• Proceedings of the Korean Society of Applied Pharmacology
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• 2001.11a
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• pp.109-109
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• 2001

The present study was done to investigate the relationship between Kupffer cells and alteration of cytochrome P-450 (CYP)-dependent drug metabolizing enzyme activities during polymicrobial sepsis. Male rats were subjected to polymicrobial sepsis by cecal ligation and puncture (CLP) followed by fluid resuscitation. The gadolinium chloride (GdC1$_3$, 10 mg/kg), blocker of Kupffer cells, was pretreated intravenously at 48 h and 24 h prior to the induction of CLP. All assay parameters were determined at 24 h after CLP or sham operation. In CLP-treated rats, the mortality rate of animals increased to 50% and serum alanine (ALT) and aspartate aminotransferase (AST) levels also significantly elevated. However, this increase was not suppressed by GdC1$_3$ pretreatment. Microsomal lipid peroxidation markedly increased after CLP operation. This increase was significantly attenuated by pretreatment. Total cytochrome P-450 content and NADPH-cytochrome P-450 reductase activity were not changed after CLP operation, but GdC1$_3$pretreatment reduced total cytochrome P-450 content, The hepatic microsomal CYP 1A1, 1A2, 2Bl and 2El activities in CLP-induced rats were also not significantly different from sham-operated rats. However, GdC1$_3$pretreatment showed a moderate increase in CYP1A1 and 1A2 activities. Our findings suggest that Kupffer cells may be partly responsible for producing hepatocellular dysfunction during sepsis.

• Journal of Preventive Medicine and Public Health
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• v.6 no.1
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• pp.71-76
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• 1973

1) The oxygen consumption was studied with albino rats under normal environment after they were given Cytochrome C intravenously (10mg/kg). The cosumption was 74.6cc/kg min. with that of control, 75.4cc/kg. min. The difference of the consumptions was not statistically significant. However, under 0.5% CO environment, the oxygen consumption of the Cytochrome C treated rats (62.5cc/kg min) was significantly greater than the control (42.1cc/kg min.) 2) The recovery time of rat acutely poisoned by 1% CO was studied. The recovery time of the Cytochrome C treated group was 37.2 minutes and in control group it was 52.2 minutes. Also significant difference of fatality was noted between the treated group (21.8%) and the untreated group (49.7%) 3) The combined effects of the hyperbaric oxygenation (100% $O_2$ at 3 atmospheric pressures) and the Cytochrome C administration was compared with the effect of the simple hyperbaric oxygenation. There was no significant difference of recovery time between the experimental group while the fatality of the experiment group was lower than control group.

• Animal cells and systems
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• v.7 no.1
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• pp.1-9
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• 2003

Programmed cell death, or apoptosis, is one of the most studied areas of modern biology. Apoptosis is a genetically regulated process, which plays an essential role in the development and homeostasis of higher organisms. Mitochondria, known to play a central role in regulating cellular metabolism, was found to be critical for regulating apoptosis induced under both physiological and pathological conditions. Mitochondria are a major source of reactive oxygen species (ROS) but they can also serve as its target during the apoptosis process. Release of apoptogenic factors from mitochondria, the best known of which is cytochrome c, leads to assembly of a large apoptosis-inducing complex called the apoptosome. Cysteine pretenses (called caspases) are recruited to this complex and, following their activation by proteolytic cleavage, activate other caspases, which in turn target for specific cleavage a large number of cellular proteins. The redox regulation of apoptosis during and after cytochrome c release is an area of intense investigation. This review summarizes what is known about the biological role of ROS and its targets in apoptosis with an emphasis on its intricate connections to mitochondria and the basic components of cell death.

• Quantitative Bio-Science
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• v.37 no.2
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• pp.103-111
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• 2018

This study was performed to investigate the cytoprotective effects of Stachys riederi var. japonica ethanol extract (SREE) to control oxidative stress induced by UVA-irradiation by examining antioxidant capacity and gene expression of cytochrome c using human dermal fibroblasts. The total polyphenolics and flavonoids in the SREE were 41.2 and 25.4 mg/g, respectively. At concentrations of 500 and $1000{\mu}g/mL$, the electron-donating ability of SREE was 48.6% and 82.0%, respectively, and the 2,2'-azino-(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radical scavenging activity was 62.3% and 78.8%, respectively. These findings showed that SREE has a fairly good antioxidant capacity. As determined by an MTT assay, the maximum permissible level for treating SREE to human dermal fibroblasts was shown to be over $200{\mu}g/mL$. SREE ($200{\mu}g/mL$) significantly decreased cytochrome c mRNA and protein expression by 31.1% (p<0.001) and 38.8% (p<0.01), respectively. These findings suggest that SREE may protect human skin cells against mitochondrial-dependent apoptosis. Therefore, SREE seems to be a natural antioxidant to protect cells against oxidative stress induced by UVA-irradiation.

• Environmental Analysis Health and Toxicology
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• v.8 no.1_2
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• pp.1-10
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• 1993

This study was done to determine the toxic effect of fthalide in rats which have oral administration at levels of 100 mg/kg/day for twelve days. It was examined the hematogram and serological parameters, and also the content of cytochrome P-450, the activity of NADPH-cytochrome c reductase, glucose-6-phosphatase, cholinesterase and carboxylesterase in liver. Any significant alteration of hematogram was not found but the value of AST, LDH and content of glucose in serum were statistically increased. The content of cytochrome P-450, the activty of NADPH-cytochrome c reductase were increased but glucose-6-phosphatase were slightly decreased compare with that of control group. The activity of cholinesterase was decreased slightly and on the contrary the activity of carboxylesterase was found to be the tendeny of increase in both of liver and serum.

• YAKHAK HOEJI
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• v.33 no.1
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• pp.54-63
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• 1989

Examination of the subacute toxicity of captafol showed that. 1) In the captafol administered group, the body weight was significantly decreased but the amounts of AST, ALT, LDH, BUN, TG in serum were remarkably elevated in comparision to those of the control group. 2) In captafol treated animals, the amount of cytochrome P-450 and the activity of NADPH-cytochrome c reductase in liver and in kidney were decreased, but TAB value in serum and in liver and total ATPase activity in liver and in kideny were found to be remakably elevated. 3) When captafol administered with ethanol to the group, the group showed elevated serum levels of AST, ALT and BUN but the amount of cytochrome P-450 and the activity of NADPH-cytochrome c reductase in liver and in kidney were decreased as the group which was treated with captafol only.

• BMB Reports
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• v.38 no.5
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• pp.619-623
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• 2005

The efficacy of chemotherapeutic agents on tumor cells has been shown to be modulated by tumor suppressor gene p53 and its target genes such as Bcl-2 family members (Bax, Noxa, and PUMA). However, various chemotherapeutic agents can induce cell death in tumor cells that do not express the functional p53, suggesting that some chemotherapeutic agents may induce cell death in a p53-independent pathway. Here we showed that etoposide can induce the similar degree of cell death in p53-deficient HCT 116 cells, whereas 5'-FU-mediated cell death is strongly dependent on the existence of functional p53 in HCT 116 cells. Further, we provide the evidence that etoposide can induce the cytochrome c release from isolated mitochondria, and etoposide-induced cytochrome c release is not accompanied with the large amplitude swelling of mitochondria. These data suggest that etoposide can directly induce the mitochondrial dysfunction irrespective of p53 status, and it may, at least in part, account for the p53-independent pathway in cell death induced by chemotherapeutic agents.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.4
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• pp.684-692
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• 2002

Cordyceps militaris has been known as a Chinese traditional medicine for the treatment of tuberculosis, asthma, kidney disease, debility and fatigue etc. This study was attempted to investigate the therapeutic effect of C. militaris extract on the cytotoxic activity of HepG2, human hepatocellular carcinoma cells and the liver damage induced by carbon tetrachloride in SD rats. C. militaris extracts inhibited significantly the proliferation of HepG2 cells in vitro. Carbon tetrachloride(CCl₄) caused a significant an increase in liver weight, serum aspartate aminotransferase(AST) and alanine aminotransferase(ALT) activity, alkaline phosphatase(ALP), serum thiobarbituric acid reactive substances (TBARS), microsomal TBARS, and decrease in microsomal detoxification enzymes (cytochrome P-450, P-450 reductase, cytochrome b5, b5 reductase). TBARS and ALP in serum pretreated with C. militaris extracts (300mg/kg/day, 600mg/kg/day) was significantly reduced compared to control group(CCl₄). Cytochrome b5 and b5 reductase activities were significantly increased in CM300 (300 mg/kg/day) and CM600 group(600 mg/kg/day), and cytochrome P-450 reductase was significantly increased in CM300 group. Pretreatment (100, 300, and 600 mg/kg/day for 7 days) of C. militaris with CCl₄ was significantly inhibited the accumulation microsomal TBARS and the significantly increased in the cytochrome P-450 activity. These results suggested that C. militaris (300mg/kg/day for 7 days) has appreciable therapeutic effect on CCl₄ induced hepatotoxicity.

• Polymer(Korea)
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• v.29 no.4
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• pp.331-337
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• 2005

In general, alkanethiolates having carboxylic acid in the tail group have been used as biorecepton. In this study, we have immobilized a cytochrome c protein using conjugated aromaticthiolates in order to improve the electrical property and physical stability of alkanethilolates. The pattern formation of self-assembled aromaticthiolate monolayers was as follow. Aromatic thiolates bound on the gold surface by the adsorption of 4'-mercapto-biphenyl-4-carboxylic acid and 4-mercapto-[1,1';4',1']terphenyl-4'-carboxylic acid were oxidized by the irradiation of deep UV light through a negative mask. The negative type pattern of the self-assembled monolayer (SAM) was obtained by developing with a deionized water. The pattern formation and electrical conductivity of aromaticthiolate SAMs was investigated by the measurements of STM and AFM. In addition, cytochrome c or ferrocene amide was immobilized onto the patterned substrate. We also studied on the effect of conjugated aromatic thiolates on the electrical activity of cytochrome c or ferrocene amide by cyclic voltammetry.

• Korean Journal of Acupuncture
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• v.36 no.4
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• pp.200-209
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• 2019

Objectives : The liver is rich in mitochondria and it plays a key role in whole-body energy homeostasis. Mitochondria is double membrane-bound organelle that supplies energy for intracellular metabolism including Krebs cycle and beta-oxidation. Acupuncture is known to stimulate and regulate the flow of energy. To explore the effect of acupuncture on the mitochondrial respiratory chain activity in the rats' livers, the activity of mitochondrial respiratory chain complexes I to IV was observed. Methods : The rats were divided into 4 groups; Normal 1 (no acupuncture treatment and anesthesia for 5 min), Normal 2 (no acupuncture treatment and anesthesia for 10 min), MA1 (acupuncture treatment at bilateral LR3 under anesthesia for 5 min), and MA2 (acupuncture treatment at bilateral LR3 under anesthesia for 10 min). All rats were sacrificed and the livers were examined for respiratory chain change. Results : There was no difference in ubiquinon oxidoreductase, succinate dehydrogenase, and ubiquinol cytochrome C oxidoreductase after acupuncture at LR3. Acupuncture at LR3 for 10 min increased the activity of cytochrome C oxidase compared with no acupuncture groups. Conclusions : Acupuncture at LR3 mediated mitochondrial respiratory chain activity via the cytochrome C oxidase signaling pathway in the livers of rats.