Reactive oxygen species are capable of damaging biomolecules such as lipids, proteins, and DNA, which can not only lead to various diseases, but also oxidative damage resulting aging. In our previous study, Cercis chinensis (Leguminosae) showed a potent antioxidant activity. Nineteen compounds were isolated through antioxidant activity-guided fractionation. The C. chinensis extract and some of the constituents exhibited a potent antioxidant activity on the free radicals and lipid peroxidation and a notable protective effect on the t-BuOOH induced oxidative damage. In vivo test of skin damage induced by UVB irradiation, the extract of C. chinensis and a constituent, piceatannol, exhibited a significant protective effect. The life-span of the HEK-N/F cells were extended by 1.21-2.12 fold as a result of the continuous administration of 3 $\mu\textrm{g}$/ml of the C. chinensis extract and the active constituents compared to that of the control. These observations were attributed to the inhibitory effect of the C. chinensis extract and its constituents on the age-dependent shortening of the telomere. Thus, C. chinensis was demonstrated to protect the skin cells against oxidative stress and inhibit thereby the cellular aging, followed by expectation as antiaging cosmetic ingredient.
Smoking is one of the most serious but preventable causes of cardiovascular disease (CVD). Key aspects of pathological process associated with smoking include endothelial dysfunction, a prothrombotic state, inflammation, altered lipid metabolism, and hypoxia. Multiple molecular events are involved in smoking-induced CVD. However, the dysregulations of reactive oxygen species (ROS) generation and metabolism mainly contribute to the development of diverse CVDs, and NADPH oxidase (NOX) has been established as a source of ROS responsible for the pathogenesis of CVD. NOX activation and resultant ROS production by cigarette smoke (CS) treatment have been widely observed in isolated blood vessels and cultured vascular cells, including endothelial and smooth muscle cells. NOX-mediated oxidative stress has also been demonstrated in animal studies. Of the various NOX isoforms, NOX2 has been reported to mediate ROS generation by CS, but other isoforms were not tested thoroughly. Of the many CS constituents, nicotine, methyl vinyl ketone, and ${\alpha}$,${\beta}$-unsaturated aldehydes, such as, acrolein and crotonaldehyde, appear to be primarily responsible for NOX-mediated cytotoxicity, but additional validation will be needed. Human epidemiological studies have reported relationships between polymorphisms in the CYBA gene encoding p22phox, a catalytic subunit of NOX and susceptibility to smoking-related CVDs. In particular, G allele carriers of A640G and $-930^{A/G}$ polymorphisms were found to be vulnerable to smoking-induced cardiovascular toxicity, but results for C242T studies are conflicting. On the whole, evidence implicates the etiological role of NOX in smoking-induced CVD, but the clinical relevance of NOX activation by smoking and its contribution to CVD require further validation in human studies. A detailed understanding of the role of NOX would be helpful to assess the risk of smoking to human health, to define high-risk subgroups, and to develop strategies to prevent or treat smoking-induced CVD.
Objectives : Peroxynitrite (ONOO-), superoxide anion radical (?O2-) and nitric oxide (NO) are cytotoxic because they can oxidize several cellular components such as proteins, lipids and DNA. They have been implicated in the aging process, and age-related diseases such as Alzheimer's disease, rheumatoid arthritis, cancer and atherosclerosis. The aim of this study was to investigate Sabohwan's activity for scavenging ONOO- and its precursors. NO and ?02-. Methods : For this study, the fluorescent probes, namely 2',7'-dichlorodihydrofluorescein diacetate (DCFDA), 4.5-diaminofluorescein (DAF-2) and dihydrorhodamine 123 (DHR 123) were used. Results : Sabohwanblocked tert-butylhydroperoxide (t-BHP)-induced cell death in a dose-dependent fashion. It scavenged t-BHP-induced ONOO-, NO and ?O2- in YPEN cells. Sabohwan inhibited the generation of ONOO-, NO and ?O2- in the lipopolysaccharide (LPS)-treated mouse kidney postmitochondria both in vitro and in vivo. The lipid peroxide level increased and glutathione level decreased in the LPS-treated mice, whereas the ones in the Sabohwanadministered group among the LPS-treated mice reversed toward their natural levels. Conclusions : These results suggest that Sabohwanis an effective ONOO-, ?O2- and NO scavenger, and thereby it might have a potential role as a therapy against the aging process and age-related diseases.
Mustafa, Ebtihal H;Mahmoud, Huda T;Al-Hudhud, Mariam Y;Abdalla, Maher Y;Ahmad, Iman M;Yasin, Salem R;Elkarmi, Ali Z;Tahtamouni, Lubna H
Asian Pacific Journal of Cancer Prevention
/
v.16
no.8
/
pp.3213-3222
/
2015
Background: Cancer metastasis depends on cell motility which is driven by cycles of actin polymerization and depolymerization. Reactive oxygen species (ROS) and metabolic oxidative stress have long been associated with cancer. ROS play a vital role in regulating actin dynamics that are sensitive to oxidative modification. The current work aimed at studying the effects of sub-lethal metabolic oxidative stress on actin cytoskeleton, focal adhesion and cell migration. Materials and Methods: T47D human breast cancer cells were treated with 2-deoxy-D-glucose (2DG), L-buthionine sulfoximine (BSO), or doxorubicin (DOX), individually or in combination, and changes in intracellular total glutathione and malondialdehyde (MDA) levels were measured. The expression of three major antioxidant enzymes was studied by immunoblotting, and cells were stained with fluorescent-phalloidin to evaluate changes in F-actin organization. In addition, cell adhesion and degradation ability were measured. Cell migration was studied using wound healing and transwell migration assays. Results: Our results show that treating T47D human breast cancer cells with drug combinations (2DG/BSO, 2DG/DOX, or BSO/DOX) decreased intracellular total glutathione and increased oxidized glutathione, lipid peroxidation, and cytotoxicity. In addition, the drug combinations caused a reduction in cell area and mitotic index, prophase arrest and a decreased ability to form invadopodia. The formation of F-actin aggregates was increased in treated T47D cells. Moreover, combination therapy reduced cell adhesion and the rate of cell migration. Conclusions: Our results suggest that exposure of T47D breast cancer cells to combination therapy reduces cell migration via effects on metabolic oxidative stress.
Reactive oxygen species (ROS) play an important role in the pathogenesis of a variety of life threatening conditions such as atherosclerosis, myocardial infarction and cerebral stroke. In this study, the effect of Sunghyangchungisan (SHCS) as a cytoproctant against ROS-induced cell injury was studied by investigating its effect on $H_{2}O_2-induced$ cell injury in cultured endothelial cells derived from the human umbilical vein. SHCS effectively proteced the cells against $H_{2}O_2-induced$ injury determined by trypan blue exclusion ability and lactate dehydrogenase (LDH) release. The effect of SHCS was concentration-dependent and the concentrations to inhibit by 50% the cell death and LDH release were $0.9{\pm}0.1$ and $1.2{\pm}0.1\;mg/ml$, respectively. In addition, SHCS effectively protected the cells against t-butylhydroperoside- and menadione-Induced injury as well. SHCS inhibited lipid peroxidation determined by malondialdehyde production. SHCS exerted as an effective scavenger of ROS produced by exposing the cells to $H_{2}O_2$ The activities of the intracellular ROS scavenging enzymes such as superoxide dismutase, catalase and glutathione peroxidase were not Influenced by SHCS.These results indicate that SHCS might exert as an effective cytoprotectant against ROS-induced cell injury. Further intensive studies would provide us insights into mechanisms of the pharmacological actions of SHCS.
Oxidative stress induced by reactive oxygen intermediates has been implicated in a variety of human diseases including neurodegenerative disorders, cancer, cardiovascular and respiratory diseases, and mode of action of environmental toxicants. Tert-butylhydroperoxide (t-BHP) is an organic lipid hydroperoxide analogue, which is commonly used as a pro-oxidant for evaluating mechanisms involving oxidative stress in cells and tissues. In this study, the underlying mechanisms involved in the protective effects of Hwabuk 94 kiwifruit (Actinidia deliciosa cv. 'Hwabuk 94'), which is cultivated in Jeju, on the t-BHP-induced cytotoxicity in PC12 cell. The pretreatment of rat pheochromocytoma cell line PC12 with Hwabuk 94 extract ($1-100\;{\mu}g/ml$) resulted in a significant recovery from t-BHP-induced cell death and increased Bcl-2 and procaspase-3 expression, whereas the expression of Bax and cleaved PARP were decreased in a dose-dependent manner compared to the control. Furthermore, Hwabuk 94 inhibited the t-BHP-induced p38 MAP kinase and extracellular signal-regulated kinase 1/2, but not c-Jun N-terminal kinase activations. Finally, these findings suggest that Hwabuk 94 kiwifruit might attenuate t-BHP-induced PC12 cell cytotoxicity, at least in part, through the inhibition of signaling pathways mediated by the ERK1/2 and p38 MAP kinase.
Journal of Korean Society of Occupational and Environmental Hygiene
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v.23
no.3
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pp.266-272
/
2013
Objectives: This study aimed to evaluate the effects of low-level exposure to toluene on T lymphocytes subpopulations.s. Methods: The study lasted from April to October 2010. The subjects were 390 male workers, among whom 137 were chronically exposed to toluene in video-tape manufacturing factories and 253 were controls had never been occupationally exposed to hazardous chemicals. The subpoupulations of CD4+, CD8+, CD16+ (natural killer cells) and total (CD3+) T lymphocytes were examined by two-color staining using monoclonal antibodies. The general and job characteristics of subjects were assessed through a self-administered questionnaire. Results: There was no significant difference in general and job characteristics between both groups. No significant difference in lipid peroxide level was observed between the control and exposed workers, but the concentration of hydrogen peroxide was significantly higher in the exposed workers. The numbers of CD16+ T lymphocytes in controls were significantly higher than those in exposed workers, but no significant differences were found in CD4+, CD8+ and CD3+ T lymphocytes. Hydrogen peroxide levels showed a significantly negative correlation with CD8+ (r = -0.29, p < 0.01), CD16+ (r = -0.56, p < 0.01) and CD3+(r = -0.22. p < 0.01), and toluene levels was significantly negative correlated with CD3+ (r = -0.29, p < 0.05). Conclusions: Our results suggest that chronic low-level exposure to toluene affects cell-mediated immunity and the effects might mediate through ROSs (Reactive Oxygen Species) such as hydrogen peroxide.
Jo, Na-Rae;Park, Min-A;Chae, Kyo-Young;Park, Su-Ah;Jeon, So-Ha;Ha, Ji-Hoon;Park, Soo-Nam
Journal of the Society of Cosmetic Scientists of Korea
/
v.38
no.3
/
pp.225-236
/
2012
In this study, the cellular protective effects on HaCaT cells and human erythrocytes and antioxidative effects of P. tricuspidata stem extracts were investigated. The ethyl acetate ($50{\mu}g/mL$) and aglycone fraction ($25{\mu}g/mL$) of P. tricuspidata stem extracts doesn't show any characteristics of cytotoxicity. When HaCaT cells were treated with 10 mM $H_2O_2$ and $30{\mu}M$ rose bengal, the ethyl acetate ($6.25{\sim}50{\mu}g/mL$) and aglycone ($6.25{\sim}25{\mu}g/mL$) fraction protected the cells against the oxidative damage in a concentration dependent manner. The P. tricuspidata stem extracts showed more prominent cellular protective effect than (+)-${\alpha}$-tocopherol, known as lipid antioxidant at $10{\mu}g/mL$. The ethylacetate fraction of P. tricuspidata stem extracts ($18.5{\mu}g/mL$) showed more free radical (1,1-diphenyl-2-picrylhydrazyl, DPPH) scavenging activity ($FSC5_{50}$). Reactive oxygen species (ROS) scavenging activity ($OSC_{50}$) of P. tricuspidata stem extracts on ROS generated in $Fe^{3+}$-EDTA/$H_2O_2$ system was investigated using the luminol-dependent chemiluminescence assay. The ethyl acetate ($1.72{\mu}g/mL$) and the aglycone fraction ($1.53{\mu}g/mL$) showed similar ROS scavenging activity of L-ascorbic acid ($1.50{\mu}g/mL$). These results indicate that extract/fractions of P. tricuspidata stem extracts can function as natural cytoprotective agents and antioxidants in biological systems, particularly skin exposed to UV radiation by protecting cellular membrane against ROS.
The purpose of the study was to investigate the content of sinigrin, an index component, in Brassica juncea extract and to evaluate the differentiation of lipocytes, inhibition of production of reactive oxygen species (ROS) and reduction of protein production by lipogenic factors (PPARγ, C/EBPα, aP2) in the processing of Brassica juncea extract and sinigrin in 3T3-L1 preadipocytes which induces Bisphenol A (BPA), an endocrine disrupting environmental hormone. From the investigation, the content of sinigrin in Brassica juncea extract, measured by HPLC, is found to be 21.27±0.2 mg/g. The XTT assay result on BPA-derived 3T3-L1 adipocytes shows there is no cytotoxicity found from 180 µM of sinigrin and 300 ㎍/mL of Brassica juncea extract. Moreover, both intracellular lipid accumulation and ROS production during differentiation of lipocyte are significantly reduced in cells processed with Brassica juncea extract and sinigrin. Lastly, it was also found that the production of transcription factors of lipocyte differentiation, PPARγ, C/EBPα and aP2, were found to be suppressed by the application of Brassica juncea extract and sinigrin. Such results reveals that Brassica juncea is effective in not only suppressing lipid accumulation in the environmental hormone bisphenol A-derived lipocyte, but also in reducing the ROS. The sinigrin-containing Brassica juncea is highly expected to be used in natural functional supplements that prevents the lipid metabolism disorders caused by BPA. There are necessities for additional clinical research and follow-up studies on the in vivo model to verify the relevant mechanisms.
So-Hap-Hyang-Won, a traditional oriental medicine used in the treatment of stroke patients, was examined for its ability to reverse the cell damage caused by lipid peroxidation products and oxidative stress in bovine aortic endothelial cells (BAEC). The effects of herbal medicine on cell proliferation and recovery of oxidative damaged situation were studied in BAEC, which was considered an appropriate in vitro model for stroke resulting from various vascular diseases prevalent in advanced age. In a clinical study of stroke patients, So-Hap-Hyang-Won appeared to improve considerably arm and leg movements as well as consciousness disturbance condition, compared with other traditional medicines used for stroke. When BAEC were treated with extracts of the lyophilized herbal medicines, only that of So-Hap-Hyang-Won stimulated cell proliferation and showed no toxicity even at high concentrations. In studies of BAEC treated with extracts of the lyophilized material of the 14 components of So-Hap-Hyang-Won, only the extract of Foeniculi Fructus stimulated cell growth at all concentrations tested. Moreover, when cells were treated with Foeniculi Fructus (10 and 100 mg/ml) extract after prior exposure to t-BHP ($l0\mu\textrm{M}$) or HNE ($0.2\mu\textrm{M}$), lipid peroxidation products which are known to be involved in aging and vascular diseases, or after the exposure to SIN-l ($500\mu\textrm{M}$), which generates nitric oxide (NO) and other reactive oxygen species, there was substantial recovery from the oxidative damage, presumably due to the radical-scavenging effect of Foeniculi Fructus extract. Foeniculi Fructus not only showed stimulatory effects on cell growth and cell damage repair in BAEC, but also appeared to show the most anti-aging activity among all the herbal components of So-Hap-Hyang-Won.
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