• The Korean Journal of Ecology
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• 제14권1호
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• pp.87-99
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• 1991

Changes of phycobiliproteins(PBP) quantity and ferredoxin-NADP reductase(FNR) activity were investigated in various light illuminated cyanobacteria, Anabaena variabilis. PBP components were increased under blue light illumination, whereas decreased under red light illumination. PBP contents were twofolds in blue light than in red light. In view of the PBP composition, allophycocyanin(APC) in red light was higher 5.5% and phycoerythrocyanin(PEC) in blue light was higher 2.2% than in white light-illuminated PBP. It was suggested that PBP changes in bule light be the results of regulation of photosysthetic efficiency and protection of photosystem, whereas PBP changes in red light be effected by adaptation of adequate harvesting of light energy in photosystem. Changes of FNR activity were highest in red light, and sequenced lower to blue light and green light. It means that light-dependent production rate of NADP is the highest in red light. The difference of values was larger than that of values in comparison of red and blue light. It was suggested that increasing of FNR activity be due not to the function of isozyme, but to the synthesis of enzymes. Because of NAD/NADP regulation-effect to metabolism, it was considered that FNR activity might influence the metabolism indirectly and explain the probability of regulation in pathways of key enzyme activation. FNR activity was directly proportional to intensity of light. Optimum temperature and pH were about 25℃ and 7.5, respectively.

• Journal of Microbiology and Biotechnology
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• 제26권2호
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• pp.226-232
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• 2016

Dihydrodipicolinate reductase is an enzyme that converts dihydrodipicolinate to tetrahydrodipicolinate using an NAD(P)H cofactor in L-lysine biosynthesis. To increase the understanding of the molecular mechanisms of lysine biosynthesis, we determined the crystal structure of dihydrodipicolinate reductase from Corynebacterium glutamicum (CgDapB). CgDapB functions as a tetramer, and each protomer is composed of two domains, an Nterminal domain and a C-terminal domain. The N-terminal domain mainly contributes to nucleotide binding, whereas the C-terminal domain is involved in substrate binding. We elucidated the mode of cofactor binding to CgDapB by determining the crystal structure of the enzyme in complex with NADP⁺ and found that CgDapB utilizes both NADH and NADPH as cofactors. Moreover, we determined the substrate binding mode of the enzyme based on the coordination mode of two sulfate ions in our structure. Compared with Mycobacterium tuberculosis DapB in complex with its cofactor and inhibitor, we propose that the domain movement for active site constitution occurs when both cofactor and substrate bind to the enzyme.

• BMB Reports
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• 제37권2호
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• pp.139-143
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• 2004

The antioxidant responsive element (ARE) is a cis-acting regulatory element of genes encoding phase II detoxification enzymes and antioxidant proteins, such as NAD(P)H: quinone oxidoreductase 1, glutathione S-transferases, and glutamate-cysteine ligase. Interestingly, it has been reported that Nrf2 (NF-E2-related factor 2) regulates a wide array of ARE-driven genes in various cell types. Nrf2 is a basic leucine zipper transcription factor, which was originally identified as a binding protein of locus control region of ss-globin gene. The DNA binding sequence of Nrf2 and ARE sequence are very similar, and many studies demonstrated that Nrf2 binds to the ARE sites leading to up-regulation of downstream genes. The function of Nrf2 and its downstream target genes suggests that the Nrf2-ARE pathway is important in the cellular antioxidant defense system. In support of this, many studies showed a critical role of Nrf2 in cellular protection and anti-carcinogenicity, implying that the Nrf2-ARE pathway may serve as a therapeutic target for neurodegenerative diseases and cancers, in which oxidative stress is closely implicated.

• Journal of Microbiology and Biotechnology
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• 제29권8호
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• pp.1221-1229
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• 2019

Mycobacterium tuberculosis, a causative pathogen of tuberculosis (TB), still threatens human health worldwide. To find a novel drug to eradicate this pathogen, we tested taurine-5-bromosalicylaldehyde Schiff base (TBSSB) as an innovative anti-mycobacterial drug using Mycobacterium smegmatis as a surrogate model for M. tuberculosis. We investigated the antimicrobial activity of TBSSB against M. smegmatis by plotting growth curves, examined the effect of TBSSB on biofilm formation, observed morphological changes by scanning electron microscopy and transmission electron microscopy, and detected differentially expressed proteins using two-dimensional gel electrophoresis coupled with mass spectrometry. TBSSB inhibited mycobacterial growth and biofilm formation, altered cell ultrastructure and intracellular content, and inhibited cell division. Furthermore, M. smegmatis adapted itself to TBSSB inhibition by regulating the metabolic pathways and enzymatic activities of the identified proteins. NDMA-dependent methanol dehydrogenase, NAD(P)H nitroreductase, and amidohydrolase AmiB1 appear to be pivotal factors to regulate the M. smegmatis survival under TBSSB. Our dataset reinforced the idea that Schiff base-taurine compounds have the potential to be developed as novel anti-mycobacterial drugs.

• Nutrition Research and Practice
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• 제13권5호
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• pp.377-383
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• 2019

BACKGROUND/OBJECTIVES: Hyperglycemia-induced hepatic damage has been recognized as one of the major cause of complications in diabetes. Hepatic complications are associated with inflammation and oxidative stress in diabetes. In this study, we investigated the hypothesis that gamma-tocopherol (GT) supplementation ameliorates NLRP3 inflammasome associated hepatic inflammation in diabetes. MATERIALS/METHODS: Diabetes was induced by the intraperitoneal injection of alloxan (150 mg/kg. BW) in ICR mice. All mice were fed with a control diet (AIN-76A). After diabetes was induced (fasting glucose level ${\geq}250mg/dL$), the mice were treated with tocopherol-stripped corn oil or GT-supplemented (35 mg/kg) corn oil, respectively, by gavage for 2 weeks. RESULTS: GT supplementation reduced fasting blood glucose levels in diabetic mice relative to non-treated diabetic mice. Moreover, GT supplementation ameliorated hyperglycemia-induced hepatic damage by regulation of NOD-like receptor protein 3 (NLRP3)-inflammasome associated inflammation represented by NLRP3, apoptosis-associated speck-like protein containing a caspase-recruitment domain, caspase-1, nuclear $factor-{\kappa}B$ pathway as well as oxidative stress demonstrated by nuclear factor erythroid 2-related factor 2, NAD(P)H dehydrogenase quinone 1, catalase and glutathione-dependent peroxidase in diabetic mice. CONCLUSION: The findings suggested that GT supplementation ameliorated hepatic damage by attenuating inflammation and oxidative stress in alloxan-induced diabetic mice. Taken together, GT could be a beneficial nutrient that can ameliorate inflammatory responses associated with NLRP3 inflammasome in hyperglycemia-induced hepatic damage.

• Toxicological Research
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• 제3권2호
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• pp.97-110
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• 1987

The effects of 5 novel hepatotrophic agents, dithiol malonate derivatives (DMDs; DMD1-DMD5), on the liver microsomal lipid peroxidation induced by carbon tetrachloride $(CCl_4)$ and the correlations with the changes of microsomal electron transport system were investigated. All DMDs were found to inhibit the lipid peroxidation induced by $CCl_4$ in mice and rats as well in vitro liver microsomal system. Therefore, each DMD seemed to have direct mode of action on liver microsomes to inhibit the lipid peroxidation. As an ex vivo study, the induced lipid peroxidation by $CCl_4$ and the changes in electron transport system were determined with liver microsomes obtained from rats chronically treated with DMDs for 7 days. The induced lipid peroxide contents in liver microsomal system were lower in DMD1, DMD2 and DMD3 treated group, but higher in DMD4 and DMD5 group when compared to the control group. Cyt. p.450 contents in the microsomes were decreased by the treatment with DMD1, DMD2 and DMD3, but increased significantly by DMD4 with great extent and by DMD5 with less extent. The cyt. p-450 isozymes induced by treatment of DMD4 and DMD5 were identified as 3-methylcholanthrene (MC) type. The NADPH cyt. -C reductase activities of the microsomes treated with DMD1, DMD2, DMD4 and DMD5 were increased in the range of around 20% to 50%, but decreased with DMD3, All DMDs increased dyt. $-b_5$ content and did not alter NAdH-cyt, $-b_5$ reductase activities in the microsomes. In summary, the 5 novel hepatotrophic agents (DMDs) markedly protected against lipid peroxidation induced by $CCl_4$ in vivo and in vitro possibly through the mechanism of direct action on the liver microsomes. The degree of inhibition produced by DMDs on lipid peroxidation induced by $CCl_4$ seemed to coincide rather with cyt. p-450 contents than with other components of liver microsomal electron transport system including NADPH-cyt, -C reductase.

• Biomolecules & Therapeutics
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• 제8권1호
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• pp.38-43
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• 2000

Several studies have shown that the stomach has sufficient alcohol dehydrogenase (ADH) activity to metabolize some amount of orally administered alcohol and the sex-related differences in the first-pass metabolism of alcohol might be associated with differences in the activity of gastric ADH(GADH). The aim of this study was to asses the sex-related differences in GADH in 48 male and 48 female Sprague-Dawley rats aged 1, 4, 10, 15, 20, and 30 weeks which each aged group had same sex ratio. The GADH activity was determined spectrophotometrically at 37$^{\circ}C$. The formation of NADH was monitored at 340nm for 10 minutes in the 1 ml of reaction mixture (0.5 M of Tris-HCl, pH 7.2 + 1.5 M of ethanol + 2.8 mM of NAD + 30 $\mu$l gastric mucosal supernatant). The GADH activity (nM of NADH/min/mg of cytosolic protein) was calculated using molecular extinction coefficient of 6.22 $\textrm{cm}^2$/$\mu$M for NADH. The GADH activities were 2.94$\pm$0.82 (n=48) in female rats and 3.34$\pm$2.17 (n=48) in male rats and had not significant difference between sex. However, the GADH activities were significantly (p<0.01) higher in female (1.91$\pm$0.59 and 3.30$\pm$0.49) than in male (0.68$\pm$0.43 and 1.92$\pm$0.81) of 1 and 4 weeks rats. However, it was significantly (p<0.05) higher in male (6.48$\pm$1.81, 3.65$\pm$1.04 and 5.13$\pm$1.30) than in female (4.23$\pm$1.23, 2.18$\pm$0.77 and 2.56$\pm$0.93) of 10, 20 and 30 weeks rats, respectively. Therefore, the results suggested that sex-related differences of the GADH activities in same aged rats were existed by age.

• Asian Pacific Journal of Cancer Prevention
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• 제17권4호
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• pp.1947-1959
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• 2016

Background: Colorectal cancer (CRC) is a major cause of morbidity and mortality, being the second most common type of cancer worldwide in both men and women. It accounts yearly for approximately 9% of all new cases of cancers. Furthermore, the current chemotherapeutic regimens seem unsatisfactory, so that exploration of novel therapeutic modalities is needed. The present study was undertaken to investigate the inhibitory effects of a crude alkaloid extract (CAERS) of a medicinal herb, Rhazya stricta, on proliferation of CRC HCT116 cells and to elucidate mechanisms of action. To achieve these aims, we utilized MTT, comet, DNA laddering and gene reporter assays, along with Western blot and RT-PCR analyses. Results: We found that CAERS inhibited cell proliferation and induced apoptotic cell death in HCT116 cells. Hallmarks of morphological and biochemical signs of apoptosis were clearly evident. CAERS down-regulated DNA-binding and transcriptional activities of NF-${\kappa}B$ and AP-1 proteins, while up-regulating expression of the Nrf-2 protein. It also down-regulated expression levels of the ERK MAPK, Bcl-2, cyclin D1, CDK-4, survivin and VEGF and up-regulated levels of Bax, caspase-3/7 and -9, p53, p21, Nrf-2. Markedly, it promoted mRNA expression levels of cytoprotective genes including the hemeoxygenase-1, NAD(P)H quinine oxidoreductase 1 and UDP-glucuronyltransferase. Conclusions: These findings indicate that CAERS exerts antiproliferative action on CRC cells through induction of apoptotic mechanisms, and suggest CAERS could be a promising agent for studying and developing novel chemotherapeutic agents aimed at novel molecular targets for the treatment of CRC.

• 대한통합의학회지
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• 제7권4호
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• pp.61-69
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• 2019

Purpose : Human gingival fibroblast cell is one of the the main cell types in periodontal tissue, which they can show anti-inflammatory activity through the production of numerous lines of inflammatory mediators such as inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2 and interleukins. Porphyromonas gingivalis, one of the oral pathogens, has reported to play a critical role in the development of periodontal diseases. This study aimed to investigate anti-inflammatory and antioxidative activities of Gracilaria textorii ethanol extract (GTEE) in P. gingivalis derived lipopolysaccharide (LPS-PG) stimulated human gingival fibroblast (HGF)-1 cell line. Methods : In order to analyze anti-inflammatory and antioxidative activities of GTEE in HGF-1 cell line, NOS enzyme activity, expression levels of iNOS, COX-2, NAD(P)H quinone dehydrogenase (NQO)1 and their transcription factors were estimated by Griess reaction and western hybridization. Results : LPS-PG induced overexpression of iNOS and COX-2, which was significantly attenuated by GTEE treatment in a dose-dependent manner without any cytotoxicity. In addition, intracellular NOS activity was in accordance with the result of iNOS expression. Due to important role in the regulation of inflammatory responses, phosphorylated status of p65 and c-jun, each subunit of nuclear factor (NF)-κB and activator protein (AP)-1, was also dose-dependently ameliorated by GTEE treatment. One of phase II enzymes, NQO1, and its transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2), were analyzed since elevated phase II enzyme expression inhibited inflammatory response, which was significantly elevated by GTEE treatment in HGF-1 cell line. Conclusion : In conclusion, GTEE mitigated LPS-PG-stimulated inflammatory responses by attenuating NF-κB and AP-1 activation as well as accelerating NQO1 and Nrf2 expression in HGF-1 cell line. These results indicate that GTEE might be utilized a promising strategy for potential anti-inflammatory agent in periodontal diseases.

• Journal of Microbiology and Biotechnology
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• 제26권2호
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• pp.277-286
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• 2016

Makgeolli lees (ML) has several physiological effects such as antioxidant, antidiabetic, and anticancer properties, but its biological functions have not been determined definitively. Here, we tested whether ML has a cytoprotective effect on paraquat (PQ)-induced oxidative stress in the human lung carcinoma cell line A549. At 0.1 mg/ml ML, viability of PQ-exposed A549 cells was restored by 12.4%, 18.5%, and 48.6% after 24, 48, and 72 h, respectively. ML also reduced production of the intracellular reactive oxygen species (ROS) that were generated by PQ treatment. Further experiments revealed that ML treatment enhanced the expression and nuclear translocation of nuclear factor erythroid 2-related factor 2 (NRF2) as well as ARE-GFP reporter activity. ML treatment also effectively increased the expression of NRF2's target genes NAD(P)H dehydrogenase quinone 1 (NQO1) and heme oxygenase 1 (HO-1). Moreover, we found that expression of cytoprotective genes, including glutathione peroxidases (GPXs), superoxide dismutase (SOD1), catalase (CAT), peroxiredoxin 3 (PRDX3), and peroxiredoxin 4 (PRDX4), was greatly enhanced by treatment with ML during PQ exposure. Taken together, the data suggest that treatment of PQ-exposed A549 cells with ML ameliorates cytotoxicity through induction of NRF2 expression and its target genes HO-1, NQO1, and other antioxidant genes. Thus, ML may serve as a functional food applicable to ROS-mediated human diseases.