• Biomolecules & Therapeutics
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• v.21 no.3
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• pp.241-245
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• 2013

Aging is the single most important risk factor that increases susceptibility to many forms of diseases. As such, much effort has been put forward to elucidate the mechanisms behind the processes of aging and to discover novel compounds that retain anti-aging activities. Korean red ginseng has been used for a variety of medical purposes in eastern countries for several thousands of years. It has been shown that Korean red ginseng affects a number of biological activities including, but not limited to, anti-inflammatory, anti-oxidative and anti-diabetic pathways. However, few studies have been performed to evaluate its anti-aging effects with an in vivo system. Here Drosophila melanogaster as an in vivo model organism demonstrates that Korean red ginseng tonic extends lifespan, increases resistance to starvation stress and prevents weight gain. This data suggest that Korean red ginseng may regulate organisms' metabolism in favor of extending lifespan.

• Environmental Analysis Health and Toxicology
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• v.18 no.3
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• pp.175-182
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• 2003

Bisphenol A shares similarities in structure, metabolism and action with DES, a known human teratogen and carcinogen. Bisphenol A, a monomer of polycarbonate and epoxy resins, has been detected in canned food and human saliva. The purpose of the this study was to evaluate the cytotoxicity, cell proliferation of bisphenol A In the presence of a rat liver S9 mix, contaning cytochrome P450 enzymes, and Cu (II). In the present study, Bisphenol A in combination with Cu (II) exhibited a enhancement in cytotoxicity which were inhibited by free radical scavengers. The content of malondialdehyde, an end product of lipid peroxidation, was also found to increase with concentration of bisphenol A. Also, we examined the change of CuZn-SOD, Mn-SOD, catalase and GPx activities in the MCF-7 cells exposed to bisphenol A. The activities of CuZn-SOD, CPx, catalase were found to decrease with bisphenol A concentration. Meanwhile, the activity of Mn-SOD was unchanged. This indicated that elevated oxidative stress caused by imbalance between the production and removal of free radicals occurred in cells.

• BMB Reports
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• v.42 no.8
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• pp.475-481
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• 2009

Emerging data demonstrate pivotal roles for brain insulin resistance and insulin deficiency as mediators of cognitive impairment and neurodegeneration, particularly Alzheimer's disease (AD). Insulin and insulin-like growth factors (IGFs) regulate neuronal survival, energy metabolism, and plasticity, which are required for learning and memory. Hence, endogenous brain-specific impairments in insulin and IGF signaling account for the majority of AD-associated abnormalities. However, a second major mechanism of cognitive impairment has been linked to obesity and Type 2 diabetes (T2DM). Human and experimental animal studies revealed that neurodegeneration associated with peripheral insulin resistance is likely effectuated via a liver-brain axis whereby toxic lipids, including ceramides, cross the blood brain barrier and cause brain insulin resistance, oxidative stress, neuro-inflammation, and cell death. In essence, there are dual mechanisms of brain insulin resistance leading to AD-type neurodegeneration: one mediated by endogenous, CNS factors; and the other, peripheral insulin resistance with excess cytotoxic ceramide production.

• Proceedings of the PSK Conference
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• 2003.10a
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• pp.66-69
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• 2003

Mast cell playa crucial role in allergic and inflammatory disease through the exocytosis of preformed granule-associated mediators, such as histamine, serotonin, proteases and the generation of newly synthesized lipid mediators such as, leucotrien (LT) $C_4$ and prostaglandin (PG) $D_2$ in response to crosslinking of high affinity for IgE (Fc$\gamma$RI). New eicosanoids are synthesized by the oxidative metabolism of arachidonic acid, which is generally esterified sn-2 position of the major classes of glycerophospholipids. (omitted)

• BMB Reports
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• v.54 no.5
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• pp.253-259
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• 2021

Aging is characterized by a functional decline in most physiological processes, including alterations in cellular metabolism and defense mechanisms. Increasing evidence suggests that caloric restriction extends longevity and retards age-related diseases at least in part by reducing metabolic rate and oxidative stress in a variety of species, including yeast, worms, flies, and mice. Moreover, recent studies in invertebrates - worms and flies, highlight the intricate interrelation between reproductive longevity and somatic aging (known as disposable soma theory of aging), which appears to be conserved in vertebrates. This review is specifically focused on how the reproductive system modulates somatic aging and vice versa in genetic model systems. Since many signaling pathways governing the aging process are evolutionarily conserved, similar mechanisms may be involved in controlling soma and reproductive aging in vertebrates.

• Asian-Australasian Journal of Animal Sciences
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• v.23 no.10
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• pp.1299-1307
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• 2010

This study was conducted to evaluate the effect of dietary antioxidant and energy density on performance and antioxidative status in transition cows. Forty cows were randomly allocated to 4 dietary treatments in a $2{\times}2$ factorial design. High or low energy density diets (1.43 or 1.28 Mcal $NE_L$/kg DM, respectively) were formulated with or without antioxidant (AOX, a dry granular blend of ethoxyquin and tertiary-butylhydroquinone; 0 or 5 g/cow per d). These diets were fed to cows for 21 days pre-partum. During the post-partum period, all cows were fed the same lactation diets, and AOX treatment followed as for the pre-partum period. Feeding a high energy diet depressed the DMI, milk yield, and 4% fat-corrected milk (FCM) of cows. However, AOX inclusion in the diet improved the milk and 4% FCM yields. There was an interaction of energy density by AOX on milk protein, milk fat and total solids contents. Feeding a high energy diet pre-partum increased plasma glucose and ${\beta}$-hydroxybutyrate, whereas dietary AOX decreased plasma ${\beta}$-hydroxybutyrate value during the transition period. There were also interactions between time and treatment for plasma glutathione peroxidase activity and malondialdehyde content during the study. Cows fed high energy diets pre-partum had higher plasma glutathione peroxidase activity 3 days prior to parturition, compared with those on low energy diets. Inclusion of AOX in diets decreased plasma glutathione peroxidase activity in cows 3 and 10 days pre-partum. Addition of AOX significantly decreased malondialdehyde values at calving. Energy density induced marginal changes in fatty acid composition in the erythrocyte membrane 3 days post-partum, while AOX only significantly increased cis-9, trans-11 conjugated linoleic acid composition. The increase in fluidity of the erythrocyte membrane was only observed in the high energy treatment. It is suggested that a diet containing high energy density pre-partum may negatively affect the anti-oxidative status, DMI and subsequent performance. Addition of AOX may improve the anti-oxidative status and reduce plasma ${\beta}$-hydroxybutyrate, eventually resulting in improved lactation performance; the response to AOX addition was more pronounced on the high energy diet.

• The Korean Journal of Physiology
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• v.3 no.1
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• pp.11-18
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• 1969

Tissue homogenates of 10 kinds of human cancer tissues were incubated in medium containing either one of $C^{14}-1,\; C^{14}-2,\;or\; C^{14}-3-lactate $ as a substrate in order to observe the oxidative pathway of lactate in cancer tissues. Lactate concentration in incubation medium was maintained at 50 mg%. At the end of incubation period, gas samples and incubation media were analyzed for total $CO_2$ production rates, radioactivities of respiratory $CO_2$, lactate uptake rates and pyruvate appearance rates. The following results were obtained. 1. Lactate uptake rates in all of cancer tissues examined were less than $2.5\;{\mu}M/hr/gm$ and much lower than those in normal tissues. 2. In the 10 kind of human cancer tissues, total $CO_2$ production rates were less than $10\;{\mu}M/hr/gm$, in all cases. These lower values impressed that oxidative metabolism in tumor tissues generally inhibited as compared with that in normal tissue. On the other hand, fractions of $CO_2$ derived from lactate to total $CO_2$ production rates were less than 15% except one case These facts showed that oxidation of lactate into $CO_2$ was greatly inhibited in tumor tissues. 3. Respiratory $CO_2$ yields from C-1 carbon of lactate in various cancer tissues were mean of 77.7% of total $CO_2$ yield from lactate and $CO_2$ yields from C-2 and C-3 carbon of lactate were mean of 9.1% and 12.6% respectively. These facts showed that carboxyl carbon of lactate oxidized more easily than ${\alpha}\;and\;{\beta}$ carbon of lactate. 4. In 10 kinds of cancer tissues, fractions of disappeared lacteate from media into $CO_2$ and pyruvate, which expressed as RLD $co_2$ and RLDpy respectively, were about 5% in except 3 cases and less than 3% except one case. These fact showed that almost of disappeared lactate from media were degraded into compounds other than $CO_2$ and pyruvate. From the above date, it was suggested that in the oxidative pathway of lactate in cancer tissues $CO_2$ was easily Produced from carboxyl carbon of lactate by oxidative decarboxylation as in the normal tissue, and further oxidation of 2 carbon unit via TCA cycle was inhibited.

• Journal of Life Science
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• v.20 no.11
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• pp.1569-1576
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• 2010

Sweet potato (Ipomoea batatas L.) is widely used in Indonesia and other countries as a traditional medicine for the treatment of diabetes mellitus (DM). The MeOH extract of white skinned sweet potatoes (WSSP) was administered orally in doses of 100 and 200 mg/kg body weight in streptozotocin (STZ)-induced diabetic rats. Experimental diabetes was induced by a single dose of STZ (45 mg/kg, i.p.) injection. Oxidative stress was measured by tissue lipid peroxide (LPO) levels, serum aspartate transaminase (AST), alanine transaminase (ALT), total triglyceride (TG), total cholesterol (TC) and by antioxidative enzymatic activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione S-transferase in the liver. An increase in blood glucose, LPO level, AST, ALT, TG and TC levels was observed in the STZ-induced diabetic rats. Administration of MeOH extract of WSSP at a dose of 200 mg/kg for two weeks caused a significant reduction in blood glucose, LPO levels, AST, ALT, TG and TC levels in the STZ-induced diabetic rats. Furthermore, oral administration of MeOH extract showed significant improvement in the activities of antioxidant enzymes (SOD, GPx, and CAT) compared to STZ-induced diabetic rats. In conclusion, the obtained results clearly indicate the role of oxidative stress in the induction of diabetes, and that the protective effects of MeOH extracts of WSSP could be used to benefit diabetic patients.

• Journal of Marine Life Science
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• v.3 no.2
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• pp.74-80
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• 2018

Mercury (Hg) poses a threat to marine ecosystem due to continuous inflow from various industries and bioaccumulation to higher trophic level via food web. Mercury can adversely affect growth, development, reproduction and metabolism to aquatic organisms. In the present study, acute toxicity and oxidative stress markers (total glutathione content, and activities of GST, GR and GPx) were investigated in brackish water flea Disphanosoma celebensis exposed to HgCl₂ for 24 h. As results, Hg showed negative effect in survival of D. celebensis. 24 h-LC₅₀ value was determined as 0.589 mg/l (95% C.I. 0.521~0.655 mg/l). After exposure to Hg (0.08 and 0.4 mg/l) for 24 h, total glutathione content was significantly decreased, whereas GST, GPx and GR activities were enhanced. These findings indicate that Hg induced oxidative stress in D. celebensis, and oxidative stress markers may be involved in cellular defense against Hg - mediated toxicity. This study provides a better understanding of molecular mode of action of Hg toxicity in this specie and potent of molecular markers for heavy metal monitoring in marine ecosystem.

• Development and Reproduction
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• v.10 no.2
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• pp.105-113
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• 2006

Reactive oxygen species(ROS) generated in cellular metabolism have an effect on cell maturation and development. In human reproductive tract, oxidative injury by ROS may induce female infertility. Also, oxidative injury may be responsible for developmental retardation and arrest of mammalian preimplantation embryos. Activating transcription factor 4(ATF4) is a member of the cyclic-AMP response element-binding(CREB) familiy of basic region- leucine zipper(bZip). ATF4 is known to regulate stress response to protect cell from various stress factors and inducer of apoptisis. The purpose of this study was to investigate whether ATF4 is involved in the defensive mechanism in oxidative stress condition during the development of mouse preimplantation embryos. To verify the expression of ATF4 in oxidative stress condition, 2-cell stage embryos were cultured in HTF media containing 0.1mM, 0.5mM or 1mM hydrogen peroxide($H_2O_2$) for 1hr(2-cell), 8hr(4-cell), 17hr(8-cell), 24hr(morula), 48hr(early blastocyst) or 64hr(late blastocyst). The developmental rate decreased in the 0.1mM $H_2O_2$ treated group compared with control group. In embryos treated with 0.5mM and 1mM $H_2O_2$ showed 2-cell block. As a results of the semi-quantitative RT-PCR analysis of SOD1, ATF4 and Bax gene expression, SOD1, ATF4 and Bax genes were increased in 0.1mM, 0.5mM, 1mM $H_2O_2$ treated groups compared with control group. In 2-cell embryos, expression of SOD1, ATF4 and Bax genes were notably increased in 0.1mM, 0.5mM, 1mM $H_2O_2$ treated groups compared with control group. Immunofluorescence analysis showed that ATF4 protein was localized at the cytoplasm of preimplantation embryos. The increase in ATF4 immunoreactivety was observed in the 0.1mM, 0.5mM, 1mM $H_2O_2$ treated groups compared with control group. It suggests that oxidative stress by $H_2O_2$ induces expression of ATF4 and may be involved in protection mechanism in preimplantation embryos from oxidative injury.