• Title/Summary/Keyword: Oxidative species

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Salsolinol, a catechol neurotoxin, induces oxidative modification of cytochrome c

  • Kang, Jung Hoon
    • BMB Reports
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    • v.46 no.2
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    • pp.119-123
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    • 2013
  • Methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (salsolinol), an endogenous neurotoxin, is known to perform a role in the pathogenesis of Parkinson's disease (PD). In this study, we evaluated oxidative modification of cytochrome c occurring after incubation with salsolinol. When cytochrome c was incubated with salsolinol, protein aggregation increased in a dose-dependent manner. The formation of carbonyl compounds and the release of iron were obtained in salsolinol-treated cytochrome c. Salsolinol also led to the release of iron from cytochrome c. Reactive oxygen species (ROS) scavengers and iron specific chelator inhibited the salsolinol-mediated cytochrome c modification and carbonyl compound formation. It is suggested that oxidative damage of cytochrome c by salsolinol might induce the increase of iron content in cells, subsequently leading to the deleterious condition which was observed. This mechanism may, in part, provide an explanation for the deterioration of organs under neurodegenerative disorders such as PD.

Oxidative Stress Resulting from Environmental Pollutions and Defence Mechanisms in Plants (환경오염(環境汚染)에 의한 산화(酸化)스트레스와 식물체(植物體)의 방어기작(防禦機作))

  • Shim, Sang-In;Kang, Byeung-Hoa
    • Korean Journal of Environmental Agriculture
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    • v.12 no.3
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    • pp.264-280
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    • 1993
  • The environmental pollutions were a serious problem in Korea recently. So many researcher have studied the effect of environmental pollution on plants and agro-ecosystem, but the basic mechanisms of environmental stresses were various. One of the important mechanisms was oxidative stress caused by active toxic oxygen. The toxic oxygen was generated by several stresses, abnormal temperature, many xenobiotics, air pollutants, water stress, fugal toxin, etc. In the species of toxic oxygen which is primary inducer of oxidative stresses, superoxide, hydrogen peroxide, hydroxyl radical and singlet oxygen were representative species. The scavenging systems were divided into two groups. One was nonenzymatic system and the other enzymatic system. Antioxidants such as glutathione, ascorbic acid, and carotenoid, have the primary function in defense mechanisms. Enzymatic system divided into two groups; First, direct interaction with toxic oxygen(eg. superoxide dismutase). Second, participation in redox reaction to maintain the active antioxidant levels(eg. glutathione reductase, ascorbate peroxidase, etc.).

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Effect of Genistein on Activity and Expression of Antioxidant Enzyme in Hamster ovary cells (Genistein이 햄스터 난소세포의 항산화효소활성과 발현에 미치는 영향)

  • Kim, Min-Hye;Kim, An-Keun
    • YAKHAK HOEJI
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    • v.51 no.1
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    • pp.75-82
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    • 2007
  • Reactive oxygen species (ROS) are produced in the metabolic process of oxygen in cells. The superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in cells systemize the antioxidant enzymes to control the oxidative stress. Genistein is one of the isoflavonoids, and its role in controlling cellular oxidative stress is presently the active issue at question. In this study; we analyzed genistein-induced survival rates of the CHO-K1 cells, activities of antioxidant enzymes, ROS levels, and expression levels of antioxidant enzyme genes in order to investigate the effect of genistein on cellular ROS production and antioxidative systems in CHO-K1 cells. As results, the survival rate of cells was decreased as the dose of genistein increases (12.5${\sim}$200 ${\mu}$M). Genistein increased cellular ROS levels, while it reduced total SOD activities and the expression of CuZnSOD. In conclusion, we suggest that genistein may induce oxidative stress via down-regulation of SOD.

Oxidative Stress and Antioxidant Defences in the Tasar Silkworm Antheraea mylitta D: Challenged with Nosema Species

  • Jena, Karmabeer;Pandey, Jay Prakash;Sinha, Ajit Kumar
    • International Journal of Industrial Entomology and Biomaterials
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    • v.28 no.2
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    • pp.85-91
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    • 2014
  • This study was designed to find out the effect of Nosema spore on oxidative damages and antioxidant defence in the midgut of tasar silkworm Antheraea mylitta. Higher level of lipid peroxidation (LPX) and total hydroperoxides indicate the resultant oxidative stress in the Nosema exposed specimen. Increased superoxide dismutase (SOD) suggests activation of physiological mechanism to scavenge the superoxide radical produced during Nosema infection. Higher activities of catalase and glutathione-S-tranferase on $18^{th}$ d indicate adaptive behaviour of the tissue against oxyradicals. The results suggest that Nosema infection is involved in altering the active oxygen metabolism by modulating LPX and reactive oxygen species (ROS), which is indicative of pebrine disease disorder.

Oxidative Modification of Cytochrome c by Tetrahydropapaveroline, an Isoquinoline-Derived Neurotoxin

  • Kang, Jung Hoon
    • Bulletin of the Korean Chemical Society
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    • v.34 no.2
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    • pp.406-410
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    • 2013
  • Tetrahyropapaveroline (THP) is compound derived from dopamine metabolism and is capable of causing dopaminergic neurodegenerative disorder, such as Parkinson's disease (PD). The aim of this study was to evaluate the potential of THP to cause oxidative damage on the structure of cytochrome c (cyt c). Our data showed that THP led to protein aggregation and the formation of carbonyl compound in protein aggregates. THP also induced the release of iron from cyt c. Reactive oxygen species (ROS) scavengers and iron specific chelator inhibited the THP-mediated cyt c modification and carbonyl compound formation. The results of this study show that ROS may play a critical role in THP-induced cyt c modification and iron releasing of cyt c. When cyt c that has been exposed to THP was subsequently analyzed by amino acid analysis, lysine, histidine and methionine residues were particularly sensitive. It is suggested that oxidative damage of cyt c by THP might induce the increase of iron content in cells and subsequently led to the deleterious condition. This mechanism is associated with the deterioration of organs under neurodegenerative disorder such as PD.

Oxidative Stress and Antioxidants in Disease and Cancer: A Review

  • Gupta, Rakesh Kumar;Patel, Amit Kumar;Shah, Niranjan;Choudhary, Arun Kumar;Jha, Uday Kant;Yadav, Uday Chandra;Gupta, Pavan Kumar;Pakuwal, Uttam
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.11
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    • pp.4405-4409
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    • 2014
  • Reactive oxygen species (ROS), highly reactive molecules, are produced by living organisms as a result of normal cellular metabolism and environmental factors, and can damage nucleic acids and proteins, thereby altering their functions. The human body has several mechanisms to counteract oxidative stress by producing antioxidants. A shift in the balance between oxidants and antioxidants in favor of oxidants is termed as "oxidative stress". Paradoxically, there is a large body of research demonstrating the general effect of oxidative stress on signaling pathways, less is known about the initial and direct regulation of signaling molecules by ROS, or what we term the "oxidative interface." This review focuses on the molecular mechanisms through which ROS directly interact with critical signaling molecules to initiate signaling in a broad variety of cellular processes, such as proliferation and survival (MAP kinases and PI3 kinase), ROS homeostasis, and antioxidant gene regulation (Ref-1 and Nrf-2). This review also deals with classification as well as mechanisms of formation of free radicals, examining their beneficial and deleterious effects on cellular activities and focusing on the potential role of antioxidants in preventing and repairing damage caused by oxidative stress. A discussion of the role of phytochemical antioxidants in oxidative stress, disease and the epigenome is included.

Increased Oxidative Stress and RUNX3 Hypermethylation in Patients with Hepatitis B Virus-Associated Hepatocellular Carcinoma (HCC) and Induction of RUNX3 Hypermethylation by Reactive Oxygen Species in HCC Cells

  • Poungpairoj, Poonsin;Whongsiri, Patcharawalai;Suwannasin, Surasit;Khlaiphuengsin, Apichaya;Tangkijvanich, Pisit;Boonla, Chanchai
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.13
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    • pp.5343-5348
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    • 2015
  • Promoter hypermethylation of the runt-related transcription factor 3 (RUNX3) gene is associated with increased risk of hepatocellular carcinoma (HCC). Oxidative stress plays a vital role in both carcinogenesis and progression of HCC. However, whether oxidative stress and RUNX3 hypermethylation in HCC have a cause-and-effect relationship is not known. In this study, plasma protein carbonyl and total antioxidant capacity (TAC) in patients with hepatitis B virus (HBV)-associated HCC (n=60) and age-matched healthy subjects (n=80) was determined. RUNX3 methylation in peripheral blood mononuclear cells (PBMC) of subjects was measured by methylation-specific PCR. Effect of reactive oxygen species (ROS) on induction of RUNX3 hypermethylation in HCC cells was investigated. Plasma protein carbonyl content was significantly higher, whereas plasma TAC was significantly lower, in HCC patients than healthy controls. Based on logistic regression, increased plasma protein carbonyl and decreased plasma TAC were independently associated with increased risk for HCC. PBMC RUNX3 methylation in the patient group was significantly greater than in the healthy group. RUNX3 methylation in hydrogen peroxide ($H_2O_2$)-treated HepG2 cells was significantly higher than in untreated control cells. In conclusion, increase in oxidative stress in Thai patients with HBV-associated HCC was demonstrated. This oxidative increment was independently associated with an increased risk for HCC development. RUNX3 in PBMC was found to be hypermethylated in the HCC patients. In vitro, RUNX3 hypermethylation was experimentally induced by $H_2O_2$. Our findings suggest that oxidative stress is a cause of RUNX3 promoter hypermethylation in HCC cells.

Relationship between oxidative stress, semen characteristics, and clinical diagnosis in men undergoing infertility investigation

  • Pasqualotto, Fabio F.;Sharma, Rakesh K.;Nelson, David R.;Thomas, Jr, Anthony J.;Agarwal, Ashok
    • 대한생식의학회:학술대회논문집
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    • 2000.06a
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    • pp.37-42
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    • 2000
  • Objective: To determine whether particular semen characteristics in various clinical diagnoses of infertility are associated with high oxidative stress and whether any group of infertile men is more likely to have high seminal oxidative stress. Reactive oxygen species (ROS) play an important role in sperm physiological functions, but elevated levels of ROS or oxidative stress are related to male infertility. Design: Measurement of sperm concentration, motility, morphology, seminal ROS, and total antioxidant capacity (TAC) in patients seeking infertility treatment and controls. Setting: Male infertility clinic of a tertiary care center. Patient(s): One hundred sixty-seven infertile patients and 19 controls. Intervention(s): None. Main Outcome Measure(s): Semen characteristics, seminal ROS, and TAC in samples from patients with various clinical diagnoses and controls. Result(s): Fifteen patients (9.0%) were Endtz positive and 152(91.0%) Endtz negative. Sperm concentration, motility, and morphology were significantly reduced in all groups compared with the controls (P = .02), except in varicocele associated With infection group. Mean (${\pm}$SD) ROS levels in patient groups ranged from 2.2 ${\pm}$ 0.13 to 3.2 ${\pm}$ 0.35, signilicantly higher than controls (1.3 ${\pm}$ 0.3; P<.005). Patient groups had a significantly lower mean (${\pm}$SD) TAC from 1014.75 ${\pm}$ 79.22 to 1173.05 ${\pm}$ 58.07 than controls (1653 ${\pm}$ 115.28, P<.001), except ill the vaseclony reversal group (1532.02 ${\pm}$ 74.24). Sperm concentration was negatively correlated with ROS both overall and within all groups (P${\leq}$.007), with the exception of idiopathic infertility. Conclusion(s): Irrespective of the clinical diagnosis and semen characteristics, the presence of seminal oxidative stress in infertile men suggests its role in the pathophysiology of infertility. Medical or surgical treatments for infertility in these men should include strategies to reduce oxidative stress.

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Protective effect of Samultang and its four herbal plants against reactive oxygen species in vitro and cellular system

  • Nam, Mi Na;Lee, Ah Young;Sin, Seung Mi;Goo, Young-Min;Cho, Eun Ju
    • Korean Journal of Agricultural Science
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    • v.46 no.3
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    • pp.427-437
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    • 2019
  • Oxidative stress and overproduction of free radicals have been reported to be a major pathological hallmark of neurodegenerative diseases. Samultang has been known as a beneficial agent to treat liver disease and cardiovascular diseases. However, the anti-oxidant activities and neuro-protective effects of Samultang against oxidative stress still have not been evaluated yet. The aim of the present study was to investigate the anti-oxidant and protective effects of Samultang and its four herbal plants, Paeonia lactiflora (PL), Ligusticum striatum (LS), Rehmannia glutinosa (RG), and Angelica gigas (AG), in vitro system and in SH-SY5Y neuronal cells. The extracts of Samultang strongly increased the radical scavenging activities of 1,1-diphenyl-2-picrylhydrazyl (DPPH), hydroxyl radical (${\cdot}OH$), and nitric oxide (NO) in a concentration-dependent manner. Furthermore, we investigated the protective effects of Samultang on cellular damage against oxidative stress induced by hydrogen peroxide ($H_2O_2$) in SH-SY5Y cells. Treatment with Samultang alleviated the oxidative stress from $H_2O_2$ by increasing the cell viability and decreasing the intracellular reactive oxygen species levels. Based on these results, we further investigated the radical scavenging effects of PL, LS, RG, and AG. In our results, PL had the highest DPPH, ${\cdot}OH$, and NO radical scavenging activities. Thus, PL has a crucial role in Samultang, which has anti-oxidative and neuro-protective effects. The present research suggests that Samultang and PL have protective roles against oxidative stress from $H_2O_2$-induced neuronal cell death.

Protective role of Populus tomentiglandulosa against hydrogen peroxide-induced oxidative stress in SH-SY5Y neuronal cells

  • Kwon, Yu Ri;Kim, Ji Hyun;Lee, Sanghyun;Cho, Eun Ju;Kim, Hyun Young
    • Journal of Applied Biological Chemistry
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    • v.63 no.4
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    • pp.357-363
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    • 2020
  • Oxidative stress caused by the overproduction of reactive oxygen species (ROS) is known as an etiology of neurodegenerative diseases. Populus tomentiglandulosa (PT), a member of the Salicaceae family, is widely grown in Korea and has been reported to exert protective effects on cerebral ischemia by attenuating of oxidative stress and neuronal damage. In the present study, we investigated the antioxidant activity and neuroprotective effects of an ethanol extract and four fractions [n-butanol, ethyl acetate (EtOAc), chloroform, and n-hexane] of PT under in vitro and cellular systems. The extract and four fractions of PT showed 1,1-diphenyl-2-picrylhydrazyl (DPPH), •OH, and O2- radical scavenging activities in a dose-dependent manner. In particular, the EtOAc fraction of PT had the strongest DPPH, •OH, and O2- radical scavenging activities among the extract and other fractions. Therefore, we further investigated the neuroprotective effect of the EtOAc fraction of PT against oxidative stress in H2O2-induced SH-SY5Y cells. Treatment with H2O2 significantly decreased cell viability and lactate dehydrogenase (LDH) release, and it also increased the ROS levels compared to the normal group. However, treatment with the EtOAc fraction of PT significantly increased cell viability. Moreover, the EtOAc fraction of PT-treated group significantly suppressed ROS production and LDH release compared to the H2O2-induced control group. In conclusion, our findings indicated that PT had in vitro antioxidant activity and neuroprotective effects against oxidative stress. Therefore, PT could be used as a natural agent for protection against oxidative stress.