• Journal of Plant Biotechnology
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• 제33권1호
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• pp.1-9
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• 2006

도처에 분포하는 peroxiredoxins (Prxs)은 세포 내 방어신호전달 과정에서 다양한 기능을 하는 것으로 나타났다. Prxs는 크게 typical 2-Cys Prx, atypical 2-Cys Prx와 1-Cys Prx의 세 부류로 분류되는데, 이것들은 cysteine 잔기의 수와 촉매기전에 따라 구분된다. 세 종류의 단백질 중, N-말단에 peroxidatic cysteine 잔기를 포함하는 typical 2-Cys Prx는 $H_2O_2$ 분해과정 동안 과산화물-의존적인 sulfenic acid로의 산화와 thiol-의존적 환원과정이 순환되어 일어난다. Sulfenic acid는 고농도의 $H_2O_2$와 Trx, Trx reductase와 NADPH를 포함하는 촉매 요소의 존재하에 cysteine sulfenic acid로 과산화 될 수 있다 과산화된 2-Cys Prx는 ATP 의존성 효소인 sulfiredoxin의 작용에 의해 천천히 환원된다. 세포가 강력한 산화나 열 충격 스트레스에 노출되면, 2-Cys Prx는 LMW 단백질에서 HMW complex로 구조를 변화시켜 peroxidase에서 chaperone으로 기능의 전환을 일으킨다. 2-Cys Prx의 C-말단 부분 역시 이러한 구조적 전환에 중요한 역할을 한다. 따라서, C-말단이 잘려진 단백질은 과산화가 되지 않고 단백질의 구조와 기능이 조절될 수 없다. 이러한 반응들은 활성 자리인 peroxidatic cysteine 잔기에 의해 일차적으로 유도되며, 그것은 세포에서 '$H_2O_2$ sensor' 로서 작용하다. 2-Cys Prx의 가역적인 구조와 기능 변화는 세포가 외부자극에 적응하는 수단으로 작용하며, 아마도 세포내 방어신호체계를 활성화 시키는 것으로 생각된다. 특히, chloroplast에 존재하는 식물 2-Cys Prx는 촉매반응 동안 주된 구조적인 변화를 나타내는 역동적인 단백질 구조를 가지고 있어서, 산화-환원 의존적으로 super-complex를 형성하고 가역적으로 thylakoid membrane에 부착한다.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 1996년도 춘계학술대회
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• pp.19-29
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• 1996

The neurological manifestations of AIDS include dementia, encountered even in the absence of opportunistic superinfection or malignancy. The AIDS Dementia Complex appears to be associated with several neuropathological abnormalities, including astrogliosis and neuronal injury or loss. How can HIV-1 result in neuronal damage if neurons themselves are only rarely, if ever, infected by the vitus\ulcorner In vitro experiments from several different laboratiories have lent support to the existence of HIV- and immune-related toxins. In one recently defined pathway to neuronal injury, HIV-infected macrophages/microglia as well as macrophages activated by HIV-1 envelope protein gp120 appear to secrete excitants/neurotoxins. These substances may include arachidonic acid, platelet-activating factor, free radicals (NO - and O$_2$), glutamate, quinolinate, cysteine, cytokines (TNF-${\alpha}$, IL1-B, IL-6), and as yet unidentified factors emanating from stimulated macrophages and possibly reactive astrocytes. A final common pathway for newonal suscepubility appears to be operative, similar to that observed in stroke, trauma, epilepsy, and several neurodegenerative diseases, including Huntington's disease, Parkinson's disease, and amyotrophic lateral sclerosis. This mechanism involves excessive activation of N-methyl-D-aspartate (NMDA) receptor-operated channels, with resultant excessive influx of Ca$\^$2+/ leading to neuronal damage, and thus offers hope for future pharmacological intervention. This chapter reviews two clinically-tolerated NMDA antagonists, memantine and nitroglycerin; (ⅰ) Memantine is an open-channel blocker of the NMDA-associated ion channel and a close congener of the anti-viral and anti-parkinsonian drug amantadine. Memantine blocks the effects of escalating levels of excitotoxins to a greater degree than lower (piysiological) levels of these excitatory amino acids, thus sparing to some extent normal neuronal function. (ⅱ) Niuoglycerin acts at a redox modulatory site of the NMDA receptor/complex to downregulate its activity. The neuroprotective action of nitroglycerin at this site is mediated by n chemical species related to nitric oxide, but in a higher oxidation state, resulting in transfer of an NO group to a critical cysteine on the NMDA receptor. Because of the clinical safety of these drugs, they have the potential for trials in humans. As the structural basis for redox modulation is further elucidated, it may become possible to design even better redox reactive reagents of chinical value. To this end, redox modulatory sites of NMDA receptors have begun to be characterized at a molecular level using site-directed mutagenesis of recombinant subunits (NMDAR1, NMDAR2A-D). Two types of redox modulation can be distinguished. The first type gives rise to a persistent change in the functional activity of the receptor, and we have identified two cysteine residues on the NMDARI subunit (#744 and #798) that are responsible for this action. A second site, presumably also a cysteine(s) because <1 mM N-ethylmaleimide can block its effect in native neurons, underlies the other, more transient redox action. It appears to be at this, as yet unidentified, site on the NMDA receptor that the NO group acts, at least in recombinant receptors.

• Nutritional Sciences
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• 제5권4호
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• pp.228-233
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• 2002

The low molecular weight zinc-binding protein metallothionein(MT) contains 32% cysteine and has been shown to efficiently scavenge hydroxyl radicals in vitro. MT expression is induced by oxidative stress and an antioxidant role for this protein has therefore been proposed. This review mainly focuses on the evidence for this role arising from studies using genetically modified animals and cells which either over- or under-express MT. Despite some considerable disparity of results in the literature, reported studies do generally support an antioxidant role. Nevertheless, oxidant stress at non-physiological treatment levels has been the preferred experimental model and there is little information about the role of MT in physiological oxidative stress. Although it is presumed that the mechanism by which MT has an antioxidant effect involves oxidation of cysteinal thiols, it is possible that zinc release from MT is in itself an important signalling factor.

• 한국영양학회:학술대회논문집
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• 한국영양학회 2002년도 추계 심포지움초록
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• pp.1171-1177
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• 2002

The low molecular weight zinc-binding protein metallothionein (MT) contains 32% cysteine and has been shown to efficiently scavenge hydroxyl radicals in vitro. MT expression is induced by oxidative stress and an antioxidant role for this protein has therefore been proposed. This review mainly focuses on the evidence for this role arising from studies using genetically modified animals and cells which either over-or under-express MT. Despite some considerable disparity of results in the literature, reported studies do generally support an antioxidant role. Nevertheless, oxidant stress at non-physiological treatment levels has been the preferred experimental model and there is little information about the role of MT in physiological oxidative stress Although it is presumed that the mechanism by which MT has an antioxidant effect involves oxidation of cysteinal thiols, it is possible that zinc release from MT is in itself an important signalling factor.

• 한국영양학회:학술대회논문집
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• 한국영양학회 2002년도 추계학술대회 및 총회
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• pp.73-82
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• 2002

The low molecular weight zinc-binding protein metallothionein (U) contains 32% cysteine and has been shown to efficiently scavenge hydroxyl radicals in vitro. MT expression is induced by oxidative stress and an antioxidant role for this protein has therefore been proposed. This review mainly focuses on the evidence for this role arising from studies using genetically modified animals and cells which either over- or under-express MT. Despite some considerable disparity of results in the literature, reported studies do generally support an antioxidant role. Nevertheless, oxidant stress at non-physiological treatment levels has been the preferred experimental model and there is little information about the role of MT in physiological oxidative stress. Although it is presumed that the mechanism by which MT has an antioxidant effect involves oxidation of cysteinal thiols, it is possible that zinc release from MT is in itself an important signalling factor.

• Journal of Ecology and Environment
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• 제29권1호
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• pp.61-67
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• 2006

Tomato (Lycopersicon esculentum Mill) seedlings exposed to various concentrations of $CdCl_2(0{\sim}100{\mu}M)$ in a nutrient solution for up to 9 days were analyzed with respect to the thiol changes and oxidative stress. The Cd exposure increased total non-protein thiols (NPT) and cysteine in both leaves and roots, total glutathione in leaves, and the ratios of oxidized glutathione (GSSG)/reduced glutathione (GSH) in both leaves and roots, but decreased the ratio of dehydroascorbate (DASA)/ascorbate(ASA) in leaves. Our results suggest that the Cd-induced GSH depletion due to thiol synthesis and oxidation alters the antioxidant activity of seedlings for $H_2O_2$, and the subsequent $H_2O_2$ accumulationand oxidative stress result in phytotoxicity.

• 생약학회지
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• 제30권3호
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• pp.306-313
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• 1999

Polyphenol Oxidase(PPO) was purified from an extract of Ginkgo biloba leaves by ammonium sulfate fractionation followed by sephadex G-150 column chromatography, which resulted in a 18-fold increase in specific activity. The enzyme was most active at pH 8.5 and the temperature optimum for the PPO catechol oxidation reaction was $45^{\circ}C$. Heat inactivation studies showed that heating for 7, 9 and 48 min, at 80, 70 and $60^{\circ}C$ respectively caused a 50% loss in enzymatic activity and that the enzyme was completely inactivated after heat treatment at $90^{\circ}C$ for 60 min. Km values of the PPO for catechol, hydroquinone and 4-methylcatechol derived from Lineweaver-Burk plots were $6.06\;{\times}\;10^{-4}M,\;1.02\;{\times}\;10^{-3}M,\;1.41\;{\times}\;10^{-3}M$ respectively. Of the substrates tested, 4-methylcatechol was oxidized most readily and the enzyme did not oxidize monophenols. The enzyme datalyzed browning reaction was completely inhibited in the presence of reducing reagents, namely ascorbic acid, cysteine, glutathione, 2-mercaptoethanol, potassium metabisulfite at 0.5 mM level. Sodium chloride showed very little inhibition effect on Ginkgo biloba leaves PPO. Lineweaver-Burk analysis of inhibition data revealed that the inhibition by cysteine, 2-mercaptoethanol, potassium cyanide was competitive with ki values of $1.1\;{\times}\;10^{-5}M,\;2.4\;{\times}\;10^{-5}M,\;8\;{\times}\;10^{-5}M$, respectively. Among the divalent cations, $Cu^{2+}ion$ was a strong activator on PPO and $Mn^{2+}ion$ was little or no effect on PPO activity $Ni^{2+}ion$ was an inhibitor on PPO.

• 한국수산과학회지
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• 제20권5호
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• pp.419-430
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• 1987

지질산화생성물에 의한 DNA손상작용 및 그 억제 기구를 밟히기 위하여 linoleic acid와 plasmid DNA와의 모델계를 통하여 검토하였는데, 그 결과를 요약하면 다음과 같다. 1. Linoleic acid의 산화에 의하여 DNA가 손상되었으며, 그 정도는 linoleic acid의 양이 많을 수록 크게 나타났다. 2. Linoleic acid의 산화에 의한 DNA손상작용은 POV 100 mea/kg이하인 산화초기에서도 빠르게 진행되었다. 산화초기의 DNA손상작용에는 활성산소 종의 관여가 크게 나타났는데, 그 중에서도 일중항 산소와 superoxide anion의 영향이 큰 것으로 나타났다. 3. 지질 2차반응생성물인 malonaldehyde와 hexanal의 DNA손상작용은 linoleic acid경우와는 달리 활성산소종과는 무관하였으며 DNA와 와의 복합체형성에 의하였다. 4. Linoleic acid hydroperoxide의 DNA 손상작용은 linoleic acid의 초기신화에 의한 DNA손상작용 보다 크게 나타났고, 활성산소종의 영향은 없었다. 5. 지진산화생성물에 의한 DNA손상 작용은 천연 항산화성분(마늘 및 생강추출물) 및 활성산소소거제($\alpha-tocopherol 및 superoxide dismutase$의 첨가에 의하여 크게 억제되었다. 특히 . 마늘 및 생강추출물은 활성산소종의 생성을 비롯하여 공액 diene 및 POV의 증가 또한 크게 억제하였다.

• Toxicological Research
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• 제31권3호
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• pp.241-253
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• 2015

Furan ($C_4H_4O$) is a volatile compound formed mostly during the thermal processing of foods. The toxicity of furan has been well documented previously, and it was classified as "possible human carcinogen (Group 2B)" by the International Agency for Research on Cancer. Various pathways have been reported for the formation of furan, that is, thermal degradation and/or thermal rearrangement of carbohydrates in the presence of amino acids, thermal degradation of certain amino acids, including aspartic acid, threonine, ${\alpha}$-alanine, serine, and cysteine, oxidation of ascorbic acid at higher temperatures, and oxidation of polyunsaturated fatty acids and carotenoids. Owing to the complexity of the formation mechanism, a vast number of studies have been published on monitoring furan in commercial food products and on the potential strategies for reducing furan. Thus, we present a comprehensive review on the current status of commercial food monitoring databases and the possible furan reduction methods. Additionally, we review analytical methods for furan detection and the toxicity of furan.

• Asian-Australasian Journal of Animal Sciences
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• 제26권5호
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• pp.732-742
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• 2013

Flavour comprises mainly of taste and aroma and is involved in consumers' meat-buying behavior and preferences. Chicken meat flavour is supposed to be affected by a number of ante- and post-mortem factors, including breed, diet, post-mortem ageing, method of cooking, etc. Additionally, chicken meat is more susceptible to quality deterioration mainly due to lipid oxidation with resulting off-flavours. Therefore, the intent of this paper is to highlight the mechanisms and chemical compounds responsible for chicken meat flavour and off-flavour development to help producers in producing the most flavourful and consistent product possible. Chicken meat flavour is thermally derived and the Maillard reaction, thermal degradation of lipids, and interaction between these 2 reactions are mainly responsible for the generation of flavour and aroma compounds. The reaction of cysteine and sugar can lead to characteristic meat flavour specially for chicken and pork. Volatile compounds including 2-methyl-3-furanthiol, 2-furfurylthiol, methionol, 2,4,5-trimethyl-thiazole, nonanol, 2-trans-nonenal, and other compounds have been identified as important for the flavour of chicken. However 2-methyl-3-furanthiol is considered as the most vital chemical compound for chicken flavour development. In addition, a large number of heterocyclic compounds are formed when higher temperature and low moisture conditions are used during certain cooking methods of chicken meat such as roasting, grilling, frying or pressure cooking compared to boiled chicken meat. Major volatile compounds responsible for fried chicken are 3,5-dimethyl-1,2,4-trithiolanes, 2,4,6-trimethylperhydro-1,3,5-dithiazines, 3,5-diisobutyl-1,2,4-trithiolane, 3-methyl-5-butyl-1,2,4-trithiolane, 3-methyl-5-pentyl-1,2,4-trithiolane, 2,4-decadienal and trans-4,5-epoxy-trans-2-decenal. Alkylpyrazines were reported in the flavours of fried chicken and roasted chicken but not in chicken broth. The main reason for flavour deterioration and formation of undesirable "warmed over flavour" in chicken meat products are supposed to be the lack of ${\alpha}$-tocopherol in chicken meat.