• The Korean Journal of Mycology
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• v.17 no.4
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• pp.169-176
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• 1989

Mitochondria in Pleurotus ostreatus was purified by stepped sucrose density gradient centrifugation. The activity of mitochondrial ATPase has been investigated during various times of illumination at each wavelength in the range of 400 nm to 700 nm. The mitochondrial ATPase activity was simulated 1,7 fold by 580 nm illumination compared with the broad wavelength group. The mitochondrial ATPase activity according to various times of illumination was stimulated 2.2 fold for 10 seconds at 580 nm compared with the broad wavelength group. The optimum pH and temperature of the mitochondrial ATPase were 7.4 and $60^{\circ}C$, respectively. The activity of this enzyme was stimulated by 5 mmol $Fe^{3+}$, 5 mmol $Mg^{2+}$, 0.1 mmol $Ca^{2+}$ and 5 mmol $Fe^{2+}$ ion, but inhibited by 5 mmol $Na^{+}$ ion.

• Toxicological Research
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• v.29 no.4
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• pp.257-261
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• 2013

${\alpha}$-Curcumene is one of the physiologically active components of Curcuma zedoaria, which is believed to perform anti-tumor activities, the mechanisms of which are poorly understood. In the present study, we investigated the mechanism of the apoptotic effect of ${\alpha}$-curcumene on the growth of human overian cancer, SiHa cells. Upon treatment with ${\alpha}$-curcumene, cell viability of SiHa cells was inhibited > 73% for 48 h incubation. ${\alpha}$-Curcumene treatment showed a characteristic nucleosomal DNA fragmentation pattern and the percentage of sub-diploid cells was increased in a concentration-dependent manner, hallmark features of apoptosis. Mitochondrial cytochrome c activation and an in vitro caspase-3 activity assay demonstrated that the activation of caspases accompanies the apoptotic effect of ${\alpha}$-curcumene, which mediates cell death. These results suggest that the apoptotic effect of ${\alpha}$-curcumene on SiHa cells may converge caspase-3 activation through the release of mitochondrial cytochrome c.

• Journal of Radiation Protection and Research
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• v.36 no.3
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• pp.119-126
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• 2011

Mitochondrial DNA (mtDNA) deletion is a well-known marker for oxidative stress and aging, and contributes to harmful effects in cultured cells and animal tissues. mtDNA biogenesis genes (NRF-1, TFAM) are essential for the maintenance of mtDNA, as well as the transcription and replication of mitochondrial genomes. Considering that oxidative stress is known to affect mitochondrial biogenesis, we hypothesized that ionizing radiation (IR)-induced reactive oxygen species (ROS) causes mtDNA deletion by modulating the mitochondrial biogenesis, thereby leading to cellular senescence. Therefore, we examined the effects of IR on ROS levels, cellular senescence, mitochondrial biogenesis, and mtDNA deletion in IMR-90 human lung fibroblast cells. Young IMR-90 cells at population doubling (PD) 39 were irradiated at 4 or 8 Gy. Old cells at PD55, and H2O2-treated young cells at PD 39, were compared as a positive control. The IR increased the intracellular ROS level, senescence-associated ${\beta}$-galactosidase (SA-${\beta}$-gal) activity, and mtDNA common deletion (4977 bp), and it decreased the mRNA expression of NRF-1 and TFAM in IMR-90 cells. Similar results were also observed in old cells (PD 55) and $H_2O_2$-treated young cells. To confirm that a increase in ROS level is essential for mtDNA deletion and changes of mitochondrial biogenesis in irradiated cells, the effects of N-acetylcysteine (NAC) were examined. In irradiated and $H_2O_2$-treated cells, 5 mM NAC significantly attenuated the increases of ROS, mtDNA deletion, and SA-${\beta}$-gal activity, and recovered from decreased expressions of NRF-1 and TFAM mRNA. These results suggest that ROS is a key cause of IR-induced mtDNA deletion, and the suppression of the mitochondrial biogenesis gene may mediate this process.

• Journal of Nutrition and Health
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• v.54 no.4
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• pp.335-341
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• 2021

Purpose: Muscle mitochondria play a key role in regulating fatty acid and glucose metabolism. Dysfunction of muscle mitochondria is associated with metabolic diseases such as obesity and type 2 diabetes. Isorhamnetin (ISOR), also known as 3-O-methylquercetin, a quercetin metabolite, is a naturally occurring flavonoid in many plants. This study evaluated the effects of ISOR on the regulation of the mitochondrial function of C2C12 muscle cells. Methods: C2C12 muscle cells were differentiated for 5 days, and then treated in various concentrations of ISOR. Cytotoxicity was determined by assessing cell viability using the water-soluble tetrazolium salt-8 assay principle at different concentrations of ISOR and time points. Levels of the mitochondrial DNA (mtDNA) content and gene expression were measured by quantitative real-time polymerase chain reaction. The citrate synthase (CS) activity was quantified by the enzymatic method. Results: ISOR at a concentration of 10 µM did not show any cytotoxic effects. ISOR increased the mtDNA copy number in a time- or dose-dependent manner. The messenger RNA levels of genes involved in mitochondrial function, such as peroxisome proliferator-activated receptor-γ coactivator-1α, and uncoupling protein 3 were significantly stimulated by the ISOR treatment. The CS activity was also significantly increased in a time- or dose-dependent manner. Conclusion: These results suggest that ISOR enhances the regulation of mitochondrial function, which was at least partially mediated via the stimulation of the mtDNA replication, mitochondrial gene expression, and CS activity in C2C12 muscle cells. Therefore, ISOR may be useful as a potential food ingredient to prevent metabolic diseases-associated muscle mitochondrial dysfunction.

• Nutrition Research and Practice
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• v.17 no.4
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• pp.660-669
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• 2023

BACKGROUND/OBJECTIVES: To investigate the effect and regulatory mechanism of resveratrol supplementation on the mitochondrial energy metabolism of rats with exercise-induced fatigue. MATERIALS/METHODS: Forty-eight Sprague-Dawley male rats were divided randomly into a blank control group (C), resveratrol group (R), exercise group (E), and exercise and resveratrol group (ER), with 12 rats in each group. Group ER and group E performed 6-wk swimming training with 5% wt-bearing, 60 min each time, 6 days a wk. Group ER was given resveratrol 50 mg/kg by gavage one hour after exercise; group R was only given resveratrol 50 mg/kg by gavage; group C and group E were fed normally. The same volume of solvent was given by gavage every day. RESULTS: Resveratrol supplementation could reduce the plasma blood urea nitrogen content, creatine kinase activity, and malondialdehyde content in the skeletal muscle, increase the total superoxide dismutase activity in the skeletal muscle, and improve the fatigue state. Resveratrol supplementation could improve the activities of Ca²⁺-Mg²⁺-ATPase, Na⁺-K⁺-ATPase, succinate dehydrogenase, and citrate synthase in the skeletal muscle. Furthermore, resveratrol supplementation could up-regulate the sirtuin 1 (SIRT1)-proliferator-activated receptor gamma coactivator-1α (PGC-1α)-nuclear respiratory factor 1 pathway. CONCLUSIONS: Resveratrol supplementation could promote mitochondrial biosynthesis via the SIRT1/PGC-1α pathway, increase the activity of the mitochondrial energy metabolism-related enzymes, improve the antioxidant capacity of the body, and promote recovery from exercise-induced fatigue.

• Clinical and Experimental Reproductive Medicine
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• v.45 no.1
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• pp.10-16
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• 2018

Objective: Placental oxidative stress is known to be a factor that contributes to pregnancy failure. The aim of this study was to determine whether selenium could induce antioxidant gene expression and regulate invasive activity and mitochondrial activity in trophoblasts, which are a major cell type of the placenta. Methods: To understand the effects of selenium on trophoblast cells exposed to hypoxia, the viability and invasive activity of trophoblasts were analyzed. The expression of antioxidant enzymes was assessed by reverse-transcription polymerase chain reaction. In addition, the effects of selenium treatment on mitochondrial activity were evaluated in terms of adenosine triphosphate production, mitochondrial membrane potential, and reactive oxygen species levels. Results: Selenium showed positive effects on the viability and migration activity of trophoblast cells when exposed to hypoxia. Interestingly, the increased heme oxygenase 1 expression under hypoxic conditions was decreased by selenium treatment, whereas superoxide dismutase expression was increased in trophoblast cells by selenium treatment for 72 hours, regardless of hypoxia. Selenium-treated trophoblast cells showed increased mitochondrial membrane potential and decreased reactive oxygen species levels under hypoxic conditions for 72 hours. Conclusion: These results will be used as basic data for understanding the mechanism of how trophoblast cells respond to oxidative stress and how selenium promotes the upregulation of related genes and improves the survival rate and invasive ability of trophoblasts through regulating mitochondrial activity. These results suggest that selenium may be used in reproductive medicine for purposes including infertility treatment.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.4
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• pp.209-213
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• 2005

Interstitial cells of Cajal (ICCs) are the pacemaker cells that generate slow waves in the gastrointestinal (GI) tract. In the present study, we investigated the effect of mitochondrial ATP-sensitive potassium (mitoKATP) channel on pacemaking activity in cultured ICCs from murine small intestine by using whole-cell patch clamp techniques. Under current clamp mode, at 10μM glibenclamide, there was no change in pacemaking activity of ICCs. At $30{\mu}M$ glibenclamide, an inhibitor of the ATP sensitive $K^+$ channels, we could find two examples. If pacemaking activity of ICCs was irregulating, pacemaking activity of ICCs was changed into regulating and if in normal conditions, membrane potential amplitude was increased. At $50{\mu}M$ glibenclamide, the resting membrane potential was depolarized. At 3mM 5-HDA, an inhibitor of the mitoKATP channels, inhibited the pacemaking activity of ICCs. Both the amplitude and the frequency were decreased. At 5 mM 5-HDA, both the amplitude and the frequency were completely abolished. Diazoxide, an opener of the mitoKATP channels, was applied to examine its effect on pacemaking activity of ICCs. At $50{\mu}M$ concentration, the pacemaking activity of ICCs was inhibited. Both the amplitude and the frequency were decreased. At 1 mM concentration, both the amplitude and the frequency were completely abolished and the resting membrane potential was shaked.These results indicate that mitoKATP channel has an important role in pacemaking activity of ICCs.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.4
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• pp.187-193
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• 2005

Several signal transduction pathways have been implicated in ischemic preconditioning induced by the activation of ATP-sensitive $K^+$ $(K_{ATP})$ channels. We examined whether protein kinase C (PKC) modulated the activity of $K_{ATP}$ channels by recording $K_{ATP}$ channel currents in rabbit ventricular myocytes using patch-clamp technique and found that phorbol 12,13-didecanoate (PDD) enhanced pinacidil-induced $K_{ATP}$ channel activity in the cell-attached configuration; and this effect was prevented by bisindolylmaleimide (BIM). $K_{ATP}$ channel activity was not increased by $4{\alpha}-PDD$. In excised insideout patches, PKC stimulated $K_{ATP}$ channels in the presence of 1 mM ATP, and this effect was abolished in the presence of BIM. Heat-inactivated PKC had no effect on channel activity. PKC-induced activation of $K_{ATP}$ channels was reversed by PP2A, and this effect was not detected in the presence of okadaic acid. These results suggest that PKC activates $K_{ATP}$ channels in rabbit ventricular myocytes.

• The Korean Journal of Mycology
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• v.15 no.4
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• pp.217-223
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• 1987

Mitochondria in the L. edodes was purified by linear sucrose density gradient centrifugation. The mitochondrial ATPase activity was investigated by various wavelength illumination for 30 min at dark state. The mitochondrial ATPase activity was stimulated 1.6 fold by 680 nm illumination compared with dark control group. The mitochondrial ATPase activity of different light illumination time at 680 nm was stimulated 2.3 fold at 5 minutes compared with dark control group. Its optimum pH and temperature were found to be 7.5 and $59^{\circ}C$ after illumination for 5 minutes at 680 nm. The mitochondrial ATPase activity was activated by 5 mmol $Fe^{3+}$, 0.1 mmol $Fe^{2+}$, 0.1 mmol $Mg^{2+}$, 0.5 mmol $K^{+}$, and 0.1 mmol $Ca^{2+}$ ion. But, the enzyme was inhibited by 5 mmol $Na^{+}$ ion.

• Toxicological Research
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• v.35 no.1
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• pp.13-24
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• 2019

Numerous ethnomedicinal uses have been attributed to different parts of Annona senegalensis (ASE), including its uses as food and food additives. The present study investigated toxicological and antioxidant effects of 28 days administration of ethanol extracts of ASE stem bark to Wistar strain albino rats. Acute toxicity test was done to determine lethal dose in Wistar rats while sub-acute toxicity test was conducted on rats divided into four groups (A - control, B - 50 mg/kg, C - 100 mg/kg, D - 150 mg/kg, respectively and treated for 28 days. Oxidative stress markers in liver and kidney as well as hepatic succinate dehydrogenase activity in the mitochondrial and post mitochondrial fractions (PMF) were evaluated. The $LD_{50}$ value of ASE was > 2,000 mg/kg. White blood cell counts gradually increased, but red blood cell counts and haematocrits level decreased significantly (p < 0.05) by about 50%. Liver enzymes in the serum and mitochondrial succinate dehydrogenase activity increased significantly (p < 0.05). Superoxide dismutase and catalase activities also increased in liver mitochondria and PMF while malondialdehyde (MDA) and reduced glutathione levels increased only in the PMF. Furthermore, only MDA levels increased significantly in the kidney after 28 days extract administration. Histopathological examination showed hepatic necrosis and no obvious signs of nephrotoxicity. Anona senegalensis is relatively safe, but prolonged ingestion could induce oxidative stress and impair ATP synthesis through the modulation of the activity of mitochondrial succinate dehydrogenase.