• Biotechnology and Bioprocess Engineering:BBE
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• v.8 no.6
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• pp.322-330
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• 2003

The unicellular green alga Haematococcus pluvialis has recently attracted great inter-est due to its large amounts of ketocarotenoid astaxanthin, 3,3'-dihydroxy-${\beta}$,${\beta}$-carotene-4,4'-dione, widely used commercially as a source of pigment for aquaculture. In the life cycle of H. pluvialis, astaxanthin biosynthesis is associated with a remarkable morphological change from green motile vegetative cells into red immotile cyst cells as the resting stage. In recent years we have studied this morphological process from two aspects: defining conditions governing astaxanthin biosynthesis and questioning the possible function of astaxanthin in protecting algal cells against environmental stress. Astaxanthin accumulation in cysts was induced by a variety of environmental conditions of oxidative stress caused by reactive oxygen species, intense light, drought, high salinity, and high temperature. In the adaptation to stress, abscisic acid induced by reactive oxygen species, would function as a hormone in algal morphogenesis from veget ative to cyst cells. Furthermore, measurements of both in vitro and in vivo antioxidative activities of astaxanthin clearly demonstrated that tolerance to excessive reactive oxygen species is greater in astaxanthin-rich cysts than in astaxanthin-poor cysts or astaxanthin-less vegetative cells. Therefore, reactive oxygen species are involved in the regulation of both algal morph O-genesis and carotenogenesis, and the accumulated astaxanthin in cysts can function as a protective agent against oxidative stress damage. In this study, the physiological roles of astaxanthin in stress response and cell protection are reviewed.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.1
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• pp.39-44
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• 2006

Type I diabetes (T1D) is an organ-specific autoimmune disease caused by the T cell-mediated destruction of the insulin-producing ${\beta}$ cells in the pancreatic islets. The onset of T1D is the consequence of a progressive destruction of islet ${\beta}$ cells mediated by an imbalance between effector $CD4^+$ T helper (Th)1 and regulatory $CD4^+$ Th2 cell function. Since interferon-alpha (IFN-${\alpha}$) has been known to modulate immune function and autoimmunity, we investigated whether administration of adenoviralmediated IFN-${\alpha}$ gene would inhibit the diabetic process in NOD mice. The development of diabetes was significantly inhibited by a single injection of adenoviral-mediated IFN-${\alpha}$ gene before 8 weeks of age. Next, we examined the hypothesis that Th2-type cytokines are associated with host protection against autoimmune diabetes, whereas Th1-type cytokines are associated with pathogenesis of T1D. The expression of IFN-${\alpha}$ induced increase of serum IL-4 and IL-6 (Th2 cytokines) levels and decrease of serum IL-12 and IFN-${\gamma}$ (Th1 cytokines) levels. Therefore, overexpression of IFN-${\alpha}$ by adenoviralmediated delivery provides modulation of pathogenic progression and protection of NOD mice from T1D.

• Journal of Microbiology and Biotechnology
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• v.30 no.7
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• pp.967-973
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• 2020

The fungal cell wall is a major target of antifungals. In this study, we report the antifungal activity of an ethanol extract from Aucklandia lappa against Candida albicans. We found that the extract caused cell wall injury by decreasing chitin synthesis or assembly and (1,3)-β-D-glucan synthesis. A sorbitol protection assay demonstrated that the minimum inhibitory concentration (MIC) of the A. lappa extract against C. albicans cells increased eight-fold from 0.78 to 6.24 mg/ml in 72 h. Cell aggregates, which indicate damage to the cell wall or membrane, were commonly observed in the A. lappatreated C. albicans cells through microscopic analysis. In addition, the relative fluorescence intensities of the C. albicans cells incubated with the A. lappa extract for 3, 5, and 6 h were 92.1, 84.6, and 79.8%, respectively, compared to the controls, estimated by Calcofluor White binding assay. This result indicates that chitin content was reduced by the A. lappa treatment. Furthermore, synthesis of (1,3)-β-D-glucan polymers was inhibited to 84.3, 79.7, and 70.2% of that of the control treatment following incubation of C. albicans microsomes with the A. lappa extract at a final concentration equal to its MIC, 2× MIC, and 4× MIC, respectively. These findings suggest that the A. lappa ethanol extract may aid the development of a new antifungal to successfully control Candidaassociated disease.

• BMB Reports
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• v.47 no.10
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• pp.575-580
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• 2014

In this study, we investigate whether arsenite-induced DNA damage leads to p53-dependent premature senescence using human glioblastoma cells with p53-wild type (U87MG-neo) and p53 deficient (U87MG-E6). A dose dependent relationship between arsenite and reduced cell growth is demonstrated, as well as induced ${\gamma}H2AX$ foci formation in both U87MG-neo and U87MG-E6 cells at low concentrations of arsenite. Senescence was induced by arsenite with senescence-associated ${\beta}$-galactosidase staining. Dimethyl- and trimethyl-lysine 9 of histone H3 (H3DMK9 and H3TMK9) foci formation was accompanied by p21 accumulation only in U87MG-neo but not in U87MG-E6 cells. This suggests that arsenite induces premature senescence as a result of DNA damage with heterochromatin forming through a p53/p21 dependent pathway. p21 and p53 siRNA consistently decreased H3TMK9 foci formation in U87M G-neo but not in U87MG-E6 cells after arsenite treatment. Taken together, arsenite reduces cell growth independently of p53 and induces premature senescence via p53/p21-dependent pathway following DNA damage.

• The Plant Pathology Journal
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• v.31 no.1
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• pp.50-60
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• 2015

The use of novel isolates of Trichoderma with efficient antagonistic capacity against Fusarium oxysporum f. sp. lycopersici (FOL) is a promising alternative strategy to pesticides for tomato wilt management. We evaluated the antagonistic activity of 30 isolates of T. asperellum against 4 different isolates of FOL. The production of extracellular cell wall degrading enzymes of the antagonistic isolates was also measured. The random amplified polymorphic DNA (RAPD) method was applied to assess the genetic variability among the T. asperellum isolates. All of the T. asperellum isolates significantly reduced the mycelial growth of FOL isolates but the amount of growth reduction varied significantly as well. There was a correlation between the antagonistic capacity of T. asperellum isolates towards FOL and their lytic enzyme production. Isolates showing high levels of chitinase and ${\beta}$-1,3-glucanase activities strongly inhibited the growth of FOL isolates. RAPD analysis showed a high level of genetic variation among T. asperellum isolates. The UPGMA dendrogram revealed that T. asperellum isolates could not be grouped by their antagonistic behavior or lytic enzymes production. Six isolates of T. asperellum were highly antagonistic towards FOL and potentially could be used in commercial agriculture to control tomato wilt. Our results are consistent with the conclusion that understanding the genetic variation within Trichoderma isolates and their biochemical capabilities are required for the selection of effective indigenous fungal strains for the use as biocontrol agents.

• Journal of Radiation Protection and Research
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• v.19 no.3
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• pp.179-188
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• 1994

Mice were whole body irradiated with dose of 2.88Gy and 7.2Gy(Co-60) in order to observe the morphological and functional changes in radio sensitive mouse ovary. Microtechnical sectionates of $7{\mu}m$ thickness from ovary were made for light microscopy and concentrations of progesterone, testosterone and estradiol in ovarian homogenates were analyzed by radioimmunoassay. Gamma radiation resulted in the increase of atretic ratio of preantral and antral follicles, the increase of progesterone concentration in ovarian homogenates, and the low level of testosterone and estradiol. It is suggested that radiation protect the activity of $3{\beta}-HSD$(hydroxysteroid dehydrogenase) and isomerase in the follicular theca cell followed by low level of testosterone and estradiol and thereafter follicular atresia proceed.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.132.1-132.1
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• 2003

Biphenyl dimethyl dicarboxylate (DDB) is a by-product produced in process of synthesizing Schizandrin-C. Generally, DDB has known to protect hepatocytes and to decrease the index of liver enzyme (e.g. GOT and GPT) in chronic hepatitis. The present study was aimed to demonstrate whether DDB can protect the brain cell, especially the Alzheimer brain in vitro. As Alzheimers disease can be induced by activated microglia, a macrophage in the brain, through Abeta peptide (A$\beta$) produced from amyloid precursor protein (APP). (omitted)

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.3
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• pp.1911-1918
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• 2013

This meta-analysis was conducted to evaluate the association between intake of carotenoids and risk of esophageal cancer. A systematic search using PubMed, Cochrane Library, Web of Science, Scopus, CNKI, and CBM (updated to 6 May 2012) identified ten articles meeting the inclusion criteria with 1,958 cases of esophageal cancer and 4,529 controls. Higher intake of beta-carotene, alpha-carotene, lycopene, beta-cryptoxanthin, lutein, and zeaxanthin reduced esophageal cancer risk with pooled ORs of 0.58 (95% CI 0.44, 0.77), 0.81 (95% CI 0.70, 0.94), 0.75 (95% CI 0.64, 0.86), 0.80 (95% CI 0.66, 0.97), and 0.71 (95% CI 0.59, 0.87), respectively. In subgroup analyses, beta-carotene showed protective effects against esophageal adenocarcinoma in studies located in Europe and North America. Alpha-carotene, lycopene, and beta-cryptoxanthin showed protection against esophageal squamous cell cancer. This meta-analysis suggested that higher intake of carotenoids (beta-carotene, alpha-carotene, lycopene, beta-cryptoxanthin, lutein, and zeaxanthin) is associated with lower risk of esophageal cancer. Further research with large-sample studies need to be conducted to better clarify the potentially protective mechanisms of carotenoid associations risk of different types of esophageal cancer.

• BMB Reports
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• v.50 no.10
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• pp.528-533
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• 2017

Peroxiredoxin I (Prx I) plays an important role as a reactive oxygen species (ROS) scavenger in protecting and maintaining cellular homeostasis; however, the underlying mechanisms are not well understood. Here, we identified a critical role of Prx I in protecting cells against ROS-mediated cellular senescence by suppression of $p16^{INK4a}$ expression. Compared to wild-type mouse embryonic fibroblasts (WT-MEFs), Prx $I^{-/-}$ MEFs exhibited senescence-associated phenotypes. Moreover, the aged Prx $I^{-/-}$ mice showed an increased number of cells with senescence associated-${\beta}$-galactosidase (SA-${\beta}$-gal) activity in a variety of tissues. Increased ROS levels and SA-${\beta}$-gal activity, and reduction of chemical antioxidant in Prx $I^{-/-}$ MEF further supported an essential role of Prx I peroxidase activity in cellular senescence that is mediated by oxidative stress. The up-regulation of $p16^{INK4a}$ expression in Prx $I^{-/-}$ and suppression by overexpression of Prx I indicate that Prx I possibly modulate cellular senescence through $ROS/p16^{INK4a}$ pathway.

• Biomolecules & Therapeutics
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• v.27 no.6
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• pp.530-539
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• 2019

Brain aging is an inevitable process characterized by structural and functional changes and is a major risk factor for neurodegenerative diseases. Most brain aging studies are focused on neurons and less on astrocytes which are the most abundant cells in the brain known to be in charge of various functions including the maintenance of brain physical formation, ion homeostasis, and secretion of various extracellular matrix proteins. Altered mitochondrial dynamics, defective mitophagy or mitochondrial damages are causative factors of mitochondrial dysfunction, which is linked to age-related disorders. Etoposide is an anti-cancer reagent which can induce DNA stress and cellular senescence of cancer cell lines. In this study, we investigated whether etoposide induces senescence and functional alterations in cultured rat astrocytes. Senescence-associated ${\beta}$-galactosidase (SA-${\beta}$-gal) activity was used as a cellular senescence marker. The results indicated that etoposide-treated astrocytes showed cellular senescence phenotypes including increased SA-${\beta}$-gal-positive cells number, increased nuclear size and increased senescence-associated secretory phenotypes (SASP) such as IL-6. We also observed a decreased expression of cell cycle markers, including PhosphoHistone H3/Histone H3 and CDK2, and dysregulation of cellular functions based on wound-healing, neuronal protection, and phagocytosis assays. Finally, mitochondrial dysfunction was noted through the determination of mitochondrial membrane potential using tetramethylrhodamine methyl ester (TMRM) and the measurement of mitochondrial oxygen consumption rate (OCR). These data suggest that etoposide can induce cellular senescence and mitochondrial dysfunction in astrocytes which may have implications in brain aging and neurodegenerative conditions.