• Title/Summary/Keyword: Glutathione levels

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Studies on the Causal Component of Rusty-Root on Panax ginseng I. Antioxidative Activity Oriented (적변인삼 유발 물질 구명 I. 항산화 활성을 중심으로)

  • 이성식;이명구;최광태;안영옥;권석윤;이행순;곽상수
    • Journal of Ginseng Research
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    • v.24 no.3
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    • pp.113-117
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    • 2000
  • To analyze the correlation between the rusty root and the antiokidative activity in ginseng (Panax ginseng C.A.Meyer) roots, the levels of antioxidative activity in various tissues of healthy and rusty roots. The superoxide dismutase activity in rusty roots (126.9 units/mg protein) was approximately 3.5 times higher than that in healthy roots. The catalase activity in rusty roots was approximately 1.6 times higher than that in healthy roots, whereas the peroxidase activity showed a slight low level in msty roots. The 1.1 diphenyl-2-picryl-hydrazyl(DPPH) free radical scavenging activity in rusty roots was approximately 2.0 times higher than that in healthy roots. The total ascorbate content in healthy roots was 166~240 $\mu\textrm{g}$/g fr. wt. depending on the tissues. Interestingly, the oxidized dehydroascorbate (DHA) content occupied more than 80% in total ascorbate content. The total ascorbate content in rusty roots was a similar level with healthy roots, but the reduced ascorbate content was 3.5~7.5 times higher than that of the healthy roots. The total glutathione content of the epidermis, cortex and stele tissues in 겨sty roots was 7.3, 4.8, 1.2 times higher than the healthy tissues, respectively. The ratio of reduced glutathione (GSH) and oxidized glutathione (GSSG) showed a similar fluctuation of total glutathione content in 겨sty roots. These results indicate that the high antioxidative activity in rusty roots may involve in overcoming the oxidative stress derived from environmental stresses.

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Dietary Tea Catechin Inclusion Changes Plasma Biochemical Parameters, Hormone Concentrations and Glutathione Redox Status in Goats

  • Zhong, Rongzhen;Xiao, Wenjun;Ren, Guopu;Zhou, Daowei;Tan, Chuanyan;Tan, Zhiliang;Han, Xuefeng;Tang, Shaoxun;Zhou, Chuanshe;Wang, Min
    • Asian-Australasian Journal of Animal Sciences
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    • v.24 no.12
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    • pp.1681-1689
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    • 2011
  • The beneficial effects of tea catechins (TCs) are related not only to their antioxidant potential but also to the improvement of animal meat quality. In this study, we assessed the effects of dietary TC supplementation on plasma biochemical parameters, hormone responses, and glutathione redox status in goats. Forty Liuyang goats were randomly divided into four equal groups (10 animals/group) that were assigned to four experimental diets with TC supplementation at 4 levels (0, 2,000, 3,000 or 4,000 mg TC/kg DM feed). After a 60-day feeding trial, all goats were slaughtered and sampled. Dietary TC treatment had no significant effect on blood biochemical parameters, however, low-density lipoprotein cholesterol (p<0.001), triglyceride (p<0.01), plasma urea nitrogen (p<0.01), and glucose (p<0.001) decreased and total protein (p<0.01) and albumin (p<0.05) increased with the feeding time extension, and day 20 was the turning point for most of changes. Interactions were found in glutathione (p<0.001) and the ratio of reduced and oxidized glutathione (p<0.05) in whole blood between treatment and feeding time. Oxidized glutathione in blood was reduced (p<0.05) by 2,000 mg TC/kg feed supplementation, and a similar result was observed in longissimus dorsi muscle. Though plasma glutathione peroxidase (p<0.01) and glutathione reductase (p<0.05) activities were affected by treatment and feeding time interactions, and glutathione S-transferases activity increased with feeding day extension, no changed values appeared in longissimus dorsi muscle. In conclusion, dietary TC supplementation affected the concentrations of some blood metabolites and accelerated GSH depletion in the blood of goats. In terms of less high-density lipoprotein cholesterol, the highest insulin and IGF-I concentrations, the highest ratio of reduced and oxidized glutathione in plasma, the dosage of 2,000 mg TC/kg feed might be desirable for growing goats to prevent glutathione depletion and keep normal physiological metabolism.

Differential Expression of Xenobiotic-Matabolizing Enzymes by Benzylisothiazole in Association with Hepatotoxicity: Effects on Rat Hepatic Epoxide Hydrolase, Glutathione S-Transferases and Cytochrome P450s

  • Cho, Min- Kyung;Kim, Sang-Geon
    • Toxicological Research
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    • v.14 no.3
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    • pp.293-300
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    • 1998
  • Previous studies have shown that the heterocycles including thiazoles are efficacious in inducing phase phase II metabolizing enzyme as well as certain cytochrome P450s and that the inductin of these matabolizing enzymes by the heterocyclic agents is highly associated with their hepatotoxicity. In the present study, the effects of benzylisothiazole (BIT), which has a isothiazole moiety, on the expression of microsomal epoxide hydrolase (mEH), major glutathione S-transerases and cytochrome P450s were studied in the rat liver in association with its hepatotoxicity. Treatment of rats with BIT(1.17 mmol/kg, 1~3d) resulted in substantial increases in the mEH. rGSTA2, rGSTA2, rGSTM1 and rGSTM2 mRNA levels, whereas rGSTA3 and rGSTA5 mRNA levels were increased to much lesser extents. A time-course study showed that the mRNA levels of mEH and rGSTs were greater at 24hr after treatment than those after 3 days of consecutive treatment. Relative changes in mEH and rGST mRNA levels were consistent with those in the proteins, as assessed by Western immunoblot analysis. Hepatic cytochrom P450 levels were monitored after BIT treatment under the assumption that metabolic activation of BIT may affect expression of the enzymes in conjunction with hepatotoxicity. Immunoblot analysis revealed that cytochrome P450 2B1/2 were 3-to 4-fold induced in rats teatd with BIT(1.17 mmol/kg/day.3days), whereas P450 1A2, 2C11 and 3A1/2 levels were decreased to 20~30% of those in unteatd rats. P450 2E1 was only slightly decreased by BIT. Thus, the levels of several cytochrome P450s were suppressed by BIT treatment. Rats treated with BIT at the dose of 1.17mmol/kg for 3 days exhibited extensive multifocal nodular necrosis with moderate to extensive diffuse liver cell degeneration. No notable toxicity was observed in the kidney. These results showed that BIT induces mEH and rGSTs in the liver with increases in the mRNA levels, whereas the agent significantly decreased major cytochrome P450s. The changes in the detoxifying enzymes might be associated with the necrotic liver after consecutive treatment.

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Effect of Reduced Glutathione and Cold Exposure on the Levels of NP-SH and NP-SS of Some Organs of the Whole-Body X-Irradiated Mouse (Reduced glutathione 및 한랭노출(寒冷露出)이 X선(線) 전신조사(全身照射)를 입은 마우스수종장기(數種臟器)의 NP-SH 및 NP-SS에 미치는 영향(影響))

  • Rhee, Kyoo-Won;Choo, Young-Eun
    • The Korean Journal of Physiology
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    • v.6 no.1
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    • pp.11-18
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    • 1972
  • In an attempt to observe the Possible radioprotective actions of single or combined application of reduced glutathione (GSH) and cold exposure in mammals, the albino mouse was subjected to GSH injection, cold exposure at $-1{\pm}0.2C$ and whole-body X-irradiation with 900r either singularly or in combination, or the X-irradiation following the cold exposure and/or GSH injection. The levels of intrinsic NP-SH and NP-SS of the liver, brain and heart were measured at one hour after each application, and the results were compared with the control, i.e., non-irradiated and non-cold exposed normal animal. NP-SH was measured by the Ellman's method, and NP-SS was measured by the electrolytic reduction method described by Dohan and Woodward. The results thus obtained are summarized as follows: 1) The levels of NP-SH in the liver, brain and heart of the normal mouse was $6.35{\pm}0.61,\;2.65{\pm}0.15\;and\;3.17{\pm}0.10{\mu}\;mol/gm\;wet\;wt.$, respectively, and NP-SS was $3.09{\pm}0.11,\;2.95{\pm}0.20\;and\;0.18{\pm}0.24{\mu}\;mol/gm\;wet\;wt.$, respectively. 2) Though there were some degrees of difference among the tissues studied, a general tendency of (1) elevated NP-SH and NP-SS levels in the GSH injection group, (2) similar or slightly elevated NP-SH and NP-SS levels in the cold-exposed group, and (3) markedly decreased levels of NP-SH and NP-SS in the X-irradiated group, was observed. When GSH was injected prior to the X-irradiation, NP-SH and NP-SS in all the tissues studied showed generally higher values than in the group where the X-irradiation was given alone, and the values were close to the normal. In the group where the cold exposure was applied immediately after the X-irradiation, no significant difference was observed in the NP-SH and NP-S5 levels comparing with the X-irradiation group. On the contrary, when GSH was injected immediately prior to the X-irradiation or cold exposure, NP-SH and NP-SS levels were either similar to, or higher than, the normal value.

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Antioxidant mechanism of black garlic extract involving nuclear factor erythroid 2-like factor 2 pathway

  • Ha, Ae Wha;Kim, Woo Kyoung
    • Nutrition Research and Practice
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    • v.11 no.3
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    • pp.206-213
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    • 2017
  • BACKGROUN/OBJECTIVES: Although studies have revealed that black garlic is a potent antioxidant, its antioxidant mechanism remains unclear. The objective of this study was to determine black garlic's antioxidant activities and possible antioxidant mechanisms related to nuclear factor erythroid 2-like factor 2 (Nrf2)-Keap1 complex. METHODS/MATERIALS: After four weeks of feeding rats with a normal fat diet (NF), a high-fat diet (HF), a high-fat diet with 0.5% black garlic extract (HF+BGE 0.5), a high-fat diet with 1.0% black garlic extract (HF+BGE 1.0), or a high-fat diet with 1.5% black garlic extract (HF+BGE 1.5), plasma concentrations of glucose, insulin,homeostatic model assessment of insulin resistance (HOMA-IR) were determined. As oxidative stress indices, plasma concentrations of thiobarbituric acid reactive substances (TBARS) and 8-isoprostaglandin $F2{\alpha}$ (8-iso-PGF) were determined. To measure antioxidant capacities, plasma total antioxidant capacity (TAC) and activities of antioxidant enzymes in plasma and liver were determined. The mRNA expression levels of antioxidant related proteins such as Nrf2, NAD(P)H: quinone-oxidoreductase-1 (NQO1), heme oxygenase-1 (HO-1), glutathione reductase (GR), and glutathione S-transferase alpha 2 (GSTA2) were examined. RESULTS: Plasma glucose level, plasma insulin level, and HOMA-IR in black garlic supplemented groups were significantly (P < 0.05) lower than those in the HF group without dose-dependent effect. Plasma TBARS concentration and TAC in the HF+BGE 1.5 group were significantly decreased compared to those of the HF group. The activities of catalase and glutathione peroxidase were significantly (P < 0.05) increased in the HF+BGE 1.0 and HF+BGE 1.5 groups compared to those of the HF group. The mRNA expression levels of hepatic Nrf2, NQO1, HO-1, and GSTA2 were significantly (P < 0.05) increased in the HF with BGE groups compared to those in the HF group. CONCLUSIONS: The improvements of blood glucose homeostasis and antioxidant systems in rats fed with black garlic extract were related to mRNA expression levels of Nrf2 related genes.

Anti-oxidative Effect of a Protein from Cajanus indicus L against Acetaminophen-induced Hepato-nephro Toxicity

  • Ghosh, Ayantika;Sil, Parames C.
    • BMB Reports
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    • v.40 no.6
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    • pp.1039-1049
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    • 2007
  • Overdoses of acetaminophen cause hepato-renal oxidative stress. The present study was undertaken to investigate the protective effect of a 43 kDa protein isolated from the herb Cajanus indicus, against acetaminophen-induced hepatic and renal toxicity. Male albino mice were treated with the protein for 4 days (intraperitoneally, 2 mg/kg body wt) prior or post to oral administration of acetaminophen (300 mg/kg body wt) for 2 days. Levels of different marker enzymes (namely, glutamate pyruvate transaminase and alkaline phosphatase), creatinine and blood urea nitrogen were measured in the experimental sera. Intracellular reactive oxygen species production and total antioxidant activity were also determined from acetaminophen and protein treated hepatocytes. Indices of different antioxidant enzymes (namely, superoxide dismutase, catalase, glutathione-S-transferase) as well as lipid peroxidation end-products and glutathione were determined in both liver and kidney homogenates. In addition, Cytochrome P450 activity was also measured from liver microsomes. Finally, histopathological studies were performed from liver sections of control, acetaminophen-treated and protein pre- and post-treated (along with acetaminophen) mice. Administration of acetaminophen increased all the serum markers and creatinine levels in mice sera along with the enhancement of hepatic and renal lipid peroxidation. Besides, application of acetaminophen to hepatocytes increased reactive oxygen species production and reduced the total antioxidant activity of the treated hepatocytes. It also reduced the levels of antioxidant enzymes and cellular reserves of glutathione in liver and kidney. In addition, acetaminophen enhanced the cytochrome P450 activity of liver microsomes. Treatment with the protein significantly reversed these changes to almost normal. Apart from these, histopathological changes also revealed the protective nature of the protein against acetaminophen induced necrotic damage of the liver tissues. Results suggest that the protein protects hepatic and renal tissues against oxidative damages and could be used as an effective protector against acetaminophen induced hepato-nephrotoxicity.

CD26: A Prognostic Marker of Acute Lymphoblastic Leukemia in Children in the Post Remission Induction Phase

  • Mehde, Atheer Awad;Yusof, Faridah;Mehdi, Wesen Adel;Zainulabdeen, Jwan Abdulmohsin
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.12
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    • pp.5059-5062
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    • 2015
  • Background: ALL is an irredeemable disease due to the resistance to treatment. There are several influences which are involved in such resistance to chemotherapy, including oxidative stress as a result of the generation of reactive oxygen species (ROS) and presence of hypodiploid cells. Cluster of differentiation 26 (CD26), also known as dipeptidyl peptidase-4, is a 110 kDa, multifunctional, membrane-bound glycoprotein. Aim and objectives: The aim of this study was to evaluate the clinical significance of serum CD26 in patients with acute lymphoblastic leukaemia patients in the post remission induction phase, as well as the relationship between CD26 activity and the oxidative stress status. Materials and Methods: CD26, total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI), in addition to activity of related enzymes myeloperoxidase, glutathione-s-transferase and xanthine oxidase, were analysed in sixty children with acute lymphoblastic leukaemia in the post remission induction phase. Results: The study showed significant elevation in CD26, TOS and OSI levels in patients with acute lymphoblastic leukaemia in the post remission induction phase in comparison to healthy control samples. In contrast, myeloperoxidase, glutathione-s-transferase and xanthine oxidase activities were decreased significantly. A significant correlation between CD26 concentration and some oxidative stress parameters was evident in ALL patients. Conclusions: Serum levels of CD26 appear to be useful as a new biomarker of oxidative stress in children with acute lymphoblastic leukaemia in the post remission induction phase, and levels of antioxidants must be regularly estimated during the treatment of children with ALL.

Effect of Cyclohexanone Treatment on the Serum Levels of Glutathione S-Transferase Activities in Acute Liver Damaged Rats

  • Park, Hye-Jung;Yoon, Chong-Guk
    • Biomedical Science Letters
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    • v.7 no.4
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    • pp.191-196
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    • 2001
  • To evaluate an effect of cyclohexanone (CHO) treatment on the serum levels of glutathione S-transferase (GST) activity in acute liver damaged animals, acute liver damage was induced in rats with pretreatment of 50% $CCl_4$ in olive oil (0.1 ml/100 g body wt) intraperitoneally 14 times every other day. To liver damaged rats, CHO (1.56 g/kg body wt, i. p.) was injected once and then rats were sacrificed at 4 hours after injection of CHO. Increasing rate of GST activity to the control in serum was higher in CHO-treated rats pretreated with CCL$_4$ than the $CCl_4$-pretreated those. All the more, the injection of CHO to the liver damaged rats led to more enhanced liver damage on the basis of liver functional findings, i. e., serum levels of alanine aminotransferase (ALT) activity, liver weight per body weight, and malondialdehyde content. The changing pattern of serum ALT activity was similar with that of GST activity, whereas that of liver in both enzymes differed more or less from each other; the liver GST activity in CHO-treated rats pretreated with $CCl_4$ being more increased tendency than that of $CCl_4$-pretreated rats. Concomitantly the injection of CHO showed a increasing tendency of liver GST activity compared with the control. Furthermore, CHO injection to the liver damaged rats showed somewhat higher Vmax in the kinetics of liver GST enzymes. In conclusion, injection of CHO to the liver damaged animals led to more increased activity of serum GST, and it may be chiefly caused by the alteration of membrane permeability.

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Effect of hydrogen-rich water on the lactic acid level in metformin-treated diabetic rats under hypoxia

  • Zhao, Chuan;Guo, Yushu;Wang, Ruoxi;Cheng, Cheng;Chen, Xiangmei
    • The Korean Journal of Physiology and Pharmacology
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    • v.25 no.6
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    • pp.517-523
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    • 2021
  • The present study aims to investigate the impact of hydrogen-rich water on the lactic acid level in metformin-treated diabetic rats under hypoxia. Thirty Sprague-Dawley rats were randomly divided into five groups, including normal diet group, and diabetes model (DM) group, DM + metformin treatment (DMM) group, DMM + hypoxia treatment (DMMH) group and DMMH + hydrogen-rich water (DMMHR) group. We found that the levels of lactic acid, pyruvate and lactate dehydrogenase were significantly lower in the blood of DMMHR group than DMMH group. Superoxide dismutase and glutathione levels in liver and heart were significantly higher in DMMH group after hydrogen-rich water treatment, while malondialdehyde and oxidized glutathione levels were decreased in DMMHR group when compared with DMMH group, which indicates that hydrogen-rich water could reduce oxidative stress. qPCR analysis demonstrated that that pro-apoptotic genes Bax/Caspase-3 were upregulated in DM group and metformin treatment suppressed their upregulation (DMM group). However, hypoxic condition reversed the effect of metformin on apoptotic gene expression, and hydrogen-rich water showed little effect on these genes under hypoxia. HE staining showed that hydrogen-rich water prevented myocardial fiber damages under hypoxia. In summary, we conclude that hydrogen-rich water could prevent lactate accumulation and reduce oxidant stress in diabetic rat model to prevent hypoxia-induced damages. It could be served as a potential agent for diabetes patients with metformin treatment to prevent lactic acidosis and reduce myocardial damages under hypoxic conditions.

Renal protective effects of zingerone in a mouse model of sepsis

  • Lee, Bong-Seon;Lee, Changhun;Yang, Sumin;Ku, Sae-Kwang;Bae, Jong-Sup
    • BMB Reports
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    • v.52 no.4
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    • pp.271-276
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    • 2019
  • Zingerone (ZGR), a phenolic alkanone isolated from ginger, has been reported to possess pharmacological activities such as anti-inflammatory and anti-apoptotic effects. This study was initiated to determine whether ZGR could modulate renal functional damage in a mouse model of sepsis and to elucidate the underlying mechanisms. The potential of ZGR treatment to reduce renal damage induced by cecal ligation and puncture (CLP) surgery in mice was measured by assessment of serum creatinine, blood urea nitrogen (BUN), lipid peroxidation, total glutathione, glutathione peroxidase activity, catalase activity, and superoxide dismutase activity. Treatment with ZGR resulted in elevated plasma levels of BUN and creatinine, and of protein in urine in mice with CLP-induced renal damage. Moreover, ZGR inhibited nuclear $factor-{\kappa}B$ activation and reduced the induction of nitric oxide synthase and excessive production of nitric acid. ZGR treatment also reduced the plasma levels of interleukin-6 and tumor necrosis $factor-{\alpha}$, reduced lethality due to CLP-induced sepsis, increased lipid peroxidation, and markedly enhanced the antioxidant defense system by restoring the levels of superoxide dismutase, glutathione peroxidase, and catalase in kidney tissues. Our study showed renal suppressive effects of zingerone in a mouse model of sepsis, suggesting that ZGR protects mice against sepsis-triggered renal injury.