• Title/Summary/Keyword: Mitochondrial activity

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Effect of Enzymatic Hydrolysate of Hamcho (Salicomia herbacea) on Antioxidative Defense System in Rats Fed High Cholesterol Diet (함초(Salicornia herbacea)의 효소적 가수분해물이 고콜레스테롤 식이 흰쥐의 항산화방어계에 미치는 영향)

  • Kim, Kyung-Ran;Choi, Jeong-Hwa;Lee, Sung-Kwon;Woo, Mi-Hee;Choi, Sang-Won
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.35 no.10
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    • pp.1356-1362
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    • 2006
  • The purpose of the present study was to investigate the effect of enzymatic hydrolysate (extract) of Salicomia herbacea L. (Korean name: Hamcho) on antioxidative defense system in rats fed high cholesterol diet. Rats were divided into six experimental groups which are composed of normal diet group, normal diet group supplemented with 2% Hamcho extract, high cholesterol diet group, high cholesterol diet groups supplemented with 1%, 2% and 4% Hamcho extracts. The activity of serum glutamate oxaloacetae transaminase in rats was not different among all experimental groups, while the activity of glutamate pyruvate transaminase in groups supplemented with Hamcho extract was significantly lower than that of high cholesterol control group. Supplementation of Hamcho extract (SHE) to the high cholesterol fed rats resulted in increased activities of hepatic superoxide dismutase and glutathione peioxidase. However, there was no significant difference in the activity of hepatic catalase among all experimental groups. SHE also resulted in decreased levels of hepatic thiobarbituric acid reactive substances and mitochondrial carbonyl values. Those effects were higher to some extent in 2% and 4% Hamcho extract groups than those of high cholesterol control group. These results suggest that enzymatic hydrolysate of Hamcho may reduce oxidative damage by activation of antioxidative defense system in rats fed high cholesterol diets.

Rapamycin Rescues the Poor Developmental Capacity of Aged Porcine Oocytes

  • Lee, Seung Eun;Kim, Eun Young;Choi, Hyun Yong;Moon, Jeremiah Jiman;Park, Min Jee;Lee, Jun Beom;Jeong, Chang Jin;Park, Se Pill
    • Asian-Australasian Journal of Animal Sciences
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    • v.27 no.5
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    • pp.635-647
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    • 2014
  • Unfertilized oocytes age inevitably after ovulation, which limits their fertilizable life span and embryonic development. Rapamycin affects mammalian target of rapamycin (mTOR) expression and cytoskeleton reorganization during oocyte meiotic maturation. The goal of this study was to examine the effects of rapamycin treatment on aged porcine oocytes and their in vitro development. Rapamycin treatment of aged oocytes for 24 h (68 h in vitro maturation [IVM]; $44h+10{\mu}M$ rapamycin/24 h, $47.52{\pm}5.68$) or control oocytes (44 h IVM; $42.14{\pm}4.40$) significantly increased the development rate and total cell number compared with untreated aged oocytes (68 h IVM, $22.04{\pm}5.68$) (p<0.05). Rapamycin treatment of aged IVM oocytes for 24 h also rescued aberrant spindle organization and chromosomal misalignment, blocked the decrease in the level of phosphorylated-p44/42 mitogen-activated protein kinase (MAPK), and increased the mRNA expression of cytoplasmic maturation factor genes (MOS, BMP15, GDF9, and CCNB1) compared with untreated, 24 h-aged IVM oocytes (p<0.05). Furthermore, rapamycin treatment of aged oocytes decreased reactive oxygen species (ROS) activity and DNA fragmentation (p<0.05), and downregulated the mRNA expression of mTOR compared with control or untreated aged oocytes. By contrast, rapamycin treatment of aged oocytes increased mitochondrial localization (p<0.05) and upregulated the mRNA expression of autophagy (BECN1, ATG7, MAP1LC3B, ATG12, GABARAP, and GABARAPL1), anti-apoptosis (BCL2L1 and BIRC5; p<0.05), and development (NANOG and SOX2; p<0.05) genes, but it did not affect the mRNA expression of pro-apoptosis genes (FAS and CASP3) compared with the control. This study demonstrates that rapamycin treatment can rescue the poor developmental capacity of aged porcine oocytes.

Effect of ${\beta}-Carotene$ Supplementation on Lipid Metabolism and Related Enzyme Activities in Rats (${\beta}-Carotene$ 공급이 흰쥐 간 조직의 지질대사와 관련효소의 활성에 미치는 영향)

  • 최은미;박정룡;서정숙
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.23 no.5
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    • pp.743-749
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    • 1994
  • This study was designed to investigate the effect of dietary ${\beta}-carotene$ level on the lipid metabolism and lipid peroxide metabolizing enzyme activities in rats. Male Sprague -Dawley rats were fed on diets containing five levels of ${\beta}-carotene$ (0, 10, 120, 1200, 12000mg/kg diet ; BC 0, BC 1, BC 2, BC 3, BC 4 group). The rats were sacrificed after 7 weeks of the feeding periods. Lipid peroxide value of mitochondrial fraction of rat liver was elevated in ${\beta}-carotene$ restriction group when compared to $\beta$ -carotene groups. Superxide dismutase activity increased significantly by ${\beta}-carotene$ supplementation. Both catalase and glutathione peroxidase activities were reduced with increasing ${\beta}-carotene$ supplementation, except only ${\beta}-carotene$ restriction group. In liver, the contents of total lipid and cholestero decreased by ${\beta}-carotene$ supplementation but triglyceride content was not different among treatment groups. HDL-and total cholesterol ratio in plasma of 12, 000 ${\beta}-carotene$ group decreased, and was similar to that of ${\beta}-carotene$ restriction group.

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Induction of Apoptosis by Citrus grandis Osbeck Peel (CGP) Extract in HL60 Cells (당유자 과피 추출물에 의한 HL60 세포의 Apoptosis 유도)

  • Hyon, Jae-Seok;Kang, Sung-Myung;Kim, Areum-Daseul;Oh, Myung-Cheol;Oh, Chang-Kyung;Kim, Dong-Woo;Jeon, You-Jin;Kim, Soo-Hyun
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.38 no.10
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    • pp.1317-1323
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    • 2009
  • In the present study, we investigated the anti-proliferation activity of Citrus grandis Osbeck peel (CGP) in HL60 (human promyelocytic leukemia) cells. It was found that 80% ethanol extract of CGP could inhibit the cell growth in a dose-dependent manner ($250{\sim}1,000{\mu}g/mL$), which was associated with morphological changes and apoptotic cell death such as depolarized mitochondrial membrane, formation of apoptotic bodies and increased populations of apoptotic sub-G1 phase. The results indicate that CGP extract inhibits the growth of HL60 cancer cells by the induction of apoptosis, which may be mediated by its ability to change the Bcl family proteins and increase the activation of caspase-3 and PARP. Therefore, it is suggested that CGP has the potential to provide a remarkable natural defense against the proliferation of HL60 cells.

Effects of Alcohol Consumption and Fat Content in Diet on Growth, Hepatic Function and Biochemical Indices of Blood in Rat (알콜과 식이지방량이 흰쥐의 성장, 간기능 및 혈액의 생화화적 특성에 미치는 영향)

  • 최영선
    • Journal of Nutrition and Health
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    • v.20 no.6
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    • pp.432-441
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    • 1987
  • This study was undertaken to investigate effects of alcohol and fat content in a balanced diet on growth, hepatic function and some biochemical indices of blood in growing rats. Fourty eight male rats of Sprague-Dawley strain weighing about 160g were divided into 4 groups ; high fat diet group, alcohol-adminstered high fat diet group, low fat diet group and alcohol-administered low fat diet group. High and low fat diet supplied 30% and 12%, respectively, of total calorie intake from fat and alcohol-treated groups received water containing 10% ethanol. Diets contained adequate amounts of all nutrients required for rats, including lipotropic agents(choline and methionine) to minimize effects of factors other than alcohol on liver function. Growth rate was lowest in alcohol-administered low-fat diet group, despite that their energy intake was equivalent to the others. For a 3-week study period, 21.86% and 23.61% of total calorie intake were derived from alcohol in alcohol-adminitered high fat diet group and low fat diet group, respectively. There was no influenced on vitamin B$_1$ status by alcohol consumption. Concentration of triglyceride in plasma increased with alcohol comsumption, and the effect was greater after 6 weeks than after 3 weeks of alcohol consumption . Difference of dietary fat content did not affect the level of triglyceride . The levels of total cholesterol and HDL-cholesterol in plasma were not influenced by alcohol consumption. Serum glutamate pyruvate transaminase activity and hepatic mitochondrial respiration rate did not differ between groups. The results indicate that neither moderate alcohol drinking for 6 weeks nor fat content with a balanced diet caused any dramatic change of metabolism and liver function in rats. However they suggest that even moderate alcohol consumption can affect growth of animals dramatically and the effect may be lessened with relatively high fat content in diet.

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A Mitochondiral Cytochrome Oxidase I gene based identification of Corbicula ssp. commercially available in South Korea (CO-I 유전자 기반 국내 유통 Corbicula 속 패류의 종 동정)

  • Park, So Young;Kang, Se Won;Hwang, Hee Ju;Chung, Jong Min;Song, Dae Kwon;Park, Hong Seog;Han, Yeon Soo;Lee, Jun-Sang;Kang, Jung-Ha;Lee, Yong Seok
    • The Korean Journal of Malacology
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    • v.32 no.2
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    • pp.127-131
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    • 2016
  • The natives of the genus Corbicula have shown worldwide dispersion in recent times, which has caused great ecological and economic impacts on the introduced ecosystems. The species reported from the genus have been consumed as food and explored for medicine with pharmacological activity. Consequently, the demand of Corbicula sp. in the South Korean domestic market has increased and so also it's associated import to the country. However, due to the absence of identification keys of imported Corbicula, the market is facing confronting situations. We hypothesized that the mitochondrial Cytochrome Oxidase I gene (CO-I) based molecular profiling could be a necessary technique for identification of Corbicula sp. in the South Korea domestic market. The genetic analysis identified both Corbicula japonica and Corbicula fluminea from the market foods. C. japonica and C. fluminea are inhabitants in Korea, but C. fluminea production has decreased in Seomjingang river basin. Therefore, C. fluminea identified from this study, is expected to be imported from China and would have a mixed sales in Seomjingang river side basin.

A Case of Glutaric Aciduria Type I with Macrocephaly (Glutaric Aciduria Type I 1례)

  • Shin, Woo Jong;Moon, Yeo Ok;Yoon, Hye Ran;Dong, Eun Sil;Ahn, Young Min
    • Clinical and Experimental Pediatrics
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    • v.46 no.3
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    • pp.295-301
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    • 2003
  • Glutaric aciduria type 1(GA1) is an autosomal recessive disorder of the lysine, hydroxylysine and tryptophan metabolism caused by the deficiency of mitochondrial glutaryl-CoA dehydrogenase. This disease is characterized by macrocephaly at birth or shortly after birth and various neurologic symptoms. Between the first weeks and the 4-5th year of life, intercurrent illness such as viral infections, gastroenteritis, or even routine immunizations can trigger acute encephalopathy, causing injury to caudate nucleus and putamen. But intellectual functions are well preserved until late in the disease course. We report a one-month-old male infant with macrocephaly and hypotonia. In brain MRI, there was frontotemporal atrophy(widening of sylvian cistern). In metabolic investigation, there were high glutarylcarnitine level in tandem mass spectrometry and high glutarate in urine organic acid analysis, GA1 was confirmed by absent glutaryl-CoA dehydrogenase activity in fibroblast culture. He was managed with lysine free milk and carnitine and riboflavin. He developed well without a metabolic crisis. If there is macrocephaly in an infant with neuroradiologic sign of frontotemporal atrophy, GA1 should have a high priority in the differential diagnosis. Because current therapy can prevent brain degeneration in more than 90% of affected infants who are treated prospectively, recognition of this disorder before the brain has been injured is essential for treatment.

Tumor Suppressor Protein p53 Promotes 2-Methoxyestradiol-Induced Activation of Bak and Bax, Leading to Mitochondria-Dependent Apoptosis in Human Colon Cancer HCT116 Cells

  • Lee, Ji Young;Jee, Su Bean;Park, Won Young;Choi, Yu Jin;Kim, Bokyung;Kim, Yoon Hee;Jun, Do Youn;Kim, Young Ho
    • Journal of Microbiology and Biotechnology
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    • v.24 no.12
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    • pp.1654-1663
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    • 2014
  • To examine the effect of tumor suppressor protein p53 on the antitumor activity of 2-methoxyestradiol (2-MeO-$E_2$), 2-MeO-$E_2$-induced cell cycle changes and apoptotic events were compared between the human colon carcinoma cell lines HCT116 ($p53^{+/+}$) and HCT116 ($p53^{-/-}$). When both cell types were exposed to 2-MeO-$E_2$, a reduction in the cell viability and an enhancement in the proportions of $G_2/M$ cells and apoptotic sub-$G_1$ cells commonly occurred dose-dependently. These 2-MeO-$E_2$-induced cellular changes, except for $G_2/M$ arrest, appeared to be more apparent in the presence of p53. Immunofluorescence microscopic analysis using anti-${\alpha}$-tubulin and anti-lamin B2 antibodies revealed that after 2-MeO-$E_2$ treatment, impaired mitotic spindle network and prometaphase arrest occurred similarly in both cell types. Following 2-MeO-$E_2$ treatment, only HCT116 ($p53^{+/+}$) cells exhibited an enhancement in the levels of p53, p-p53 (Ser-15), $p21^{WAF1/CIP1}$, and Bax; however, the Bak level remained relatively constant in both cell types, and the Bcl-2 level decreased only in HCT116 ($p53^{+/+}$) cells. Additionally, mitochondrial apoptotic events, including the activation of Bak and Bax, loss of ${\Delta}{\psi}m$, activation of caspase-9 and -3, and cleavage of lamin A/C, were more dominantly induced in the presence of p53. The Bak-specific and Bax-specific siRNA approaches confirmed the necessity of both Bak and Bax activations for the 2-MeO-$E_2$-induced apoptosis in HCT116 cells. These results show that among 2-MeO-$E_2$-induced apoptotic events, including prometaphase arrest, up-regulation of Bax level, down-regulation of Bcl-2 level, activation of both Bak and Bax, and mitochondria-dependent caspase activation, the modulation of Bax and Bcl-2 levels is the target of the pro-apoptotic action of p53.

Physiological Effects of TOPE, a Photo - independent Diphenylether, on Higher Plants (비광요구형 디페닐에테르계 TOPE 의 생리적 작용에 관한 연구)

  • Kim, J.S.;Cho, K.Y.;Pyon, J.Y.
    • Korean Journal of Weed Science
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    • v.16 no.2
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    • pp.160-170
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    • 1996
  • Several physiological responses were investigated in plants treated with TOPE as a preliminary step to know its action site. Unlike photo-dependent diphenylethers, herbicidal activity of TOPE appeared slowly and its typical symptoms were both burning of leaf blades and abnormal division of meristem in grasses, Similarly, both leakage of cell electrolytes and the curling of cotyledon margin were also shown in cucumber(Cucumis sativus L.). Biosynthesis of chlorophyll in etiolated cucumber cotyledon was not inhibited directly by treatment of TOPE at low light intensity(5.5${\mu}$ mol $m^{-2}s^{-1}$ PAR) and protoporphyrin IX was not also accumulated. The contents of phytoene, phytofluene and ${\beta}$-carotene were abnormaly increased. Photosynthesis was inhibited only at high concentration. Mitochondrial respiration was inhibited at high concentration but rather increased significantly at 10${\mu}$M of TOPE. However, respiration inhibitors did not alleviate the two symptoms of TOPE in cucumber cotyledon. In the same experiments, using inhibitors of protein or nucleic acid biosynthesis, only one of the two symptoms was alleviated by chloramphenicol and cycloheximide. In contrast, both symptoms were alleviated by actinomycin-D and hydroxyurea, suggesting that nucleic acid metabolism might be preferentially related to the mode of action of TOPE. DNA, RNA and protein contents were accumulated in both cucumber cotyledon and rice (Oryza sativa L.) routs treated with TOPE, and the DNA of them was increased at first. Thus, it is conjectured that TOPE increase nucleic acid metabolism directly or indirectly, and then disturb various metabolic pathways causing abnormal physiological and morphological effects followed by final death.

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Protective effects skin keratinocyte of Oenothera biennis on hydrogen peroxide-induced oxidative stress and cell death via Nrf2/Ho1 pathway.

  • Lee, Seung Young;Jung, Ji Young;Choi, Hee Won;Choi, Kyung Min;Jeong, Jin-Woo
    • Proceedings of the Plant Resources Society of Korea Conference
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    • 2018.10a
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    • pp.103-103
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    • 2018
  • Oenothera biennis, commonly known as evening primrose, a potential source of natural bioactive substances: flavonoids, steroids, tannins, fatty acids and terpenoids responsible for a diverse range of pharmacological functions. However, whether extract prepared from aerial part of O. biennis (APOB) protects skin against oxidative stress remains unknown. To investigate the protective effects of APOB against oxidative stress-induced cellular damage and elucidated the underlying mechanisms in the HaCaT human skin keratinocytes. Our results revealed that treatment with APOB prior to hydrogen peroxide ($H_2O_2$) exposure significantly increased viability, and the highest DPPH radical-scavenging activities and reducing power of HaCaT cells. APOB also effectively attenuated H2O2-induced comet tail formation and inhibited the $H_2O_2$-induced phosphorylation levels of the histone ${\gamma}H2AX$, as well as the number of apoptotic bodies and Annexin V-positive cells. In addition, APOB exhibited scavenging activity against intracellular reactive oxygen species (ROS) accumulation and restored the mitochondrial membrane potential loss by $H_2O_2$. Moreover, $H_2O_2$ enhanced the cleavage of caspase-3 and degradation of poly (ADP-ribose)-polymerase (PARP), a typical substrate protein of activated caspase-3, as well as DNA fragmentation; however, these events were almost totally reversed by pretreatment with APOB. Furthermore, APOB increased the levels of heme oxygenase-1 (HO-1), which is a potent antioxidant enzyme, associated with the induction of nuclear factor-erythroid 2-related factor 2 (Nrf2). According to our data, APOB is able to protect HaCaT cells from $H_2O_2$-induced DNA damage and cell death through blocking cellular damage related to oxidative stress through a mechanism that would affect ROS elimination and activating the Nri2/HO-1 signaling pathway.

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