• Korean Journal of Soil Science and Fertilizer
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• v.20 no.3
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• pp.251-259
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• 1987

Humic acids extracted from decomposing plant residues were characterized by infrared(IR) spectra. The IR spectra were further interpreted by chemical analyses for oxygen-containing functional groups such as carboxyl, phenolic, alcoholic, carbonyl, and quinionic groups. 1. The IR spectra obtained in this study were divied into three categories: spectra of humic acids from grain crop straws of rice, barley, wheat and rye produced Type I, while that from wild grass hay yielded Type II, and those from forest tree litter of the deciduous and conifers were led to give Type III. 2. There were no significant changes in the absorption bands observed among humic acids extracted at various stages of decomposition of a given Plant material. 3. The absorption band at about $3,430cm^{-1}$ represents the presence of hydrogen-bonded hydroxyl groups, phenolic-OH groups being the major component. 4. A close relationship was found between the total acidity and the content of phenolic-OH groups of humic acids. The content of carboxyl groups maintains a direct relationship with the content of total hydroxyl groups, and such a close relationship also exists between the content of alcoholic hydroxyls and that of total hydroxyl groups. 5. Overlapping of the absorption bands of carbonyl groups and quinones renders it difficult to make differentiation between the two. 6. A variety of non-armoatic cyclic hydrocarbons appears to be a structural component as evidenced by a sharp absorption peak near $995-1000cm^{-1}$.

• Korean Journal of Microbiology
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• v.52 no.3
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• pp.319-326
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• 2016

An antimicrobial bacterium to pathogenic microorganisms, strain $W5-1^T$ was isolated from Korean fermented-food Kimchi. The isolate was Gram-staining-variable, strictly aerobic, rod-shaped, endospore-forming, and motile with peritrichous flagella. It grew at $15-40^{\circ}C$, at pH 6.0-10.0, and in the presence of 0-4% NaCl. Strain $W5-1^T$ could hydrolyze esculin and xylan, and assimilate $\small{D}$-mannose, but not $\small{D}$-mannitol. Strain $W5-1^T$ showed antimicrobial activity against Listeria monocytogens, Pseudomonas aeruginosa, Staphylococcus aureus, and Salmonella typhi. The G+C content of the DNA of strains $W5-1^T$ was 52.6 mol%. The predominant respiratory quinone was menaquinone-7 (MK-7) and the major cellular fatty acids were $C_{16:0}$, antieiso-$C_{15:0}$, $C_{18:0}$, and $C_{12:0}$. The strain contained meso-diaminopimelic acid in cell-wall peptidoglycan. On the basis of 16S rRNA gene sequence and phylogenetic analysis, the strain W5-1 was shown to belong to the family Paenibacillaceae and was most closely related to Paenibacillus pinihumi $S23^T$ (98.4% similarity) and Paenibacillus tarimensis $SA-7-6^T$ (96.4%). The DNA-DNA relatedness between the isolate and Paenibacillus pinihumi $S23^T$ was 8.5%, indicating that strain $W5-1^T$ represented a species in the genus Paenibacillus. On the basis of the evidence from this polyphasic study, it is proposed that strain $W5-1^T$ is considered to represent a novel species of the genus Paenibacillus, for which the name Paenibacillus kimchicus sp. nov. is proposed. The type strain is $W5-1^T$ (=KACC $15046^T$ = $LMG 25970^T$).

• Proceedings of the Korean Biophysical Society Conference
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• 2003.06a
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• pp.80-80
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• 2003

${\beta}$-lapachone(${\beta}$-Lap), a natural o-naphthoquinone, presents in the bark of the Lapacho tree. ${\beta}$-Lap is cytotoxic against a variety of human cancer cells and it potentiates the anti-tumor effect of Taxol. In addition, ${\beta}$-Lap has been reported to radiosensitize cancer cells by inhibiting the repair of radiation-induced DNA damage.In the present study, we investigated the cytotoxicity of ${\beta}$-Lap against RKO human colorectal cancer cells as well as the combined effect of ${\beta}$-LaP and ionizing radiation. An incubation of RKO cells with 5 ${\mu}$M of ${\beta}$-Lap for 4 h killed almost 90％ of the clonogenic cells. An incubation of RKO cells with 5 ${\mu}$M of ${\beta}$-Lap for 4 h or longer also caused massive apoptosis. Unlike other cytotoxic agents, ${\beta}$-Lap did not increase the expression of p53 and p21 and it suppressed the NFkB expression. The expression of Caspase 9 and 3 was minimally altered by ${\beta}$-Lap. Radiation and ${\beta}$-Lap acted synergistically in inducing clonogenic cell death and apoptosis in RKO cells when ${\beta}$-Lap treatment was applied after but not before the radiation exposure of the cells. Interestingly, a 4 h treatment with 5 ${\mu}$M of ${\beta}$-Lap starting 5 h after irradiation was as effective as that starting immediately after irradiation. The mechanisms of ${\beta}$-Lap-induced cell killing is controversial but a recent hypothesis is that ${\beta}$-Lap is activated by NAD(P)H: quinone-onidoreductase (NQO1) in the cells followed by an elevation of cytosolic Ca$\^$2+/ level and activation of proteases leading to apoptosis. It has been reported that NQO1 level in cells is markedly up-regulated for longer than 10 h after irradiation. Indeed, using immunological staining of NQO1, we observed a significant elevation of NQO1 expression in RKO cells 5h after 2-4 Gy irradiation. Such a prolonged elevation of NQO1 level after irradiation may be the reasons why the ${\beta}$-Lap treatment applied S h after irradiation was as effective as that applied immediately after irradiation in killing the cells. In view of the fact that the repair of radiation-induced damage is usually completed within 1-2 h after irradiation, it is highly likely that the ${\beta}$-Lap treahment applied 5 h after irradiation could not inhibit the repair of radiation-induced damage. For in vivo study, RKO cells were injected S.C. into the hind-leg of Nu/Nu mice, and allowed to grow to 130 mm3 tumor. The mice were i.p. injected with ${\beta}$-lapachone or saline 2 h after irradiation of tumors with 10 Gy of X-rays. The radiation induced growth delay was increased by 2.4 $\mu\textrm{g}$/g of ${\beta}$-lapachone. Taken together, we may conclude that the synergistic interaction of radiation and ${\beta}$-Lap in killing cancer cells is not due to radiosensitization by ${\beta}$-Lap but to an enhancement of ${\beta}$-Lap cytotoxicity by radiation through an upregulation of NQO1. The fact that NQO1 is elevated in tumors and that radiation causes prolonged increase of the NQO1 expression may be exploited to preferentially kill tumor cells using ${\beta}$-Lap in combination with radiotherapy.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.26 no.1
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• pp.149-162
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• 2000

Coenzyme Q10 is found in all tissues including skin and it is the well-known coenzyme for mitochondrial enzymes. The electron and proton transfer functions of the quinone ring are of fundamental importance for the oxidative phosphorylation pathway to generate energy in the cells. Coenzyme Q10 has been studied as a potent antioxidant molecule in the skin. It is involved in the skin's response to UVR irradiation. The concentration of this antioxidant in UVR exposed skin is higher than in non-exposed skin. However, recent studies have also shown that coenzyme Q10 is one of the first antioxidants to be depleted when skin is UVR-irradiated. This indicates that coenzyme Q10 is primarily involved in defense mechanisms of the skin. Therefore, we questioned whether coenzyme Q10 shows reulatory effect of melanogenesis. Here we report that coenzyme Q10 inhibits melanin neosynthesis of normal human melanocytes grown in culture, and lightens UVB-induced hyperpigmentation of the guinea pig skin in vivo. We treated human melanocytes with 0.05mM to 0.5mM of coenzyme Q10 for a total of two days. This inhibited melanin neosynthesis of cultured human melanocytes dose-dependently. The inhibitory effect of coenzyme Q10 was as effective as kojic acid or vitamin C on cultured human melanocytes. CoQ10 didn't have direct inhibitory effect on tyrosinase activity in in vitro tyrosine hydroxylase activity To further clarify the effect of coenzyme Q10 on the melanogenesis, we established UVB-induced hyperpigmentation on the shaved backs of brownish guinea pigs. The UVB intensity was 500mJ/$\textrm{cm}^2$ and the total energy dose was 1,500 mJ/$\textrm{cm}^2$. The animals were exposed to UVB radiation one times a week for three consecutive weeks. Coenzyme Q10, kojic acid, Arbutin, vitamin C(1% in vehicle) or vehicle alone as a control were then topically applied daily to the hyperpigmented areas twelve times per week far four successive weeks. The lightening effect was evaluated by visual scoring, chromameter and immunohistochemistry. Coenzyme Q10 had lightening effect on the UVB-induced hyperpigmentation without any other side effects, whereas another compounds showed weak lightening efficacies. Therefore, these results suggest that coenzyme Q10 may be useful for solving physiological hyperpigmenting problems for cosmetic purposes.

• Korean Journal of Plant Resources
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• v.35 no.5
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• pp.565-573
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• 2022

Gingival inflammation is one of the main causes that can be related to various periodontal diseases. Human gingival fibroblast (HGF) is the major constituent in periodontal connective tissue and secretes various inflammatory mediators, such as nitric oxide (NO) and prostaglandin E₂ (PGE₂), upon lipopolysaccharide stimulation. This study is aimed at investigating the anti-inflammatory and antioxidative activities of Lotus Root extract (LRE) in Porphyromonas gingivalis derived lipopolysaccharide (LPS-PG)-stimulated HGF-1 cells. The concentration of NO and PGE₂, as well as their responsible enzymes, inducible NO synthase (iNOS), and cyclooxygenase-2 (COX-2), was analyzed by Griess reaction, ELISA, and western blot analysis. LPS-PG sharply elevated the production and protein expression of inflammatory mediators, which were significantly attenuated by LRE treatment in a dose-dependent manner. LRE treatment also suppressed activation of Toll-like receptor 4 (TLR4)/myeloid differentiation primary response gene 88 (MyD88) and nuclear factor-κB (NF-κB) in LPS-PG-stimulated HGF-1 cells. In addition, one of phase II enzyme, NAD(P)H quinone dehydrogenase (NQO)-1, and its transcription factor, Nuclear factor erythroid 2-related factor 2 (Nrf2), were significantly induced by LRE treatment. Consequently, these results suggest that LRE ameliorates LPS-PG-induced inflammatory responses by attenuating TLR4/MyD88-mediated NF-κB, and activating NQO-1/Nrf2 antioxidant response element signaling pathways in HGF-1 cells.