• 생약학회지
• /
• 제37권4호
• /
• pp.258-265
• /
• 2006

Brassica rapa L. (Turnip) which is one of the specialized crops in Ganghwa island, has been used for diuretic, digestive, and curative for jaundice, etc. In this study, the anti oxidative effects and hepatoprotective effects of turnip in vitro and in vivo were investigated in order to evaluate the possibility as hepatoprotective agents. Ethanol extract of turnip potently showed the scavenging effect on DPPH and inhibitory effect on lipid peroxidation. Oral administration of turnip extract to dgalactosamine-induced experimental liver injured rats was significantly reduced the serum AST, ALT and LDH enzyme activities. And the decrease of catalase and SOD activities in liver microsolmal cytosol was significantly improved by the treatment of turnip. Based on these findings, it is presumed that ethanol extract of turnip may have the hepatoprotective effect on d-galactosamine-induced hepatotoxicity rat.

• 한국환경농학회지
• /
• 제28권4호
• /
• pp.462-467
• /
• 2009

Exposure of formaldehyde (FA), one of the major compounds in pesticides and in the onset of sick house syndrome, has been implicated in the development of diverse diseases. Liver is a very important organ to body metabolism and drug detoxification. Apotosis of hepatocytes is associated with the onset of liver diseases such as hepatitis. However, the apoptotic effect of FA in hepatocytes is not clear. Therefore, this study was conducted to investigate the effect of FA on the apoptosis in HepG2 cells, a human hepatocyte cell line. As a result, FA (> $500\;{\mu}M$) decreased cell viability and increased lactate dehydrogenase activity in HepG2 cells, which was blocked by the treatment of vitamin E and N-acetylcysteine (NAC). In addition, FA decreased glutathione (GSH) contents and Bcl-2 levels, while increasing lipid peroxide formation and Bax levels. It also cleaved caspase-3 form, which was blocked by the treatment of vitamin E and NAC. It is insisted that FA induced apoptosis via oxidative stress in human hepatocytes.

• Molecules and Cells
• /
• 제41권1호
• /
• pp.35-44
• /
• 2018

Mitochondria are responsible for supplying of most of the cell's energy via oxidative phosphorylation. However, mitochondria also can be deleterious for a cell because they are the primary source of reactive oxygen species, which are generated as a byproduct of respiration. Accumulation of mitochondrial and cellular oxidative damage leads to diverse pathologies. Thus, it is important to maintain a population of healthy and functional mitochondria for normal cellular metabolism. Eukaryotes have developed defense mechanisms to cope with aberrant mitochondria. Mitochondria autophagy (known as mitophagy) is thought to be one such process that selectively sequesters dysfunctional or excess mitochondria within double-membrane autophagosomes and carries them into lysosomes/vacuoles for degradation. The power of genetics and conservation of fundamental cellular processes among eukaryotes make yeast an excellent model for understanding the general mechanisms, regulation, and function of mitophagy. In budding yeast, a mitochondrial surface protein, Atg32, serves as a mitochondrial receptor for selective autophagy that interacts with Atg11, an adaptor protein for selective types of autophagy, and Atg8, a ubiquitin-like protein localized to the isolation membrane. Atg32 is regulated transcriptionally and post-translationally to control mitophagy. Moreover, because Atg32 is a mitophagy-specific protein, analysis of its deficient mutant enables investigation of the physiological roles of mitophagy. Here, we review recent progress in the understanding of the molecular mechanisms and functional importance of mitophagy in yeast at multiple levels.

• Biomolecules & Therapeutics
• /
• 제26권1호
• /
• pp.29-38
• /
• 2018

During cancer progression, cancer cells are repeatedly exposed to metabolic stress conditions in a resource-limited environment which they must escape. Increasing evidence indicates the importance of nicotinamide adenine dinucleotide phosphate (NADPH) homeostasis in the survival of cancer cells under metabolic stress conditions, such as metabolic resource limitation and therapeutic intervention. NADPH is essential for scavenging of reactive oxygen species (ROS) mainly derived from oxidative phosphorylation required for ATP generation. Thus, metabolic reprogramming of NADPH homeostasis is an important step in cancer progression as well as in combinational therapeutic approaches. In mammalian, the pentose phosphate pathway (PPP) and one-carbon metabolism are major sources of NADPH production. In this review, we focus on the importance of glucose flux control towards PPP regulated by oncogenic pathways and the potential therein for metabolic targeting as a cancer therapy. We also summarize the role of Snail (Snai1), an important regulator of the epithelial mesenchymal transition (EMT), in controlling glucose flux towards PPP and thus potentiating cancer cell survival under oxidative and metabolic stress.

• Journal of Microbiology
• /
• 제38권1호
• /
• pp.18-23
• /
• 2000

Streptomyces coelicolor produces three kinds of catalases to cope with oxidative stress and to allow normal differentiation. Catalase A is the major vegetative catalase which functions in removing hydrogen peroxide generated during the process of aerobic metabolism. To understand the regulatory mechanism of response against oxidative stress, hydrogen peroxide-resistant mutant (HR4O) was isolated from S. coelicolor J1501 following UV mutagenesis. The mutant overproduced catalase A more than 50-fo1d compared with the wild type. The mutation locus catRI was mapped closed to the mthB2 locus by genetic crossings. An ordered cosmid library of S. coelicolor encompassing the mthB2 locus was used to isolate the regulator gene (catR) which represses catalase overproduction when introduced into HR4O. A candidate catR gene was found to encode a Fur-like protein of 138 amino acids (15319 Da).

• 동의신경정신과학회지
• /
• 제22권1호
• /
• pp.37-51
• /
• 2011

Objectives : This experiment was designed to investigate the effect of Gamisoyo-san(Jiaweixiaoyaosan, SYS) on serotonin activity of P815 Mast Cell. Methods : The effects of SYS on activation of TPH-1 mRNA and AAADC mRNA in P815 mast cell were investigated. The effect of SYS on content of serotonin in P815 mast cell was investigated. The effects of SYS on activation of DPPH and SOD in P815 mast cell were investigated. Results : 1. The SYS increased the activation of SOD and DPPH in P815 mast cell. 2. The SYS decreased the manifestation TPH-1 mRNA in P815 mast cell. 3. The SYS decreased the manifestation AAADC mRNA in P815 mast cell. Conclusions : This experiment shows that Gamisoyo-san might not be effective for treating depression in terms of biogenic amine theory. However, Gamisoyo-san showed significant anti-oxidative effect and it can not yet be ruled out for treating depression. Therefore, pathogenesis of depression and clinical research of Gamisoyo-san is suggested for future research.

• The Plant Pathology Journal
• /
• 제29권3호
• /
• pp.323-329
• /
• 2013

The stationary-phase sigma factor, RpoS, influences the expression of factors important in survival of Pseudomonas chlororaphis O6 in the rhizosphere. A partial proteomic profile of a rpoS mutant in P. chlororaphis O6 was conducted to identify proteins under RpoS regulation. Five of 14 differentially regulated proteins had unknown roles. Changes in levels of proteins in P. chlororaphis O6 rpoS mutant were associated with iron metabolism, and protection against oxidative stress. The P. chlororaphis O6 rpoS mutant showed increased production of a pyoverdine-like siderophore, indole acetic acid, and altered isozyme patterns for peroxidase, catalase and superoxide dismutase. Consequently, sensitivity to hydrogen peroxide exposure increased in the P. chlororaphis O6 rpoS mutant, compared with the wild type. Taken together, RpoS exerted regulatory control over factors important for the habitat of P. chlororaphis O6 in soil and on root surfaces. The properties of several of the proteins in the RpoS regulon are currently unknown.

• International Journal of Industrial Entomology and Biomaterials
• /
• 제23권1호
• /
• pp.115-122
• /
• 2011

The effect of dietary feeding of silk fibroin/sericinmixtureson the antioxidative status and glucose metabolism in high fat-fed mice was investigated. The mice weregiven experimental diets for 6 weeks: normal control (NC),high fat (HF) andhigh fat supplemented with F100 (pure fibroin, HF-F100), F81 (81:19 fibroin-sericin, w/w, HF-F81) or F50 (50:50 fibroin-sericin, w/w, HF-F50). The silk protein-fed mice showed decreased lipid peroxidation, enhancedantioxidant enzymesactivities and lower blood glucose level relative to HF group. The HF-F50 animals exhibited significantly lower insulin level, higher glycogen concentration, enhanced hepatic glucokinaseactivity and reduced glucose-6-phosphate and phosphoenolpyruvatecarboxynaseactivities than the HF ones. The $in$ $vivo$ antioxidant activity and hypoglycemic action tended to increase with increased amount of sericin and decreased fibroin content in the diet. These findings demonstrate that silk protein, particularly sericin, may be beneficial in suppressing high fat diet-induced hyperglycemiaand oxidative stress.

• BMB Reports
• /
• 제49권1호
• /
• pp.45-50
• /
• 2016

Salsolinol (SAL), a compound derived from dopamine metabolism, is the most probable neurotoxin involved in the pathogenesis of Parkinson's disease (PD). In this study, we investigated the modification and inactivation of human ceruloplasmin (hCP) induced by SAL. Incubation of hCP with SAL increased the protein aggregation and enzyme inactivation in a dose-dependent manner. Reactive oxygen species scavengers and copper chelators inhibited the SAL-mediated hCP modification and inactivation. The formation of dityrosine was detected in SAL-mediated hCP aggregates. Amino acid analysis post the exposure of hCP to SAL revealed that aspartate, histidine, lysine, threonine and tyrosine residues were particularly sensitive. Since hCP is a major copper transport protein, oxidative damage of hCP by SAL may induce perturbation of the copper transport system, which subsequently leads to deleterious conditions in cells. This study of the mechanism by which ceruloplasmin is modified by salsolinol may provide an explanation for the deterioration of organs under neurodegenerative disorders such as PD. [BMB Reports 2016; 49(1): 45-50]

• 약학회지
• /
• 제40권5호
• /
• pp.563-573
• /
• 1996

The system most likely responsible for the accelerated metabolism of alcohol with chronic ingestion or at high blood ethanol levels, is the microsomal ethanol-oxidizing system(M EOS). While the increase in the MEOS with chronic ethanol ingestion is thought to be adaptive, it may also have serious adverse effects on the liver. The rates of the NADPH-dependent oxygen consumption by the liver microsomes from the prolonged ethanol fed rats were 2 times higher than the rates from the non-treated rats. With the alcohol ingestion, the total SH and nonprotein SH contents showed the significant decrease and at the same time, MDA in liver and GOT and GPT levels in blood showed the significant increase, which suggests the occurrence of liver damage due to the oxidative stress caused by chronic alcohol consumption. The mitochondrial aldehyde dehydrogenase(ALDH) activity was decreased by chronic ethanol ingestion, whereas the alcohol dehydrogenase activity and the cytosolic ALDH activity were not altered. These results suggest that the induction of cytochrome P450 by the chronic alcohol ingestion increases the oxidative stress which seems to result in the altered the physiological states of the liver including the ALDH activity, which may in turn to lead to the liver disease.