• Journal of Food Hygiene and Safety
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• v.9 no.3
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• pp.105-109
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• 1994

Lysosomal enzymes might play a most important role in the pathogenesis od diabetic microangiopathy. Some glycosidases, which participate in the catabolism of glycoprotein, are significantly decreased in diabetic mice. In search of new potential lysosomal enzyme inducers, we examined the effects of crude red-ginseng saponin fraction on N-acetyl-$\beta$-D-glucosaminidase, $\beta$-D-galactosidase and $\alpha$-D-mannosidase activities in the liver and kidney of normal and streptozotocin induced diabetic mice. It was found that i.p. administration of ginseng saponin produced the induction of lysosomal enzymes in the kidney more intensively than in the liver. The obtained results suggest the possibility that ginseng saponin might prevent the diabetic microangiopathy.

• Journal of Environmental Health Sciences
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• v.17 no.2
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• pp.121-126
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• 1991

To clarify a cause of increased serum level of acid phosphatase in CCl$_{4}$-treated rats, the acid phosphatase activity of liver was compared with that serum. Concomitantly, the serum and liver acid phosphatase activity of CCl$_{4}$-treated rats were compared with that of CCl$_{4}$-treated rats pretreated with prednisolone or actinomycin D. In CCl$_{4}$-treated rats, the activity of serum acid phosphatase was significiantly increased whereas that of liver acid phosphatase was rather slightly decreased. the pretreatment of prednisolone led to the decreased activity of serum and liver acid phosphatase in CCl$_{4}$-treated rats. But the pretreatment of actinomycin D rather increased the activity of liver and serum enzyme. In conclusion, it is likely the increased activity of serum acid phosphatase is based on the excess leaking of acid phosphatase into blood by the increased membrane permeability of both liver cell and lysosome in it.

• Biomolecules & Therapeutics
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• v.28 no.6
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• pp.503-511
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• 2020

Autophagy is a major catabolic process that maintains cell metabolism by degrading damaged organelles and other dysfunctional proteins via the lysosome. Abnormal regulation of this process has been known to be involved in the progression of pathophysiological diseases, such as cancer and neurodegenerative disorders. Although the mechanisms for the regulation of autophagic pathways are relatively well known, the precise regulation of this pathway in the treatment of cancer remains largely unknown. It is still complicated whether the regulation of autophagy is beneficial in improving cancer. Many studies have demonstrated that autophagy plays a dual role in cancer by suppressing the growth of tumors or the progression of cancer development, which seems to be dependent on unknown characteristics of various cancer types. This review summarizes the key targets involved in autophagy and malignant transformation. In addition, the opposing tumor-suppressive and oncogenic roles of autophagy in cancer, as well as potential clinical therapeutics utilizing either regulators of autophagy or combinatorial therapeutics with anti-cancer drugs have been discussed.

• Archives of Pharmacal Research
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• v.28 no.1
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• pp.93-99
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• 2005

Intracellular trafficking of transferrin-conjugated dimethyldioctadecyl-ammonium bromide liposome $(T_f-liposome)/DNA$ complexes in HeLa cells was studied using the double-labeled fluorescence technique and confocal microscopy. The size of the $T_f-liposome/DNA$ complex was about 367 nm in diameter and the zeta-potential of it at a 5:1 (w/w) ratio was almost neutral. The intracellular pathway of the $T_f-liposome/DNA$ complex, noted as green (FITC), red (rhodamine) or yellow (FITC + rhodamine) fluorescence, was elucidated from the plasma membrane to the endosome (or lysosome), and finally to the nucleus. The results of this study indicate that plasmid DNA enters into the nucleus not only as a free form but as an associated form complexed with $T_f-liposome$. More interestingly, the $T_f-liposome$ undergoes a nuclear location in the form of ordered structures. This could be a very useful piece of information in designing a safe and advanced gene delivery system.

• Molecules and Cells
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• v.41 no.1
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• pp.18-26
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• 2018

Mitochondrial quality control systems are essential for the maintenance of functional mitochondria. At the organelle level, they include mitochondrial biogenesis, fusion and fission, to compensate for mitochondrial function, and mitophagy, for degrading damaged mitochondria. Specifically, in mitophagy, the target mitochondria are recognized by the autophagosomes and delivered to the lysosome for degradation. In this review, we describe the mechanisms of mitophagy and the factors that play an important role in this process. In particular, we focus on the roles of mitophagy adapters and receptors in the recognition of damaged mitochondria by autophagosomes. In addition, we also address a functional association of mitophagy with mitochondrial dynamics through the interaction of mitophagy adaptor and receptor proteins with mitochondrial fusion and fission proteins.

• Biomedical Science Letters
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• v.10 no.4
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• pp.429-434
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• 2004

The effects of intravenous administration of high concentration of taurocholic acid (TCA) on cathepsin B and D, and acid phosphatase activities in rat liver lysosome were studied. These liver lysosomal enzymes were determined from the experimental rats with choledocho-caval shunt (CCS). The activities of liver lysosomal cathepsin B and D, and acid phosphatase were found to be significantly increased in the CCS plus TCA injection group than in control group, such as group of CCS alone group. However, these hepatic enzyme activities did not change in the CCS plus tauroursodeoxycholic acid injection group. The above results suggest that TCA stimulates the biosynthesis of the lysosomal cathepsin B and D, and acid phosphatase in the liver.

• Journal of Nutrition and Health
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• v.20 no.1
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• pp.15-24
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• 1987

To study effects of heated oil on lipid peroxidation in rat liver, rats were fed 3 and 6 weeks by intubating oils heated for l1(HA group) and 24 hours (HB group) at 18$0^{\circ}C$. The contents of lipid peroxides and vitamin E, and the activities of super oxide dismutase and glutathione peroxidase in liver were measured. Histological changes of the liver tissue were observed. In both HA and HE groups, the contents of lipid peroxides and the activities of superoxide dismutase were increased, but the activities of glutathione peroxidase and the contents of vitamin E in liver were decreased when compared to the control group which was fed fresh cora oils. During the oil feeding period, the activities of superoxide dismutase and the contents of vitamin E were not significantly changed, but the activities of glutathione peroxidase were decreased, and lipid peroxides were increased in the 3 weeks than in 6 weeks. In HB liver, the heterochromatin of nucleus increased, mitochondria swellen, cristae in mitochondria disappeared, fat droplet and secondary lysosome increased and lumen of rough endoplasmic reticulum enlarged, compared with that of the control group. These phenomena in HA group were less pronounced.

• Molecules and Cells
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• v.38 no.5
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• pp.381-389
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• 2015

Autophagy is a lysosome-dependent intracellular degradation process that allows recycling of cytoplasmic constituents into bioenergetic and biosynthetic materials for maintenance of homeostasis. Since the function of autophagy is particularly important in various stress conditions, perturbation of autophagy can lead to cellular dysfunction and diseases. Accumulation of abnormal protein aggregates, a common cause of neurodegenerative diseases, can be reduced through autophagic degradation. Recent studies have revealed defects in autophagy in most cases of neurodegenerative disorders. Moreover, deregulated excessive autophagy can also cause neurodegeneration. Thus, healthy activation of autophagy is essential for therapeutic approaches in neurodegenerative diseases and many autophagy-regulating compounds are under development for therapeutic purposes. This review describes the overall role of autophagy in neurodegeneration, focusing on various therapeutic strategies for modulating specific stages of autophagy and on the current status of drug development.

• Korean Journal of Veterinary Research
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• v.22 no.2
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• pp.187-195
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• 1982

This paper dealt with the light microscopical and electron microscopical findings on the morphological changes of the liver of Korean native goat injected with toxin (culture filtrate) of Clostridium perfringens which was isolated from Korean native cattle died of acute Clostridium perfringens enterotoxemia. The results observed are summarized as follows. In the microscopical findings, hyperemia and minute hemorrhage of the liver parenchyma, dilatation of hepatic central vein and centrilobular necrosis of liver, cloudy swelling and hydropic degeneration of hepatic cells, and appearance of light eosinophilic granular bodies in the vacuoles were recognized. In the electron microscopical findings, appearance of pinocytotic vesicle (coated vesicle), fusion of these vesicles, formation of vacuole and accumulation of minute granular proteinous materials in the vacuole were observed in the hepatic cells. Decreased number of glycogen granules, swelling and destruction of mitochondria, proliferation of smooth-surfaced endoplasmic reticulum, enlargement of rough-surfaced endoplasmic reticulum, dispersal of thready agranular membranous structure and appearance of secondary lysosome were recognized in the hepatic cell cytoplasm.

• Molecules and Cells
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• v.40 no.7
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• pp.441-449
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• 2017

Proteolysis in eukaryotic cells is mainly mediated by the ubiquitin (Ub)-proteasome system (UPS) and the autophagy-lysosome system (hereafter autophagy). The UPS is a selective proteolytic system in which substrates are recognized and tagged with ubiquitin for processive degradation by the proteasome. Autophagy is a bulk degradative system that uses lysosomal hydrolases to degrade proteins as well as various other cellular constituents. Since the inception of their discoveries, the UPS and autophagy were thought to be independent of each other in components, action mechanisms, and substrate selectivity. Recent studies suggest that cells operate a single proteolytic network comprising of the UPS and autophagy that share notable similarity in many aspects and functionally cooperate with each other to maintain proteostasis. In this review, we discuss the mechanisms underlying the crosstalk and interplay between the UPS and autophagy, with an emphasis on substrate selectivity and compensatory regulation under cellular stresses.