• 한국식품영양과학회지
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• 제35권9호
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• pp.1159-1165
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• 2006

제2형 당뇨 동물모델(C57BL/KsJ-db/db)을 대상으로 대두 이소플라본의 주성분인 genistein과 daidzein의 항산화효능을 검증하고자 5주령의 수컷 C57BL/KsJ-db/db 마우스와 그의 이형접합체인 C57BL/KsJ-db/+ 마우스를 2주간 환경에 적응시킨 후 비당뇨군(db/+), 당뇨대조군(db/db), genistein 급여군(db/db-genistein), daidzein 급여군(db/db- daidzein)으로 나누어 6주간 사육하였다. 실험동물의 간, 부고환지방과 신주변지방의 조직무게는 당뇨군(db/db)이 비당뇨군(db/+)에 비해 유의적으로 높았으나, 심장무게는 유의적으로 낮았다. Genistein과 daidzein 급여는 장기무게 변화에 영향을 미치지 않았다. 적혈구의 SOD와 CAT활성은 혈당과 양의 상관성을 보였으나 GSH-Px활성은 음의 상관성을 나타내었다. 따라서 SOD와 CAT활성은 db/db군이 db/+군에 비해 유의적으로 높은 반면, GSH-Px 활성은 유의적으로 낮았다. Genistein과 daidzein 급여로 db/db군의 증가된 CAT활성은 감소되었으며 GSH-Px활성은 높게 나타났다. 적혈구의 GSH함량은 당뇨군들이 비당뇨군에 비해 유의적으로 높았으나 genistein과 daidzein에 의한 영향은 관찰되지 않았다. 간, 신장 및 심장조직 내 SOD활성은 유의적인 변화가 없었으나 간조직 중 CAT와 GSH-Px활성과 신장조직 중의 GSH-Px활성은 db/db군이 db/+군에 비하여 유의적으로 높게 나타난 반면 신장조직 중의 CAT활성과 심장조직 중의 CAT와 GSH-Px활성은 낮았다. 그러나 genistein과 daidzein 급여는 고혈당으로 인한 조직 내 CAT와 GSH- Px활성을 유의적으로 개선하였다. 적혈구를 비롯하여 모든 조직 내 지질과산화물 함량은 db/db군이 db/+군에 비하여 유의적으로 높았으나 genistein과 daidzein 급여로 간, 신장과 심장조직 중의 지질과산화물 생성이 유의적으로 억제되었다. 이와 같이 genistein과 daidzein은 제2형 당뇨동물에서 고혈당으로 야기되는 적혈구와 조직 내 항산화효소 변화를 완화하고 간, 신장 및 심장조직의 지질과산화물을 낮추는 것으로 관찰됨으로써 이들의 항산화작용을 통한 당뇨 합병증을 예방할 것으로 사료된다.

• 사상체질의학회지
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• 제22권1호
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• pp.49-58
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• 2010

1. Objectives: The purpose of this study is to find out the Anti-Oxidative effects of Soyangin Hyeongbangpaedok-san(HBP) in kidney and spleen cells of aged rats. 2. Methods: Aged rats used in this experiment were 6, 52, 68 weeks old. Each age group was divided into three groups again. One group was given no treatment, another group was dosed normal saline and the other group was dosed HBP decoction. The antioxidant effects of HBP decoction were measured by the levels of SOD, GSH, MDA and NO. 3. Results: and Conclusions: 1) The activity of SOD was significantly increased in kidney cells of 68w-HBP group. Deterioration of the activity of SOD in kidney cells was significantly suppressed according to increasing in age of the week. 2) The level of NO was significantly decreased in kidney cells of 68w-HBP group. Deterioration of The level of NO in kidney cells was significantly suppressed according to increasing in age of the week. 3) The activity of SOD was increased in spleen cells of 52w and 68w-HBP group. 4) The level of GSH was significantly increased in spleen cells of 68w-HBP group.

• 생명과학회지
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• 제13권6호
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• pp.911-916
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• 2003

The effects of Opuntia ficus-indica (OF) administration on the biochemical parameters of function in liver tissue and serum of $CCl_4$ treated rats were investigated. Opuntia ficus-indica (200 mg/kg) was administered into rats intraperitoneally for two weeks. $3.3m\ell$ of $CCl_4$$_4$ (50% $CCl_4$ : Olive oil = 1 : 1) was treated to rats on the 14th day and 15th day and they were operated on 15th day. We examined the antioxidative enzymatic activity by measuring the level of AST (Aspartate aminotransferase), ALT (Alanine aminotransferase), GSH (Glutathione reduced form), GSSG (Glutathione oxidezed form), GPx (GSH-peroxidase), SOD (Superoxide dismutase) and CAT (Catalase) in serum and liver tissue of rats. OFC administered group showed 24.8% of inhibitory effect in AST activity compared to $CCl_4$ -treated abnormal group (CTA). ALT level of OF administered group was decreased by 60.7% to the level of CTA. GSH, GSSG and GPx of OFC administered group were significantly higher than those of CTA group. SOD and CAT in OFC administered group were increased by 28.3% and by 16.9% respectively compared to those of CTA group.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2003년도 정기총회 및 학술발표회
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• pp.61-61
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• 2003

We have cloned the CGR1 gene encoding glutathione reductase (GR) which catalyzes the reduction of oxidized glutathione (GSSG) to reduced glutathione (GSH) from Candida albicans. The cgr1/cgr1 mutants were not viable when CaMAL2 promoter repressed the CGR1 expression. The growth of the mutants could be partially overcome by thiol compounds such as GSH, dithiothreitol, cysteine, N-acetylcysteine and GSSG. Interestingly, C. albicans with CGR1 overexpressed showed defective hyphal growth on solid medium and attenuated virulence. We have also cloned the GCS1 gene encoding ${\gamma}$-glutamylcysteine synthetase which catalyzes the first step of glutathione biosynthesis. The gcs1/gcs1 mutants were nonviable in minimal defined medium. The growth of the mutants could be resumed by supplementing with GSH, GSSG and ${\gamma}$-glutamylcysteine in the medium. The mutants had increased intracellular D-erythroascorbic acid level up to 2.25-fold when transferred to GSH-free medium. When the mutants were depleted of GSH, they showed typical markers of apoptosis. In conclusion, these results suggest that glutathione is an essential metabolite, and involved in hyphal growth, virulence and apoptosis in C. albicans.

• Toxicological Research
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• 제3권2호
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• pp.129-141
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• 1987

Hepatocytes isolated from rats which have been pretreated with phenobarbital (80 mg/kg for 3 days), were able to take up N-acetylcysteine from surrounding medium and were able to synthesize the reduced glutathione ($GSH^{\ast}-3$) intracellularly. The N-acetylcysteine is quickly deacetylated after the uptake and increases the pool size of cysteine, which was very low initially (5 nmol/$10^6$ cells). From this increased intracellular cysteine pool, GSH was synthesized. Freshly isolated rat hepatocytes contained a high level of GSH (30 nmol/$10^6$ cells), but upon incubation with the diethylmaleate, it was markedly decreased (10 nmol/$10^6$ cells). The hepatocytes with depleted GSH have lost viability upon incubations with acetaminophen (5mM) and paraquat (2 mM). However, when the N-acetylcysteine (1 mM) was added to this incubation condition, these chemical induced hepatocellular necrosis were prevented for longer durations. This N-acetylcysteine dependent protective effect against the hepatotoxic chemicals was lost by adding methionine sulfoximine (10 mM), an inhibitor of GSH biosynthesis. Both the carbontetrachloride (5 mM) and chioroform (5 mM) added to the incubation medium caused rapid losses of GSH and cell viability, even without the prior depletion of cellular GSH. However, again, if the 1mM N-acetylcysteine was supplemented, the rates of losses of GSH and cell viability were retarded in both cases. Even though large amounts of the added N-acetylcysteine was present in the cell, N-acetylcysteine conjugate of acetaminophen was not formed. Instead, only large amounts of GSH conjugate of the drug was produced. Thus, it is concluded that the added N-acetylcysteine is taken up and utilized for resynthesis of GSH. In turn, this resynthesized GSH contributes to the protection against cytotoxicity inducible with hepatotoxic drugs.

• Toxicological Research
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• 제24권4호
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• pp.281-287
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• 2008

Impairment of hepatic metabolism of sulfur-containing amino acids has been known to be linked with induction of liver injury. We determined the early changes in the transsulfuration reactions in liver of rats challenged with a toxic dose of $CCl_4$ (2 mmol/kg, ip). Both hepatic methionine concentration and methionine adenosyltransferase activity were increased, but S-adenosylmethionine level did not change. Hepatic cysteine was increased significantly from 4 h after $CCl_4$ treatment. Glutathione (GSH) concentration in liver was elevated in $4{\sim}8$ h and then returned to normal in accordance with the changes in glutamate cysteine ligase activity. Cysteine dioxygenase activity and hypotaurine concentration were also elevated from 4 h after the treatment. However, plasma GSH concentration was increased progressively, reaching a level at least several fold greater than normal in 24 h. ${\gamma}$-Glutamyltransferase activity in kidney or liver was not altered by $CCl_4$, suggesting that the increase in plasma GSH could not be attributed to a failure of GSH cycling. The results indicate that acute liver injury induced by $CCl_4$ is accompanied with extensive alterations in the metabolomics of sulfurcontaining amino acids and related substances. The major metabolites and products of the transsulfuration pathway, including methionine, cysteine, hypotaurine, and GSH, are all increased in liver and plasma. The physiological significance of the change in the metabolomics of sulfur-containing substances and its role in the induction of liver injury need to be explored in future studies.

• 식물조직배양학회지
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• 제27권1호
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• pp.57-61
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• 2000

식물배양세포의 항산화기구를 이해하기 위하여 다양한 유도조건에서 확립된 24종의 세포주를 대상으로 환원형 (GSH)과 산화형 (GSSG)의 glutathione 함량을 조사하였다. 배양세포의 전체 glutathione 함량 ($\mu$g/g cell fresh wt)은 98$\pm$27로 식물종에 따라 큰 차이가 없었다. 배양세포의 환원형 GSH과 산화형 GSSG의 평균함량 ($\mu$g/g fr wt)은 각각 72$\pm$20와 26$\pm$10을 나타내었다. 배양세포의 전체 glutathione 중에서 평균 환원형 GSH는 약 73%를 차지하였다. 황금 (Scutellaria baicalensis)배양세포의 현탁배양에 따른 GSH 함량 ($\mu$g/g cell fresh wt)은 계대배양부터 대수증식기까지는 계속하여 감소하여 세포생장 정지기인 배양후 13일에는 84까지 감소한 후 다시 증가하였다가 배양후기에는 크게 감소하였다. 한편 GSSG의 함량 ($\mu$g/g cell fresh wt)은 오히려 대수증식기까지는 증가하여 배양후 13일에는 31을 나타내었고 배양후기인 25일에는 48로 오히려 산화형 GSSG의 비율이 높았다. 이러한 결과는 GSH와 GSSG의 비율이 배양세포의 생장과 항산화기구에 주요하게 관여하고 있음을 시사한다.

• Archives of Pharmacal Research
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• 제28권3호
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• pp.311-318
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• 2005

Oxidative stress has been reported to elevate ceramide level during cell death. The purpose of the present study was to modulate cell death in relation to cellular glutathione (GSH) level and GST (glutathione S-transferase) expression by regulating the sphingolipid metabolism. LLC­PK1 cells were treated with H$_2$O$_2$ in the absence of serum to induce cell death. Subsequent to exposure to H$_2$O$_2$, LLC-PK1 cells were treated with desipramine, sphingomyelinase inhibitor, and N-acetylcysteine (NAC), GSH substrate. Based on comparative visual observation with H202-treated control cells, it was observed that 0.5 $\mu$M of desipramine and 25 $\mu$M of NAC exhibited about 90 and $95\%$ of cytoprotection, respectively, against H$_2$O$_2$-induced cell death. Desipramine and NAC lowered the release of LDH activity by 36 and $3\%$ respectively, when compared to $71\%$ in H$_2$O$_2$-exposed cells. Cellular glutathione level in 500 $\mu$M H202-treated cells was reduced to 890 pmol as compared to control level of 1198 pmol per mg protein. GST P1-1 expression was decreased in H$_2$O$_2$-treated cells compared to healthy normal cells. In conclusion, it has been inferred that H$_2$O$_2$-induced cell death is closely related to cellular GSH level and GST P1-1 expression in LLC-PK1 cells and occurs via ceramide elevation by sphingomyelinase activation.

• The Korean Journal of Physiology
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• 제5권2호
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• pp.55-62
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• 1971

In an attempt to better understand the effects of whole body X-irradiation on the levels of non-protein sulfhydryl (NP-SH), non-protein disulfide (NP-SS) and oxygen consumption rate $(QO_2)$ of the mouse duodenum, and to clarify the possible radioprotective action of reduced glutathione (GSH), a whole body X-irradiation of 1,000r was given to albino mouse either singularly or immediately after injecting GSH intraperitoneally to mouse 1 mg per gm of body weight. NP-SH was measured by Ellman's method, NP-SS was measured by the electrolytic reduction method described by Dohan and Woodward, and $(QO_2)$ by the Warburg's standard manometric method. The experiment was performed at 1, 6, 12 and 24 hours post-irradiation, and the comparison was made with the control. The results thus obtained are summarized as follows: 1) Comparing with the intrinsic NP-SH level of $3.31{\pm}0.27{\mu}\;mol/gm$ wet weight in the duodenum of the normal mouse, either whale body X-irradiation or injection of GSH alone produced no significant change in NP-SH from the normal. However, when GSH was injected prior to X-irradiation, markedly elevated NP-SH levels were observed throughout the entire experiment with the highest value of $4.70{\pm}0.10$ at 6 experimental hours. 2) The normal value of NP-SS in the mouse duodenum was $1.57{\pm}0.17{\mu}\;mol/gm$ wet weight, while in the group where injection of GSH and X-irradiation were combined, NP-SS increased to $2.36{\pm}0.33$ at 12 hours and $2.15{\pm}0.53$ at 24 hours, showing the intermediate value between the GSH injection group and X·irradiation group. 3) The normal value of $(QO_2)$ was $4.16{\pm}0.73{\mu}l\;O_2/hr./gm$ D.W., and no noticeable change was observed comparing with the GSH injection group. However, in the group where X·irradiation alone was given, $(QO_2)$ of the duodenum increased significantly throughout the entire experiment with the highest value of $6.35{\pm}1.07$ at 6 experimental hours. When GSH was injected before X-irradiation was given, the levels of $(QO_2)$ were in the middle of the GSH injection group and X-irradiation group. 4) The above results suggest that GSH may be effective as a radioprotector in terms of NP-SH, NP-SS and $(QO_2)$ of the mouse duodenum.

• Journal of Nutrition and Health
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• 제40권2호
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• pp.105-110
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• 2007

The study was designed to observe antioxidant activities of conjugated linoleic acid (CLA) by determining antioxidant enzyme protein levels [cytochrome P4502 El (CYP2E1), Copper, Zinc-superoxide dismutase (CuZn-SOD), glutathione peroxidase (CSH-Px), glutathione S-transferase (GST)] by Western blot analysis and the levels of ${\alpha}$-tocopherol and 2-thiobarbituric acid reactive substances (TBARS) in the liver of chronically ethanol-treated rats. Sixty Sprague Dawley male rats were divided into 3 groups (Control, EtOH, EtOH+CLA). All rats were fed Lieber-DeCarli liquid diet for 4 weeks by pair-feeding against the EtOH group. The liquid diet was supplemented with 1.77g CLA mixture per kg diet in the EtOH+CLA group. Isocaloric maltose dextrin was added in replace of 50g ethanol (36%kcal) for the Control group. Ethanol ingestion significantly increased the levels of CYP2E1 protein and TBARS, but significantly reduced CuZn-SOD protein level and increased GST protein level. There was no significant effect on the level of GSH-Px protein and ${\alpha}$-tocopherol in the liver by ethanol. CLA supplementation with ethanol significantly increased the levels of CuZn-SOD, GSH-Px and GST and also significantly attenuated TBARS level, whereas there was no significant effect on the levels of CYP2E1 protein and ${\alpha}$-tocopherol by CLA. Overall, the CLA supplemented to ethanol could significantly increase the levels of CuZn-SOD, GSH-Px and GST proteins and reduce the level of TBARS in the liver of chronically ethanol-treated rats.