• Journal of Nutrition and Health
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• v.24 no.3
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• pp.166-178
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• 1991

This present study was designed to evaluate whether supplementaion of dietary coenzyme $Q_{10}$ protects the lipid peroxidation damage in adriamycin (ADR)-treated rats. Two experiments were conducted in this study. Experiment I was undertaken under the condition of simultaneous administration of ADR and coenzyme $Q_{10}$ for 4 weeks. Experiment 2 was undertaken under the same condition as experiment I after feeding the experimetal diets alone without administration of ADR for 4 weeks. Results obtained from the present study were as follows. Lipid peroxide value of plasma and heart mitochondria was elevated by ADR treatment. but decreased according to dietary coenzyme $Q_{10}$ supplementation. Pretreatment with dietary coenzyme $Q_{10}$ was more efficient in reducing ADR-induced lipid peroxide value. The simultaneous use of ADR and coenzyme $Q_{10}$ enhanced the heart glutathione peroxidase (GSH-Px) activity. particularly at higher level of coenzyme $Q_{10.}$ The change of superoxide dismutase(SOD) activity was similar to that of GSH-Px activity. In case of pretreatment with coenzyme $Q_{10, }$ these enzyme activities were more enhanced by dietary coenzyme $Q_{10.}$ However, there was little difference in catalase activity.

• Applied Microscopy
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• v.19 no.1
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• pp.1-18
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• 1989

It has been debated whether postischemic reperfusion is necessarily beneficial to salvage the myocardium after ischemic insult or not. Therefore, this study was undertaken to compare the ultrastructural changes as well as the distribution of $Ca^{2+}$ in the ventricular myocardial cells after transient ischemia and after postischemic reperfusion, and to suspect to what extent the postischemic reperfusion is beneficial. After 10 minutes of ischemia, the heart developed wide I bands, glycogen depletion, intramyofibrillar edema, mitochondrial swelling, clumping and migration of chromatin, ghosts of lipid droplets, disintegration of cell junctions, sarcolemmal disruption, and loss of $Ca^{2+}$ binding capacity of the sarcolemma and the mitochondria. In spite of reperfusion, in a large number of cells, the ultrastructure was more severely damaged, however, $Ca^{2+}$ binding capacity of the sarcolemma and the mitochondria restored. These results suggest that postischemic reperfusion may help the myocardial cells to restore their function to control $Ca^{2+}$ to a certain extent, but that it could aggravate the ischemic insult.

• 한국생물공학회:학술대회논문집
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• 2005.10a
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• pp.884-884
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• 2005

• Korean Journal of Clinical Laboratory Science
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• v.51 no.2
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• pp.221-234
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• 2019

Cancer is genetically, metabolically and infectiously induced life threatening disorder showing aggressive growing pattern with invasive tendency. In order to prevent this global menace from jeopardizing human life, enormous studies on carcinogenesis and treatment for chemotherapy resistance have been intensively researched. Hinokitiol (${\beta}$-thujaplicin) extracted from heart wood of cupressaceous is a well-known bioactive compound demonstrating anti-inflammation, anti-bacteria and anti-cancer effects on several cancer types via apoptosis and autophagy. This study proposed that hinokitiol activates transcription factor EB (TFEB) nuclear translocation for autophagy and lysosomal biogenesis regardless of nutrient condition in cancer cells. Mitophagy and ${\beta}$-catenin translocation into the nucleus under treatment of hinokitiol on non-small cell lung cancer (NSCLC) cells and HeLa cells were investigated. Hinokitiol exerted cytotoxicity on HeLa and HCC827 cells; moreover, artificially induced autophagy by overexpression of TFEB granted imperfect sustainability onto HeLa cells. Taken together, hinokitiol is the prominent autophagy inducer and activator of TFEB nuclear translocation. Alternative cancer therapy via autophagy is pros and cons since the autophagy in cancer cells is related to prevention and survival mechanism depending on nutrition. To avoid paradox of autophagy in cancer therapy, fine-tuned regulation and application of hinokitiol in due course for successful suppressing cancer cells are recommended.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.4
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• pp.333-342
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• 2001

Adriamycin is a commonly used chemotherapeutic agent for cancer, including acute leukemia, lymphoma, and a number of solid human tumors. However, recent studies have recognized severe cardiotoxicity after an acute dose, which are likely the result of generation of free radicals and lipid peroxidation. Therefore, the clinical uses of adriamycin have been limited. Melatonin, the pineal gland hormone known for its ability to modulate circardian rhythm, has recently been studied in its several functions, including cancer growth inhibition, stimulating the immune system, and acting as an antioxidant and radical scavenging effects. In the present study, we evaluated the effect of melatonin administration on adriamycin-induced cardiotoxicity in rat. Heart slices were prepared using a Stadie-Riggs microtome for the measurement of malondialdehyde (MDA) content used as an index of lipid peroxidation and lactate dehydrogenase (LDH) release as an indicator of lethal cell injury. Serious adriamycin-induced lethality was observed in rat by a single intraperitoneal injection in a dose-dependent manner. A single injection of adriamycin (25 mg/kg, i.p.) induced a lethality rate of 86%, with melatonin (10 mg/kg s.c. for 6 days) treatment reducing the adriamycin-induced lethality rate to 20%. The severe body weight loss caused by adriamycin was also significantly attenuated by melatonin treatment. Treatment of melatonin marked reduced adriamycin-induced the levels of MDA formation and LDH release. A cell damage indicated by the loss of myofibrils, swelling of the mitochondria as well as cytoplasmic vacuolization was seen in adriamycin-treated group. Melatonin attenuated the adriamycin-induced structural alterations. These data provide evidence that melatonin prevents adriamycin-induced cardiotoxicity and might serve as a combination with adriamycin to limit free radical-mediated cardiotoxicity.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.6
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• pp.1733-1739
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• 2004

The water extract of Hwangryunhaedog-tang(HRHDT} has been traditionally used for treatment of ischemic heart and brain damage in oriental medicine. However, little is known about the mechanism by which the water extract of HRHDT rescues cells from these damages. This study was designed to investigate the protective mechanisms of HRHDT on hypoxia-induced cytotoxicity in H9c2 cardiomyoblast cells. Hypoxia, markedly decreased the viability of H9c2 cells, which was characterized with apparent apoptptic features such as chromatin condensation as well as fragmentation of genomic DNA and nuclei. However, HRHDT significantly reduced hypoxia-induced cell death and apoptotic characteristics. Also, HRHDT prevented the mitochondrial dysfunction including the disruption of mitochondria membrane permeability transition (MPT) and an increase in expression of anti-apoptotic Bcl-2 proteins in hypoxia-H9c2 cells. Taken together, this study suggests that the protective effects of the water extract of HRHDT against hypoxic damages may be mediated by the modulation of Bcl-2 and Bak expression.

• Journal of Nutrition and Health
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• v.33 no.7
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• pp.725-732
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• 2000

The purpose of this study was to investigate the effects of green tea catechin on renal dysfunction and blood presure change in chronic cadmium poisoned rats. Sprague-Dawley male rats weighing 100$\pm$10g were randomly assigned to one normal group and three cadmium poisoned groups. Cadmium groups were classified to catechin free diet(Cd-0C group) 0.25% catechin diet(Cd-0.25C group) and 0.5% catechin diet(Cd-0.5C group) according to the levels of catechin supplement. Animals were raids for 20weeks. Cadmium were supplied as drinking water of 50ppm Cd2+ Morphological changes shown through a light microscope and an electro-microscope revealed the mitochondria and tubule epithelial cell edema in Cd -0C group but they were alleviated in catechin supplementation. The urinary $\beta$2-microglobulin that measured to observe the glomerular injury were higher in Cd-poisoned groups than in normal group but they was lowered by catechin supplementation. Glomerular filtration ratios(GFR) in Cd-poisoned groups were significantly lower than in normal group but that of catechin supplementation group was similar to normal group. This suggested that catechin protected the kidney from the functional damage. Angiotensin converting enzyme(ACE) activity and blood pressure(BP) in Cd-poisoned groups were significantly higher than in normal group. Heart rate was tended to increase in Cd-poisoned groups. The results indicate that green tea catechin supplementation on chronic cadmium-poisoned rats normalized the renal dysfunction and blood pressure system.

• Applied Microscopy
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• v.19 no.2
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• pp.99-118
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• 1989

The cardiotoxic effects of acute and chronic administration of adriamycin (ADR) were evaluated in A/J Swiss albino mice. In acute studies, male mice received intravenous ADR, 5mg or 15mg/kg per day for 3 or 1day and were sacrifice 12 hours later. Because the glutathione-glutathione peroxidase system is major pathway for free radical detoxication, glutathione levels and glutathione peroxidase activity was measured. In acute studies, ADR-treated mice exhibited significantly decreased levels(p<0.05) of total glutathione and unchanged levels of oxidized glutathione and percentage of oxidized glutathione. The earliest myocardial fine structural alterations included swelling and degeneration of mitochondria and dilatation of sarcoplasmic reticulum at all dosage of acute models. In chronic studies, mice received 5mg/kg ADR once a week for up to 16 weeks. Levels of total and reduced glutathione were decreased significantly(p<0.01) and oxidized glutathione and percentage of oxidized glutathione were increased significantly (p<0.05). Chronic myocardial lesions included perinuclear vacuolization, seperation of myofibrils and the fasciae adherens of intercalated disc and hypercontraction band within myocyte. Glutathione peroxidase activity reduced significantly (p<0.01) in any group of acute and chronic ADR-treated animals. Test for lipid peroxidation(malondialdehyde) was increased significantly(P<0.01). Thus, we conclude 1) ADR significantly lowers glutathione levels in heart tissue, and 2) cellular damage progress produced by alteration of this system in mouse models of ADR cardiotoxicity. These results suggest that the glutathione-glutathione peroxidase system may be involved in the modulation of ADR-induced cardiotoxicity.

• Applied Microscopy
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• v.22 no.2
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• pp.30-45
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• 1992

An experimental study on the acute irradiation effects on the substantia nigra of head-irradiated rats were carried out. Rats anesthetized with sodium thiopental, were exposed only on their head areas with a single dose of 3,000 rads or 6,000 rads, respectively. Radiation was produced by Mitsubishi linear accelerator at the speed of 200 rads/min. Aminals were sacrificed on 6 hours, 2 days and 6 days following irradiations. By the perfusion fixation through the heart, rats were fixed with 1% glutaraldehyde-1% paraformaldehyde solution. Two hours later, brains were exposed and immersed in the same fixatives over night. Tissue blocks from subtantia nigra were punched out, and they were refixed in the 2% osmium tetroxide solution. Blocks were dehydrated through alcohol series, and embedded in the araldite mixture. Ultrathin sections were stained with uranyl acetate and lead citrate solutions, From the ultrastructural study, following results were made: 1. Six hours after irradiation, severe depletion of synaptic vesicles was occurred in the many axon terminals of the nigral neuropil. 2. Dramatical decrease of lysosomes and dense granules was observed. 3. Two days following irradiation, alterations of ribosomes, granular endoplasmic reticula, mitochondria, etc, were noticed. 4. Many of the malformations were seen to be repaired on the 6th day. 5. Above results were interpreted as follows. At the acute stage of heavy irradiation, neurotransmitters in the substantia nigra are released severely. But they are recovered within 6 days. It is concluded that acute head-irradiation may result severe disturbance of nigral motor control function during the first few days.

• Journal of Life Science
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• v.14 no.3
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• pp.514-520
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• 2004

The antioxidative effects of fermented milk, mushroom extract and fermented milk containing its extract (Lentinus edodes, Ganoderna lucidum, and Pleurotus ostreatus) on the lipid peroxidation in the tissues of female Sprague-Dawley rats and on the DPPH ($\alpha,\alpha$' -diphenyl-$\beta$-picrylhydrazyl) radical donating ability were studied. The total concentrations of polyphenolic compound in Lentinus edodes, Ganoderma lucidum and Pleurotus ostreatus were 0.34, 0.20 and 0.34%, respectively. The DPPH donating abilities of mushroom extract, fermented milk, fermented milk containing its extract and BHT (butylated hydorxytoluene) as standard were 33.9, 34.9, 51.9 and 95.6%, respectively. Experimental diet groups were divided into five groups: the normal diet (ND), the cholesterol diet (CD), and cholesterol + fermented milk diet (CDFM), cholesterol + mushroom extract diet (CDME) and cholesterol + fermented milk containing mushroom extract diet (CDFMME). The concentrations of lipid peroxide in liver and its microsome were significantly lower in both CDFM and CDFMME groups than in the other groups. The kidney concentration of lipid peroxide was significantly higher in the CD group than in the ND group, but this rise were significantly decreased in the CDFM and CDFMME groups. Meanwhile, the concentrations of heart and spleen and their fractions were not significantly different among dietary groups. This study was suggested that the fermented milk diet containing mushroom extract effectively reduced the lipid peroxidation in liver and kidney of cholesterol-fed female rats.