxins, heavy metals, drugs with different chemical origin and effects, radiation, electromagnetic fields, alcohol, cigarette smoke, stresses, allergies, dietary factors, temperature and microscopic form of life, such as bacteria, yeasts, viruses etc. The oxidative stress in biological systems is often characterized by increase in the formation of radicals; decrease in small-molecular-weight and lipid soluble antioxidants; disturbance in cellular redox balance; oxidative damage to cellular components (biomacromolecules). The presence of oxidative stress may be tested in one of three ways: direct measurement of the ROS; measurement of the resulting damage to biomolecules; and detection of antioxidant levels. Directly measuring ROS might seem the preferred method, but many reactive oxygen species are extremely unstable and difficult to measure directly. Many markers of damage are extremely stable and therefore provide a more reliable method to measure oxidative stress. Another approach is to measure the levels of antioxidant enzymes and other redox molecules which serve to counterbalance ROS generated in the cell. At the same time, it must emphasize that oxidative stress not only has a cytotoxic effect, but also plays an important role in the modulation of messengers that regulate essential cell membrane functions, which are vital for survival. For prevention of oxidative stress cells produce or uptake antioxidants – substance significantly delays or prevents oxidation of that substrate. Antioxidants may be enzymatic and non-enzymatic in nature in which enzymatic system directly or indirectly help in defence against the ROS. Antioxidants are involved in the prevention of oxidants and ROS formation; exhibits scavenger of ROS; and repairs the oxidized molecules through sources like dietary or consecutive antioxidants. Among non-enzymatic antioxidants distinguished glutathione, α-tocopherol, ascorbic acid, beta-carotene, and uric acid; these are mostly considered to be chain-breaking antioxidants in that they interrupt the auto-catalytic spread of radical reactions. Among enzymatic antioxidants most known superoxide dismutase, catalase, glutathione-SH peroxidase. The significant correlation found between ROS, parameters of oxidative stress and pathology indicate that there is a need in finding of measures of prevention of endo- and exogenous factors provoke their generation. There is a need to continue to explore the relationship between free radicals, pathological processes and the complications of them, and to elucidate the mechanisms by which increased oxidative stress accelerates the development of complications, in an effort to expand treatment options. Improvement of complications control seems to be a beneficial factor to decrease oxidative stress. For a better investigation of oxidative stress, it would be wise to supplement the clinical research by determination of special products typical for oxidative stress that let to understand mechanism of some pathological processes more clearly.

93 EFFECT OF ANTIOXIDANTS SUPPLEMENTATION ON THE QUALITY OF CRYOPRESERVED SPERM OF DOGS

2011 ◽  
Vol 23 (1) ◽  
pp. 152
Author(s):  
C. A. B. Sobrinho ◽  
M. Nichi ◽  
P. A. A. Góes ◽  
A. Dalmazzo ◽  
S. E. Crusco ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Vitamin E ◽  
Reactive Oxygen ◽  
The Other ◽  
Mitochondrial Activity ◽  
Enzymatic Antioxidants ◽  
Oxygen Species ◽  
Intact Membrane

One of the main causes of poor quality of frozen–thawed dog sperm is oxidative stress (i.e. higher production of reactive oxygen species not compensated by improved antioxidant protection). This event is known to impair sperm functionality by attacking plasma membrane, acrosome, mitochondria, and DNA. Spermatozoa are particularly susceptible the oxidative stress, mainly due to the reduced cytoplasm and the high content of polyunsaturated fatty acids (PUFA) in the membrane, which allows the spermatozoa to be motile and confers a higher resistance against the damages caused by cryopreservation, but makes the sperm more susceptible to the attack of the reactive oxygen species (ROS). The present study aimed to evaluate the effects of antioxidant supplementation on semen extender (Tris-egg yolk-citrate-glicerol) with glutathione (GSH) and vitamin E on the quality of cryopreserved dog sperm. Ejaculates of 12 dogs were divided in pools of 3 ejaculates with at least 70% of motility. Each pool was diluted with 7 different extenders for treatment groups as follows: control, vitamin E (1, 5, and 10 mM), and reduced glutathione (GSH; 1, 5, and 10 mM) and submitted to cryopreservation. Samples were thawed (37°C/30′) and evaluated for motility, vigor, percentage of sperm showing intact membrane (eosin/nigrosin), and acrosome (simple stain fast-green and bengal rose), mitochondrial activity (3–3′-diaminobenzidine-DAB), and sperm susceptibility to oxidative stress (TBARS). Statistical analyses were performed using the SAS system for Windows (SAS Institute Inc., Cary, NC, USA; least significant differences test and Spearman correlation; P < 0.05). Samples treated with 1 mM of GSH showed a higher percentage of sperm with intact membrane when compared with the control (11.21 ± 2.84 and 6.21 ± 1.16%, respectively; P < 0.05). On the other hand, treatment with 5 mM of GSH showed better results regarding mitochondrial activity. Vitamin E supplementation also played a protective role on mitochondrial activity; samples treated with 1 mM showed a lower percentage of DAB III sperm (cells with severely compromised mitochondrial activity) when compared with the control group (5.61 ± 0.7 and 8.62 ± 1.05%, respectively; P < 0.05). Both vitamin E and GSH are important non-enzymatic antioxidants responsible for the destruction of the hydroxyl radical. Despite the positive influence of these antioxidants on mitochondrial status, no effect was found on the other variables studied. These results indicate that the action of both antioxidants in dog sperm would be mainly intracellular. Furthermore, other ROS could be responsible for the other damages caused by cryopreservation on the other sperm functionalities (i.e. membrane, acrosome, DNA, oxidative status). Therefore, the use of a combination of enzymatic and non-enzymatic antioxidants could be an alternative to overcome the deleterious influence of oxidative stress in cryopreserved semen of dogs. The authors thank the Brazilian army for the dogs used in this study.

scholarly journals Antioxidants Maintain Cellular Redox Homeostasis by Elimination of Reactive Oxygen Species

2017 ◽  
Vol 44 (2) ◽  
pp. 532-553 ◽  
Author(s):  
Long He ◽  
Ting He ◽  
Shabnam Farrar ◽  
Linbao Ji ◽  
Tianyi Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Signaling Molecules ◽  
Antioxidant Systems ◽  
Enzymatic Antioxidants ◽  
Oxygen Species ◽  
Cytochrome P450 Enzymes ◽  
Cell Death Pathway

Reactive oxygen species (ROS) are produced by living cells as normal cellular metabolic byproduct. Under excessive stress conditions, cells will produce numerous ROS, and the living organisms eventually evolve series of response mechanisms to adapt to the ROS exposure as well as utilize it as the signaling molecules. ROS molecules would trigger oxidative stress in a feedback mechanism involving many biological processes, such as apoptosis, necrosis and autophagy. Growing evidences have suggested that ROS play a critical role as the signaling molecules throughout the entire cell death pathway. Overwhelming production of ROS can destroy organelles structure and bio-molecules, which lead to inflammatory response that is a known underpinning mechanism for the development of diabetes and cancer. Cytochrome P450 enzymes (CYP) are regarded as the markers of oxidative stress, can transform toxic metabolites into ROS, such as superoxide anion, hydrogen peroxide and hydroxyl radical which might cause injury of cells. Accordingly, cells have evolved a balanced system to neutralize the extra ROS, namely antioxidant systems that consist of enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidases (GPxs), thioredoxin (Trx) as well as the non-enzymatic antioxidants which collectively reduce oxidative state. Herein, we review the recent novel findings of cellular processes induced by ROS, and summarize the roles of cellular endogenous antioxidant systems as well as natural anti-oxidative compounds in several human diseases caused by ROS in order to illustrate the vital role of antioxidants in prevention against oxidative stress.

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

scholarly journals 4-Hydroxychalcone Induces Cell Death via Oxidative Stress in MYCN-Amplified Human Neuroblastoma Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Amnah M. Alshangiti ◽  
Eszter Tuboly ◽  
Shane V. Hegarty ◽  
Cathal M. McCarthy ◽  
Aideen M. Sullivan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cytotoxic Effect ◽  
Neuroblastoma Cells ◽  
Reactive Oxygen ◽  
Prognostic Indicator ◽  
Oxygen Species ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

Neuroblastoma is an embryonal malignancy that arises from cells of sympathoadrenal lineage during the development of the nervous system. It is the most common pediatric extracranial solid tumor and is responsible for 15% of childhood deaths from cancer. Fifty percent of cases are diagnosed as high-risk metastatic disease with a low overall 5-year survival rate. More than half of patients experience disease recurrence that can be refractory to treatment. Amplification of the MYCN gene is an important prognostic indicator that is associated with rapid disease progression and a poor prognosis, highlighting the need for new therapeutic approaches. In recent years, there has been an increasing focus on identifying anticancer properties of naturally occurring chalcones, which are secondary metabolites with variable phenolic structures. Here, we report that 4-hydroxychalcone is a potent cytotoxin for MYCN-amplified IMR-32 and SK-N-BE (2) neuroblastoma cells, when compared to non-MYCN-amplified SH-SY5Y neuroblastoma cells and to the non-neuroblastoma human embryonic kidney cell line, HEK293t. Moreover, 4-hydroxychalcone treatment significantly decreased cellular levels of the antioxidant glutathione and increased cellular reactive oxygen species. In addition, 4-hydroxychalcone treatment led to impairments in mitochondrial respiratory function, compared to controls. In support of this, the cytotoxic effect of 4-hydroxychalcone was prevented by co-treatment with either the antioxidant N-acetyl-L-cysteine, a pharmacological inhibitor of oxidative stress-induced cell death (IM-54) or the mitochondrial reactive oxygen species scavenger, Mito-TEMPO. When combined with the anticancer drugs cisplatin or doxorubicin, 4-hydroxychalcone led to greater reductions in cell viability than was induced by either anti-cancer agent alone. In summary, this study identifies a cytotoxic effect of 4-hydroxychalcone in MYCN-amplified human neuroblastoma cells, which rationalizes its further study in the development of new therapies for pediatric neuroblastoma.

scholarly journals Protective Effects of Gintonin on Reactive Oxygen Species-Induced HT22 Cell Damages: Involvement of LPA1 Receptor-BDNF-AKT Signaling Pathway

Molecules ◽  
2021 ◽  
Vol 26 (14) ◽  
pp. 4138
Author(s):  
Yeon-Jin Cho ◽  
Sun-Hye Choi ◽  
Ra-Mi Lee ◽  
Han-Sung Cho ◽  
Hyewhon Rhim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Signaling Pathway ◽  
Reactive Oxygen ◽  
Akt Signaling ◽  
Atp Depletion ◽  
Oxygen Species ◽  
Akt Signaling Pathway ◽  
Neuroprotective Effects ◽  
Lpa1 Receptor

Gintonin is a kind of ginseng-derived glycolipoprotein that acts as an exogenous LPA receptor ligand. Gintonin has in vitro and in vivo neuroprotective effects; however, little is known about the cellular mechanisms underlying the neuroprotection. In the present study, we aimed to clarify how gintonin attenuates iodoacetic acid (IAA)-induced oxidative stress. The mouse hippocampal cell line HT22 was used. Gintonin treatment significantly attenuated IAA-induced reactive oxygen species (ROS) overproduction, ATP depletion, and cell death. However, treatment with Ki16425, an LPA1/3 receptor antagonist, suppressed the neuroprotective effects of gintonin. Gintonin elicited [Ca2⁺]i transients in HT22 cells. Gintonin-mediated [Ca2⁺]i transients through the LPA1 receptor-PLC-IP3 signaling pathway were coupled to increase both the expression and release of BDNF. The released BDNF activated the TrkB receptor. Induction of TrkB phosphorylation was further linked to Akt activation. Phosphorylated Akt reduced IAA-induced oxidative stress and increased cell survival. Our results indicate that gintonin attenuated IAA-induced oxidative stress in neuronal cells by activating the LPA1 receptor-BDNF-TrkB-Akt signaling pathway. One of the gintonin-mediated neuroprotective effects may be achieved via anti-oxidative stress in nervous systems.

scholarly journals How to express the antioxidant properties of substances properly?

2021 ◽  
Author(s):  
Małgorzata Olszowy-Tomczyk
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Literature Review ◽  
Antioxidant Activities ◽  
Antioxidant Properties ◽  
Reactive Oxygen ◽  
The Body ◽  
Universal Method ◽  
Oxygen Species ◽  
Good Tool

AbstractOxidative stress, associated with an imbalance between the oxidants (reactive oxygen species) and the antioxidants in the body, contributes to the development of many diseases. The body’s fight against reactive oxygen species is supported by antioxidants. Nowadays, there are too many analytical methods, but there is no one universal technique for assessing antioxidant properties. Moreover, the applied different ways of expressing the results lead to their incompatibility and unreasonable interpretation. The paper is a literature review concerning the most frequent ways of antioxidant activities expression and for an easy and universal method of the obtained results discussion. This paper is an attempt to point out their disadvantages and advantages. The manuscript can support the searching interpretation of the obtained results which will be a good tool for the development of a number of fields, especially medicine what can help in the future detection and treatment of many serious diseases. Graphic abstract

scholarly journals The role of oxidative/nitrosative stress in pathogenesis of paracetamol-induced toxic hepatitis

2010 ◽  
Vol 63 (11-12) ◽  
pp. 827-832 ◽  
Author(s):  
Tatjana Radosavljevic ◽  
Dusan Mladenovic ◽  
Danijela Vucevic ◽  
Rada Jesic-Vukicevic
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Liver Injury ◽  
Kupffer Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Severe Liver ◽  
Hepatocellular Necrosis

Introduction. Paracetamol is an effective analgesic/antipyretic drug when used at therapeutic doses. However, the overdose of paracetamol can cause severe liver injury and liver necrosis. The mechanism of paracetamol-induced liver injury is still not completely understood. Reactive metabolite formation, depletion of glutathione and alkylation of proteins are the triggers of inhibition of mitochondrial respiration, adenosine triphosphate depletion and mitochondrial oxidant stress leading to hepatocellular necrosis. Role of oxidative stress in paracetamol-induced liver injury. The importance of oxidative stress in paracetamol hepatotoxicity is controversial. Paracetamol induced liver injury cause the formation of reactive oxygen species. The potent sources of reactive oxygen are mitochondria, neutrophils, Kupffer cells and the enzyme xatnine oxidase. Free radicals lead to lipid peroxidation, enzymatic inactivation and protein oxidation. Role of mitochondria in paracetamol-induced oxidative stress. The production of mitochondrial reactive oxygen species is increased, and the glutathione content is decreased in paracetamol overdose. Oxidative stress in mitochondria leads to mito?chondrial dysfunction with adenosine triphosphate depletion, increase mitochondrial permeability transition, deoxyribonu?cleic acid fragmentation which contribute to the development of hepatocellular necrosis in the liver after paracetamol overdose. Role of Kupffer cells in paracetamol-induced liver injury. Paracetamol activates Kupffer cells, which then release numerous cytokines and signalling molecules, including nitric oxide and superoxide. Kupffer cells are important in peroxynitrite formation. On the other hand, the activated Kupffer cells release anti-inflammatory cytokines. Role of neutrophils in paracetamol-induced liver injury. Paracetamol-induced liver injury leads to the accumulation of neutrophils, which release lysosomal enzymes and generate superoxide anion radicals through the enzyme nicotinamide adenine dinucleotide phosphate oxidase. Hydrogen peroxide, which is influenced by the neutrophil-derived enzyme myeloperoxidase, generates hypochlorus acid as a potent oxidant. Role of peroxynitrite in paracetamol-induced oxidative stress. Superoxide can react with nitric oxide to form peroxynitrite, as a potent oxidant. Nitrotyrosine is formed by the reaction of tyrosine with peroxynitrite in paracetamol hepatotoxicity. Conclusion. Overdose of paracetamol may produce severe liver injury with hepatocellular necrosis. The most important mechanisms of cell injury are metabolic activation of paracetamol, glutathione depletion, alkylation of proteins, especially mitochondrial proteins, and formation of reactive oxygen/nitrogen species.

scholarly journals Role of mitochondria-derived reactive oxygen species in microvascular dysfunction in chronic kidney disease

2018 ◽  
Vol 314 (3) ◽  
pp. F423-F429 ◽  
Author(s):  
Danielle L. Kirkman ◽  
Bryce J. Muth ◽  
Meghan G. Ramick ◽  
Raymond R. Townsend ◽  
David G. Edwards
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Local Heating ◽  
Reactive Oxygen ◽  
Microvascular Dysfunction ◽  
Healthy Controls ◽  
Oxygen Species ◽  
Cutaneous Vasodilation

Cardiovascular disease is the leading cause of mortality in chronic kidney disease (CKD). Mitochondrial dysfunction secondary to CKD is a potential source of oxidative stress that may impair vascular function. This study sought to determine if mitochondria-derived reactive oxygen species contribute to microvascular dysfunction in stage 3–5 CKD. Cutaneous vasodilation in response to local heating was assessed in 20 CKD patients [60 ± 13 yr; estimated glomerular filtration rate (eGFR) 46 ± 13 ml·kg−1·1.73 m−2] and 11 matched healthy participants (58 ± 2 yr; eGFR >90 ml·kg−1·1.73 m−2). Participants were instrumented with two microdialysis fibers for the delivery of 1) Ringer solution, and 2) the mitochondria- specific superoxide scavenger MitoTempo. Skin blood flow was measured via laser Doppler flowmetry during standardized local heating (42°C). Cutaneous vascular conductance (CVC) was calculated as a percentage of the maximum conductance achieved with sodium nitroprusside infusion at 43°C. Urinary isofuran/F2-isoprostane ratios were assessed by gas-chromatography mass spectroscopy. Isofuran-to-F2-isoprostane ratios were increased in CKD patients (3.08 ± 0.32 vs. 1.69 ± 0.12 arbitrary units; P < 0.01) indicative of mitochondria-derived oxidative stress. Cutaneous vasodilation was impaired in CKD compared with healthy controls (87 ± 1 vs. 92 ± 1%CVCmax; P < 0.01). Infusion of MitoTempo significantly increased the plateau phase CVC in CKD patients (CKD Ringer vs. CKD MitoTempo: 87 ± 1 vs. 93 ± 1%CVCmax; P < 0.01) to similar levels observed in healthy controls ( P = 0.9). These data provide in vivo evidence that mitochondria-derived reactive oxygen species contribute to microvascular dysfunction in CKD and suggest that mitochondrial dysfunction may be a potential therapeutic target to improve CKD-related vascular dysfunction.

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.

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