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Oxidant-induced senescence in G6PD-deficient cells

Oxidant-induced senescence in G6PD-deficient cells

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第六届全国自由基生物学与自由基医学学术会议和海峡两岸自由基生物学与自由基医学学术会议

作者： Daniel Tsun-yee Chiu Graduate Institute of Medical Biotechnology and School of Medical Technology Chang Gung University Kwei-san Tao-yuan Taiwan Department of Clinical Pathology Chang Gung Memorial Hospital Kwei-san Tao-yuan Taiwan

Glucose-6-phosphate dehydrogenase (G6PD) is involved in the generation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) and the maintenance of the cellular redox balance. At cellular level, reactive oxygen species (ROS) can induce cellular oxidative damage and cause senescence. In our previous data, the accelerated senescence in G6PD-deficient human foreskin fibroblast (HFF1) cell was accompanied by an early increase in intracellular oxidative stress. In the present study, we tested for their sensitivities of hydrogen peroxide (H2O2) to a sub-lethal oxidative insult;HFF1 cells exhibited an increased susceptibility to induction of senescent phenotypes. These cells exhibited signs of aging as indicated by large, flattened morphology and senescence-associated β-galactosidase (SA-β-gal) staining. Ectopic expression of active G6PD in the deficient cells prevented their senescence, which induced by H2O2. Treated with H2O2, the intracellular G6PD activity was significant decrease and the ratio of NADPH/NADP was the same manner. The amount of 8-OHdG in the cellular DNA increased markedly when HFF1 cells were treated with H2O2 Such increase in 8-OHdG was also according with the population double levels. We found that G6PD activity is important role of cellular senescence when exposed to hydrogen peroxide. Moreover, our G6PD-deficient HFF is envisaged as a model system to delineate the effect of oxidative stress and cellular senescence.

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Susceptibility of G6PD-deficient human fibroblast to enterovirus 71 infection

Susceptibility of G6PD-deficient human fibroblast to enterov...

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第六届全国自由基生物学与自由基医学学术会议和海峡两岸自由基生物学与自由基医学学术会议

作者： Hung-vao Ho T.T.Yen Daniel Tsun-yee Chiu Graduate Institute of Medical Biotechnology and School of Medical Technology Chang Gung University Kwei-san Tao-yuan Taiwan Graduate Institute of Medical Biotechnology and School of Medical Technology Chang Gung University Kwei-san Tao-yuan Taiwan Department of Clinical Pathology Chang Gung Memorial Hospital Kwei-san Tao-yuan Taiwan

Accumulating evidence suggests that the cellular redox status plays an important role in regulating viral replication and infectivity. G6PD-deficient human foreskin fibroblast (HFF) is under higher oxidative stress. In this study, experiments were performed to compare the susceptibility of normal (HFF3) and G6PD-deficient (HFF1) cells to enterovirus7l (EV71) infection. After EV71 infection, both types of cells developed cytopathic effect. There was a significant difference in cell viability of both types of cells: cell viability of HFF1 was 71% of uninfected control whereas the viability of HFF3 was 83% of uninfected control. The amount of viral particles collected from HFF1 (2.2×104 PFU/ml) was larger than HFF3 (1.2×104 PFU/ml). G6PD plays a role in the protection of cells from viral infection was further supported by the results that ectopic expression of G6PD in the deficient cells prevented the loss of viability upon viral infection and inhibited the amplification ability of virus. The GSH/GSSG ratio in G6PD-deficient cells was lower than G6PD over-expressing cells. Taken together, our new findings support the notion that G6PD-deficient HFF is more susceptible to EV71 infection.

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OXIDATIVE STRESS IN MITOCHONDRIAL ENCEPHALOM-YOPATHIES ASSOCIATED WITH MITOCHONDRIAL DNA MUTATIONS

OXIDATIVE STRESS IN MITOCHONDRIAL ENCEPHALOM-YOPATHIES ASSOC...

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第六届全国自由基生物学与自由基医学学术会议和海峡两岸自由基生物学与自由基医学学术会议

作者： Yau-Huei Wei. Ching-You Lu, Yin-Cheu Chen, Yi-Shing Ma, and Chun-Yi Liu Department of Biochemistry, Yang-Ming University, Taipei 112, Taiwan

More than one hundred mutations in mtDNA have been found in the affected tissues of patients with mitochondrial encephalomyopathies. It is well established that some of the mtDNA mutations may impair mitochondrial respiratory function and generate more superoxide anions and hydrogen peroxide via electron leakage in affected cells. We have hypothesized that oxidative stress is a contributory factor for the pathogenesis of mitochondrial diseases. It is of our interest to understand the consequences of oxidative stress in human cells harboring pathogenic mutations of mtDNA. Recently, we found that RNA, protein, and activity levels of Mn-SOD are increased two- to three-fold in skin fibroblasts of patients with CPEO syndrome. However, the other antioxidant enzymes were not changed by the same way at RNA, protein, and activity levels. The imbalance in the expression of these antioxidant enzymes may result in a condition that the production of ROS is in excess of their removal, which in turn may elicit an increase of oxidative stress in the fibroblasts. We detected higher intracellular levels of superoxide anions and hydrogen peroxide and oxidative damage to DNA and lipids in skin fibroblasts from patients with mitochondrial encephalomyopathies as compared with those of age-matched controls. On. the other hand, by cDNA microarray and RT-PCR, we identified several clusters of genes whose expression are altered in the skin fibroblasts of our MERRF patients. Several clusters of the genes related to oxidative stress response were up-regulated, and another gene clusters related to energy metabolism and protein synthesis were down-regulated. One of the most striking findings is the increase in the levels of mRNA, protein, and activities of matrix metalloproteinases (MMPs) 1 and 2, which could be induced by hydrogen peroxide. By using confocal microscopy, we observed distinct derangement of mitochondrial network in skin fibroblasts of the MERRF patients. Taken together, we sugges

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Inhibition of early atherosclerosis by total flavonoids of Astragalus and combination of vitamin E plus C in rabbits with diet-induced hypercholesterolemia

Inhibition of early atherosclerosis by total flavonoids of A...

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第六届全国自由基生物学与自由基医学学术会议和海峡两岸自由基生物学与自由基医学学术会议

作者： Critchley J.A.J.H Thomas G Neil James A.E Tomlinson Brine Division of Clinical Pharmacology Department of Medicine and Therapeutics The Laboratory Animal Services Centres CUHK HK

Antioxidants are hypothesized to help prevent atherosclerosis, in part, by blocking lipoprotein oxidation. We investigated the effect of total flavonoids of Astragalus (TEA) and a combination of vitamin E plus C on atherogensis in high cholesterol-fed rabbits. Seventy-four males New Zealand White rabbits were divided into 5 groups. The rabbits were given either normal chow (A group, n=14) or 1% high cholesterol food (B to E groups, which were either untreated (group B) or receiving vitamin E (400 IU/day) plus vitamins C (500 mg/day) or TFA (60 or 120 mg/day) respectively by gavage, n=15/group) for 12 weeks. The study demonstrated that feeding the high cholesterol diet, as expected, caused a significant increase in total- and LDL-cholesterol, triglyceride, aortic fatty streak area and cholesterol content and the ratio of intima to media average thickness. TFA significantly reduced plasma levels of total- (p<0.05) and LDL-cholesterol (p<0.05 to 0.01) and enhanced HDL-cholesterol levels (p<0.01). TFA markedly reduced the fatty streak area by 43.6 and 63.6% (p<0.01), respectively. The combination of vitamin E plus C significantly reduce plasma total cholesterol (p<0.01) and triglyceride levels (p<0.05), the cholesterol content of the aortic arch (p<0.05), the ratio of intima to media average thickness (p<0.05) and fatty streak area by 51.8% (p<0.05). The vitamin combination increased the plasma antioxidant activity, including the ferric reducing ability of plasma (FRAP) (p<0.01 to 0.001) and as expected, α-tocopherol levels (p<0.01). There was no correlation between the fatty streak area of the aorta levels of total cholesterol in plasma or antioxidants indices, suggesting that TFA and the vitamin combination reduced the development of atherosclerosis by mechanisms in addition to their potent antioxidative activity.

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Over-expression of wild type UCP2,but not its mutant form UCP2 (D212N),induces mitochondrial dysfunctions and cell senescence of hepatocarcinoma cells

Over-expression of wild type UCP2,but not its mutant form UC...

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第六届全国自由基生物学与自由基医学学术会议和海峡两岸自由基生物学与自由基医学学术会议

作者： Lei Gao, Yingli Shang, Fang Yang, Honggang Wang, Shusen Liu and Quan Chen The State Key Laboratory of Biomembrane and Membrane Biotechnology, Chinese Academy of Sciences, Beijing 100080, P.R. China, chenq@*** Drug Discovery Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA

Uncoupling protein 2 (UCP2), discovered in 1997, belongs to a family of inner mitochondrial membrane proteins that, in general, function as proton transporter. The physiological function of UCP2 is to uncouple respiration from ATP synthesis and thus, to dissipate the energy stored in the proton electrochemical gradient as heat. In addition to functioning as a thermogen, the ubiquitously expressed uncoupling protein-2 (UCP2) was suggested to play critical roles in regulating cellular reactive oxygen species (ROS) production and modulating cellular stress responses. However, the underlying mechanisms of how this mitochondrial inner membrane protein achieves such diverse functions are not *** this study, we found that, when stably over-expressed in HepG 2 cells, wild type (wt) UCP2 induced significant proportion of the cells to have a senescent-like phenotype characterized by growth retardation, increased cell size, and positive p-Galactosidase (β-gal) staining. Over-expression of wtUCP2 caused significant reduction of mitochondrial membrane potential (ΔΨm), increased mitochondrial mass enhanced cellular oxygen consumption and intracellular ROS production, indicating impaired mitochondrial functions. In contrast, cells over-expressing identical levels of mutant UCP2 (D212N), which lack proton translocation activity, or cells treated with siRNA that specifically knock down the expression of UCP2, did not show senescent-like phenotypes and associated mitochondrial abnormalities. Furthermore, we found telomere shortening, mitochondrial DNA (mtDNA) mutations and rearrangements in cells that over-expressed wtUCP2, but not in siRNA treated cells or in cells that over-expressed mutant UCP2 (D212N). Our data suggest that the over-expression of wtUCP2 in HepG2 cells causes abnormal mitochondrial physiology that lead to mtDNA and telomere damage and ultimately cellular senescence. Taken together, UCP2 may be a potential regulator of cell senescence through regulating cellul

关键词： Uncoupling protein 2 (UCP2) Reactive Oxygen Species (ROS) Cell senescence Mitochondria

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Ischemic preconditioning attenuate postischemic leukocyte-endothelial cell adhesive interactions:the role of TNF-α

Ischemic preconditioning attenuate postischemic leukocyte-en...

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第六届全国自由基生物学与自由基医学学术会议和海峡两岸自由基生物学与自由基医学学术会议

作者： Li-Man Hung and Fu-Chan Wei Department of Life Science, College of Medicine, Chang Gung University, No. 259, Wen-Hwa 1st Road, Kwei-Shan, Tao-Yuan 333. Taiwan, E-mail: lisahung@mail.cgu.edu.tw

Ischemia-reperfusion (I/R) injury is a complex process involving the generation and release of inflammatory cytokines, accumulation and infiltration of neutrophils and macrophages, that disturb the microcirculatory hemodynamics. Nonetheless, ischemic preconditioning (IPC) is known to produce immediate tolerance to subsequent prolonged I/R insults, although its underlying mechanism remains largely unknown. Our study investigated the role of IκB-α-NF-κB-TNF-α(tumor necrosis factor-α) pathway in IPC’s ability to ameliorate I/R-induced microcirculatory disturbances in cremaster muscle flaps. Male Sprague Dawley rats were randomized (n=8 per group) into three groups: sham-operated control group, I/R group (4 h of pudic epigastric artery ischemia followed by 2 h of reperfusion), and IPC + I/R group (three cycles of 10 min ischemia followed by 10 min reperfusion before I/R). Intravital microscopy was used to observe leukocyte/endothelial cell interactions and quantify functional capillaries in cremaster muscles. I/R markedly increased the number of rolling, adhering, and migrating leukocytes. It was also observed that I/R significantly increased the TNF-αexpressions in these injured tissues. On the other hand, IPC prevented the I/R-induced increases in leukocyte rolling, adhesion, and transmigration. Moreover, TNF-αprotein production and its mRNA expression were downregulated in the IPC group. Finally, I/R-induced IβB-αphosphorylation and NF-βB (p65) nucleus translocation were both suppressed by IPC. These results indicated that IPC attenuated NF-βB activation and subsequently reduced TNF-αexpression, which resulted in the amelioration of microcirculatory disturbances in I/R-injured cremaster muscles.

关键词： ischemic preconditioning ischemia-reperfusion microcirculation leukocyte TNF-α NF-κB

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EFFECTS OF 17β-ESTRADIOL AND ICI 182,780 ONPARAQUAT-INDUCED LIPID PEROXIDATION AND VASCULARNITRIC OXIDE （NO） IN FEMALE SD RATS

EFFECTS OF 17β-ESTRADIOL AND ICI 182,780 ONPARAQUAT-INDUCED...

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第六届全国自由基生物学与自由基医学学术会议和海峡两岸自...

作者：黄秋峰楼迎统 Department of Physiology Chang Gung UniversityTao-YuanTaiwan Department of Life Science Chang Gung UniversityTao-YuanTaiwan

＜正＞ Estrogen （E2） is known to protect cardiovascular functions partially via direct vascular actions. Recent evidence suggest that females exhibit less oxidative stress than males but whether such observations reflect E2’s antioxidative effects and whether estrogen receptor （ER） is involved is not known. We thus experimentally induce oxidative stress by injecting paraquat （40 mg/kg） peritoneally in sham operated and ovariectomized （OVX） SD rats. In half of the sham rats, ER antagonist （ICI 182,780） was injected daily for 12d. Tissue malondialdehyde level （MDA） was determined in aorta, lung, and liver. We found that ovariectomy decreased plasma E2 level significantly and ICI 182,780 did not alter plasma E2 level but eliminated natural hormone cycle of the treated animals. In our preliminary data, lower level of E2 in OVX rats significantly increased body weight and paraquat-induced MDA level in aorta （vs. sham, P＜0.001）. However, ICI 182,780 altered MDA level of aorta （vs. sham, P=0.056） and liver but only significantly in liver （vs. sham, P＜0.01）. We also determined the aortic concentration of NO and found that both OVX and ICI 182,780-treatments slightly reduced NO concentration （sham vs. OVX, P=0.1696 , sham vs. ICI 182,780, P=0.2349）. These data suggest that E2 play a crucial role to protect paraquat-induced lipid peroxidation of aorta and liver in female rats. In addition, ER may be associated with the protection of E2 on paraquat-induced lipid peroxidation.

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Use of whole blood directly for single-cell gel electrophoresis （comet） assay of DNA strand breaks both in vivo and in vitro

Use of whole blood directly for single-cell gel electrophore...

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第六届全国自由基生物学与自由基医学学术会议和海峡两岸自...

作者： Cheng-Hung Chuang and Miao-Lin Hu Department of Food Science, Chung-Hsing University, 250 Kuo-Kuang Raod, Taichung, 402 Taiwan,

＜正＞ The present study investigated the use of whole blood from human and rats directly for single-cell gel electrophoresis （comet） assay of DNA strand breaks. As little as 20 μL of whole blood was sufficient for comet assay, and the comet images obtained from whole blood were not different from those obtained from isolated lymphocytes. The DNA remained intact up to 4 h at 4℃after isolation and had no observable strand breakage when whole blood was cryopreserved （at -80℃） in 10% pre-cooled DMSO up to 60 days. To demonstrate that the whole blood technique could be applied to in vivo studies, we injected rats with a known carcinogen Fe/NTA and measured DNA strand breaks in whole blood in comparison with isolated lymphocytes. We showed that Fe/NTA injection resulted in similar extent of DNA strand breakage in both whole blood and lymphocytes, indicating that whole blood method can be used for in vivo genotoxic studies. One disadvantage of the whole blood technique is that whole blood cannot be used for in vitro studies because of the interferences from red blood cell （RBC） components. However, this problem can be overcome by prior hemolysis of RBCs and a brief centrifugation to obtain white blood cells （WBCs）, which can then be used for in vitro incubation with genotoxic compounds before comet assay. Overall, this whole-blood technique for comet assay is expected to provide a simple, rapid and cost-effective alternative for the existing comet assay using isolated lymphocytes in situations such as when time and cost are limiting factors.

关键词： Comet assay whole blood lymphocytes white blood cells cryopreservation.

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