Reactive oxygen species (Apex, N.C.)最新文献

{"title":"Grape Seed Extract Exerts an Anti-Apoptotic Effect and Attenuates the Decrease in Striatal Tyrosine Hydroxylase in Rotenone-Treated Mice","authors":"O. Abdel-Salam, M. El-Shamarka, E. Omara","doi":"10.20455/ROS.2019.805","DOIUrl":"https://doi.org/10.20455/ROS.2019.805","url":null,"abstract":"The potential neuroprotective effect of grape seed extract (GSE) was evaluated in the rotenone-induced Parkinson’s disease in mice. Rotenone was administered at the dose of 1.5 mg/kg subcutaneously (sc) three times per week for 2 weeks alone or in combination with GSE at doses of 13.5 and 27 mg/kg, sc, daily. The control group received the vehicle. The brain levels of the lipid peroxidation product malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (nitrite), and paraoxonase-1 (PON-1) were determined. Histopathology, caspase-9 immunohistochemistry in different brain regions, and tyrosine hydroxylase immunoreactivity (TH-ir) in the substantia nigra were performed. Behavioral testing included rearing activity, locomotor activity, and stair test paradigms. Results indicated significantly increased lipid peroxidation and nitric oxide contents along with a significant decrease in GSH level and marked inhibition of PON-1 activity in the striatum and in the rest of the brain tissue in rotenone-treated mice. Rotenone caused significant decreases in rearing and locomotor activities and impaired motor strength. Treatment with GSE at 27 mg/kg resulted in decreased MDA and nitric oxide by 22.8%/17.9% and 38.5%/45.5%, respectively, in the striatum and the rest of the brain. GSH was increased by 20.8% and 26%, while PON-1 activity increased by 204% and 142.9% after GSE treatment in the striatum and in the rest of the brain tissue, respectively, compared with the corresponding rotenone control values. GSE given at 27 mg/kg almost completely corrected the decrease in motor activity and motor strength caused by rotenone. Neuronal degeneration and the increase in caspase-9 expression caused by rotenone in different brain regions as well as the loss of substantia nigra TH-ir were markedly reduced by GSE. These data indicate that GSE was effective in improving brain oxidative stress and in preventing the behavioral deficits and neurodegeneration induced by rotenone in the mouse brain. It is suggested that GSE might be useful as an adjunctive treatment in patients with Parkinson’s disease.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67595148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Antioxidants in the Protection of Plants against Inhibitors of Protoporphyrinogen Oxidase","authors":"F. Dayan, Abigail L. Barker, Lauren Dayan, Karl Ravet","doi":"10.20455/ROS.2019.811","DOIUrl":"https://doi.org/10.20455/ROS.2019.811","url":null,"abstract":"Protoporphyrin IX (proto), a photodynamic chlorophyll synthesis intermediate, is present in trace amounts in plant tissues. However, plants treated with protoporphyrin IX oxidase (PPO) inhibitors (e.g., acifluorfen-methyl) accumulate high levels of proto leading to the formation of reactive oxygen species (ROS) responsible for rapid light-dependent loss of cellular membrane integrity and subsequent cell death. We show that increasing the level of certain antioxidants protects plants against the herbicidal effect of PPO inhibitors. In particular, hydrophilic antioxidants such as reduced glutathione and ascorbic acid (ascorbate) had superior protective effects than the lipophilic antioxidant ?-tocopherol. Conversely, inhibiting glutathione biosynthesis with 5 mM l-buthionine sulfoximine rendered plants more sensitive to acifluorfen-methyl. These reducing agents protect plants by quenching the ROS generated by the photoactivation of proto. The quenching of superoxide by ascorbate and reduced glutathione provided superior protection than quenching of hydrogen peroxide by ascorbate. Additionally, the absolute amounts of proto present in the tissues were also reduced in the presence of the more active antioxidants, suggesting that these molecules further protect plants by enhancing the degradation of proto.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67595541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mind-Body Interventions Significantly Decrease Oxidative DNA Damage in Sperm Genome: Clinical Implications","authors":"V. Dhawan, Manoj Kumar, P. Chaurasia, R. Dada","doi":"10.20455/ROS.2019.801","DOIUrl":"https://doi.org/10.20455/ROS.2019.801","url":null,"abstract":"Mind-body interventions (MBIs) have been broadly categorized into a group of interventions which facilitate mind’s capacity to affect the functions of the body. There is a growing body of evidence suggesting the adoption of MBIs like yoga, meditation, Tai Chi, and Qigong as an adjunct in the management of various complex lifestyle-related disorders. This review summarizes the importance of simple yoga- and meditation-based lifestyle intervention as a critical component of male infertility therapy. Defective chromatin integrity is one of the hallmarks of male factor infertility. Regular practice of yoga and meditation affects and targets the whole body, decreases free radical levels, and causes collateral increase in levels of antioxidants, not only resulting in improvement in standard sperm parameters, but also becoming ideal in treating oxidative stress and oxidative DNA damage and modulating levels of sperm transcripts through affecting the sperm methylome. This may aid in reversing testicular aging and improving the overall health and quality of life of male infertility patients and of the next generation.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67594838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Effects of the Peroxisome-Proliferator Activated Receptor-alpha Agonist, Fenofibrate, on the Antioxidant Capacity of the Brain in Pentylenetetrazol Kindling Seizures in Mice","authors":"N. Sarahian, M. Mohammadi, Shamsi Darabi, F. Salem","doi":"10.20455/ROS.2019.807","DOIUrl":"https://doi.org/10.20455/ROS.2019.807","url":null,"abstract":"It has been demonstrated that peroxisome-proliferator activated receptor-alpha (PPARα) has a potent neuroprotective role in various pathological events of the nervous tissue. Since oxidative damage is associated with development of seizure, we aimed to examine whether the PPARα agonist, fenofibrate, exerts protective effects against the repeated seizures in pentylenetetrazol (PTZ) kindling model in mice through improving the brain antioxidant capacity. The experiment was carried out in two groups of mice (each group, n = 12): PTZ-kindled mice and fenofibrate-treated kindled mice. Repetitive intraperitoneal injections of PTZ (65 mg/kg) once every 48 h were used to achieve the kindling seizures till day 21. The mice were administered orally fenofibrate (30 mg/kg/day) during the test. Latency and the brain activities of catalase and superoxide dismutase (SOD) as well as the brain content of reduced glutathione (GSH) were determined at termination of the experiment. The latency following the last injection of PTZ was considerably decreased in untreated kindled mice (49 ± 8 s), whereas fenofibrate treatment prevented this reduction in kindled mice (105 ± 16 s). Treatment with fenofibrate significantly increased the GSH content in kindled mice (20.22 ± 9.87 nmol/mg protein) compared to untreated kindled mice (5.37 ± 0.84 nmol/mg protein), (p < 0.05). Likewise, treatment with fenofibrate considerably increased the activities of catalase and SOD in kindled mice compared to untreated kindled mice by 78% and 55%, respectively. In view of the critical protective role of antioxidants in seizures, the findings of the present study suggested that the PPARα agonist, fenofibrate, might modulate the seizure behaviors in the PTZ kindling model in mice through improving the brain antioxidant capacity.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67595202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective Effects of Organic Acids against Xanthine/Xanthine Oxidase-Induced Cell Death by Reducing the Intracellular Level of Hydrogen Peroxide","authors":"Hung-Yu Chou, Marie-Noëlle Takahashi, Aoi Hozono, T. Umehara, Takashi Nomiya, Ryunosuke Kaiho, M. Ninomiya, Sayaka Kamijima, T. Satoh","doi":"10.20455/ROS.2019.803","DOIUrl":"https://doi.org/10.20455/ROS.2019.803","url":null,"abstract":"Enhanced production of superoxide is considered to play a pivotal role in the pathogenesis of various chronic diseases. In the present study, we examined the toxic effects of superoxide and hydrogen peroxide (H2O2) produced by xanthine (XA) plus xanthine oxidase (XO), and the protective effects of various organic acids against them by use of a cellular model of COS7 cells, an African green monkey cell line. Here, we report that superoxide and H2O2 generated by XA/XO triggered cell death associated with the increase in the intracellular level of H2O2. The reactive oxygen species (ROS) levels were measured by use of 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) and a multi-well fluorescence spectrophotometer. XA/XO induced an ROS burst before initiating the loss of cell viability. Catalase and N-acetylcysteine protected the cells from the XA/XO-induced cell death, indicating that the effector of the cell death was indeed H2O2. Further, we found that organic acids involved in aerobic energy metabolism, such as pyruvate, oxaloacetate, and α-ketoglutarate, had significant protective effects against the cells death by reducing the levels of H2O2. These organic acids all shared a common chemical structure, i.e., that of α-keto acid, which directly reacted with H2O2. In contrast, other organic acids, such as lactate, succinate, fumarate, and malate, which do not have the α-keto acid structure, but may produce it by dehydrogenase systems, did not efficiently protect the cells, suggesting that this structure was essential for the protective action of organic acids against oxidative stress.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"7 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67595097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reactive Oxygen Species, Biomarkers of Microvascular Maturation and Alveolarization, and Antioxidants in Oxidative Lung Injury.","authors":"Arwin M Valencia,&nbsp;Maria A Abrantes,&nbsp;Jamal Hasan,&nbsp;Jacob V Aranda,&nbsp;Kay D Beharry","doi":"10.20455/ros.2018.867","DOIUrl":"https://doi.org/10.20455/ros.2018.867","url":null,"abstract":"<p><p>The lungs of extremely low gestational age neonates (ELGANs) are deficient in pulmonary surfactant and are incapable of efficient gas exchange necessary for successful transition from a hypoxic intrauterine environment to ambient air. To improve gas exchange and survival, ELGANs often receive supplemental oxygen with mechanical ventilation which disrupts normal lung developmental processes, including microvascular maturation and alveolarization. Factors that regulate these developmental processes include vascular endothelial growth factor and matrix metalloproteinases, both of which are influenced by generation of oxygen byproducts, or reactive oxygen species (ROS). ELGANs are also deficient in antioxidants necessary to scavenge excessive ROS. Thus, the accumulation of ROS in the preterm lungs exposed to prolonged hyperoxia, results in inflammation and development of bronchopulmonary dysplasia (BPD), a form of chronic lung disease (CLD). Despite advances in neonatal care, BPD/CLD remains a major cause of neonatal morbidity and mortality. The underlying mechanisms are not completely understood, and the benefits of current therapeutic interventions are limited. The association between ROS and biomarkers of microvascular maturation and alveolarization, as well as antioxidant therapies in the setting of hyperoxia-induced neonatal lung injury are reviewed in this article.</p>","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"6 18","pages":"373-388"},"PeriodicalIF":0.0,"publicationDate":"2018-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6284827/pdf/nihms-994132.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36768467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Graphene Quantum Dots Potently Block Copper-Mediated Oxidative DNA Damage: Implications for Cancer Intervention.","authors":"Rachel E Li,&nbsp;Y Robert Li,&nbsp;Hong Zhu,&nbsp;Zhenquan Jia","doi":"10.20455/ros.2018.865","DOIUrl":"https://doi.org/10.20455/ros.2018.865","url":null,"abstract":"<p><p>Our early work suggested that graphene quantum dots (GQDs) block Cu(II)/Cu(I) redox cycle in biological systems. Here we report that GQDs could also potently protect against copper redox-mediated oxidative DNA damage. Using Cu(II)/hydrogen peroxide, Cu(II)/hydroquinone, and Cu(II)/ascorbic acid as three biologically relevant systems for inducing oxidative DNA damage, we demonstrated that GQDs protected against the above system-induced DNA strand breaks in ϕx-174 plasmid DNA in a concentration-dependent manner. Notably, a significant protection was observed with GQDs at 1 μg/ml, and a nearly complete protection was shown with 10 and 100 μg/ml of GQDs. Using electron paramagnetic resonance (EPR) spectrometry in conjunction with α-(4-pyridyl-1-oxide)-<i>N</i>-tert-butylnitrone (POBN)-spin trapping, we showed that the above three systems generated hydroxyl radicals, as evidenced by the formation of a POBN-CH₃ radical adduct in the presence of 0.5 M dimethyl sulfoxide (DMSO). Consistent with the protective effects of GQDs on DNA damage, the hydroxyl radical formation was markedly reduced in the presence of GQDs in a concentration dependent manner. A nearly complete blockage of the hydroxyl radical generation was seen with GQDs at 10 and 100 μg/ml. Taken together, our results showed that GQDs potently protected against oxidative DNA damage. Considering the critical role of copper in cancer development, our findings might have important implications for cancer intervention with GQD-based nanotech modality.</p>","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"6 18","pages":"406-413"},"PeriodicalIF":0.0,"publicationDate":"2018-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.20455/ros.2018.865","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36695891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Graphene Quantum Dots Protect against Copper Redox-Mediated Free Radical Generation and Cardiac Cell Injury.","authors":"Y Robert Li,&nbsp;Arben Santo,&nbsp;Hong Zhu,&nbsp;Zhenquan Jia,&nbsp;Michael A Trush","doi":"10.20455/ros.2018.855","DOIUrl":"https://doi.org/10.20455/ros.2018.855","url":null,"abstract":"<p><p>In this work, we investigated the effects of graphene quantum dots (GQDs) on copper redox-mediated free radical generation and cell injury. Using electron paramagnetic resonance (EPR) spectrometry in conjunction with 5,5-dimethyl-1-pyrroline <i>N</i>-oxide (DMPO) as a spin trap, we found that GQDs at a concentration as low as 1 μg/ml significantly inhibited Cu(II)/H₂O₂-mediated hydroxyl radical formation. GQDs also blocked Cu(II)-catalyzed nucleophilic addition of H₂O to DMPO to form a DMPO-OH adduct in the absence of H₂O₂, suggesting a potential for GQDs to inhibit copper redox activity. Indeed, we observed that the presence of GQDs prevented H₂O₂-mediated reduction of Cu(II) to Cu(I) though GQDs themselves also caused the reduction of Cu(II) to Cu(I). To further investigate the effects of GQDs on copper redox activity, we employed the Cu(II)/hydroquinone system in which copper redox activity plays an essential role in the oxidation of hydroquinone to semiquinone radicals with consequent oxygen consumption. Using oxygen polarography as well as EPR spectrometry, we demonstrated that the presence of GQDs drastically blocked the oxygen consumption and semiquinone radical formation resulting from the reaction of Cu(II) and hydroquinone. These results suggested that GQDs suppressed free radical formation via inhibiting copper redox activity. Lastly, using cultured human cardiomyocytes, we demonstrated that the presence of GQDs also protected against Cu(II)/H₂O₂-mediated cardiac cell injury as indicated by morphological changes (e.g., cell shrinkage and degeneration). In conclusion, our work shows, for the first time, the potential for using GQDs to counteract copper redox-mediated biological damage.</p>","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"6 17","pages":"338-348"},"PeriodicalIF":0.0,"publicationDate":"2018-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6112819/pdf/nihms984762.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36458505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidant Stress and Lipid Peroxidation in Acetaminophen Hepatotoxicity.","authors":"H. Jaeschke, A. Ramachandran","doi":"10.20455/ROS.2018.835","DOIUrl":"https://doi.org/10.20455/ROS.2018.835","url":null,"abstract":"Acetaminophen (APAP) overdose is the most frequent cause of liver injury and acute liver failure in many western countries. The mechanism of APAP-induced hepatocyte necrosis has been investigated extensively. The formation of a reactive metabolite and its binding to cellular proteins was initially thought to be responsible for cell death. A competing hypothesis was introduced that questioned the relevance of protein binding and instead suggested that P450-derived oxidant stress and lipid peroxidation causes APAP-induced liver injury. However, work over the last 15 years has reconciled some of these apparent contradictory hypotheses. This review summarizes the present state of knowledge on the role of reactive oxygen species (ROS) in APAP hepatotoxicity. Detailed investigations into the sources and relevance of the oxidant stress have clearly shown the critical role of the electron transport chain of mitochondria as main source of the oxidant stress. Other potential sources of ROS such as cytochrome P450 enzymes or NADPH oxidase on phagocytes are of limited relevance. The mitochondria-derived superoxide and peroxynitrite formation is initiated by the binding of the reactive metabolite to mitochondrial proteins and the amplification by mitogen activated protein kinases. The consequences of this oxidant stress are the opening of the mitochondrial membrane permeability transition pore with cessation of ATP synthesis, nuclear DNA fragmentation and ultimately cell necrosis. Lipid peroxidation is not a relevant mechanism of cell death but can be a marker of ROS formation. These mechanistic insights suggest that targeting mitochondrial oxidant stress is a promising therapeutic option for APAP hepatotoxicity.","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"5 15 1","pages":"145-158"},"PeriodicalIF":0.0,"publicationDate":"2018-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48077791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidant Stress and Lipid Peroxidation in Acetaminophen Hepatotoxicity.","authors":"Hartmut Jaeschke,&nbsp;Anup Ramachandran","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Acetaminophen (APAP) overdose is the most frequent cause of liver injury and acute liver failure in many western countries. The mechanism of APAP-induced hepatocyte necrosis has been investigated extensively. The formation of a reactive metabolite and its binding to cellular proteins was initially thought to be responsible for cell death. A competing hypothesis was introduced that questioned the relevance of protein binding and instead suggested that P450-derived oxidant stress and lipid peroxidation causes APAP-induced liver injury. However, work over the last 15 years has reconciled some of these apparent contradictory hypotheses. This review summarizes the present state of knowledge on the role of reactive oxygen species (ROS) in APAP hepatotoxicity. Detailed investigations into the sources and relevance of the oxidant stress have clearly shown the critical role of the electron transport chain of mitochondria as main source of the oxidant stress. Other potential sources of ROS such as cytochrome P450 enzymes or NADPH oxidase on phagocytes are of limited relevance. The mitochondria-derived superoxide and peroxynitrite formation is initiated by the binding of the reactive metabolite to mitochondrial proteins and the amplification by mitogen activated protein kinases. The consequences of this oxidant stress are the opening of the mitochondrial membrane permeability transition pore with cessation of ATP synthesis, nuclear DNA fragmentation and ultimately cell necrosis. Lipid peroxidation is not a relevant mechanism of cell death but can be a marker of ROS formation. These mechanistic insights suggest that targeting mitochondrial oxidant stress is a promising therapeutic option for APAP hepatotoxicity.</p>","PeriodicalId":91793,"journal":{"name":"Reactive oxygen species (Apex, N.C.)","volume":"5 15","pages":"145-158"},"PeriodicalIF":0.0,"publicationDate":"2018-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5903282/pdf/nihms956703.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36031931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}