• Journal of Environmental Health Sciences
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• v.23 no.2
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• pp.98-105
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• 1997

The study on the cytotoxicity of heavy metals was carried out to evaluate the cytotoxic effect of those on mouse L929 fibroblast cell in 96-well microtiter plates. The cytotoxicity was assayed by the neutral red, tetrazolium MTT, total protein, micronuclei test. The cytotoxicity of the heavy metals by neutral red and tetrazolium MTT was showed in order, cadmium > zinc > nickel for the cationic metals tested. The effect of metal-metal interaction on the cytotoxicity showed a marked reduction of cadmium toxicity by zinc, to a lesser degree, by nickel. The amount of total protein in treated group added heavy metals was less than that of the control and treated cadmium alone was less than those of combination with nickel or zinc. At midpoint cytotoxicity values of heavy metals, the frequency of micronuclei on the cell treated heavy metals was more than that of control and treated cadmium alone was more than those of combination with nickel or zinc. From those results, it could be suggested that the heavy metals decreased the viability of mouse fibroblast L929 cells in a concentration-dependent manner and have cytogenic toxic effects, but mixed group decreased the cytotoxic and cytogenic toxicity on L929 cells.

• Journal of Pharmaceutical Investigation
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• v.32 no.2
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• pp.113-117
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• 2002

Cyto-toxic effect of silver sulfadiazine (Ag-SD) on keratinocytes and its implication on wound healing process were investigated in $2^{nd}$ degree bum hairless mouse model. As a dermal model, HaCat (immortalized keratinocytes) monolayer culture in DMEM with 10% FBS was used. Cyto-toxicity of Ag-SD was estimated by measuring the cell viability using neutral red assay after adding the drug. The $2^{nd}$ degree bum was prepared on hairless mouse back skin (1 cm diameter) and dressings with Ag-SD were applied for 96 hr. The process of re-epithelialization and the presence of inflammatory cells were investigated and histology with Hematoxylin-Eosin staining was performed. Ag-SD displayed highly cyto-toxic effect on cultured HaCat cells in a concentration dependent manner $(1-100\;{\mu}g/mL)$. Topical application of Ag-SD (2%) could control the infection: no inflammatory cells were observed in histology. However the cyto-toxic effect of Ag-SD on skin cells induced the impairment in epidermal regeneration.

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.2
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• pp.65-71
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• 2008

The present study examined the inhibitory effect of licorice compounds glycyrrhizin and a metabolite $18{\beta}$-glycyrrhetinic acid on the neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the mouse and on the 1-methyl-4-phenylpyridinium ($MPP^+$)-induced cell death in differentiated PC12 cells. MPTP treatment increased the activities of total superoxide dismutase, catalase and glutathione peroxidase and the levels of malondialdehyde and carbonyls in the brain compared to control mouse brain. Co-administration of glycyrrhizin (16.8 mg/kg) attenuated the MPTP effect on the enzyme activities and formation of tissue peroxidation products. In vitro assay, licorice compounds attenuated the $MPP^+$-induced cell death and caspase-3 activation in PC12 cells. Glycyrrhizin up to $100{\mu}M$ significantly attenuated the toxicity of $MPP^+$. Meanwhile, $18{\beta}$-glycyrrhetinic acid showed a maximum inhibitory effect at $10{\mu}M$; beyond this concentration the inhibitory effect declined. Glycyrrhizin and $18{\beta}$-glycyrrhetinic acid attenuated the hydrogen peroxide- or nitrogen species-induced cell death. Results from this study indicate that glycyrrhizin may attenuate brain tissue damage in mice treated with MPTP through inhibitory effect on oxidative tissue damage. Glycyrrhizin and $18{\beta}$-glycyrrhetinic acid may reduce the $MPP^+$ toxicity in PC12 cells by suppressing caspase-3 activation. The effect seems to be ascribed to the antioxidant effect.

• Journal of the Korean Society of Food Science and Nutrition
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• v.18 no.2
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• pp.175-180
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• 1989

Toxins from Vibrio vulnificus cause Vibrio septicemia. Study was carried out for localization, characterization and toxicity of these toxins by injection thorough introspectional route to ICR(Insititude cancer research) mouse using Vibrio vulnificus M -1 isolated from patient and Vibrio vulnificus S-1 from sea water. No significant differences in lethal toxicity were observed between Vibrio vulnificus M-1 and Vibrio vulnificus $S-1.\;LD_{50}$ was $7.80{\times}10^6$ cells when these bacteria were injected to ICR mouse thorough intraperitoneal route. Crude hemolysin from Vibrio vulnificus S-1 did not show lethal toxiity and this lethal toxin were found to be endotoxin. This endotoxin were completely inactivated upon incubation at $80^{\circ}C$ for 20min.

• Journal of Food Hygiene and Safety
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• v.11 no.4
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• pp.299-306
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• 1996

6-[(N-3,4-Dibromophenyl)amino]-7-chloro-5,8-quinolinedione(FCK13) was tested for antifungal activities. The MIC values were determined by the two-fold dilution method. The therapeutic potential of RCK13 had been assessed in comparison with ketoconazole and fluconazole against systemic infections with candida albicans in normal mice. RCK13 had ED50,0.80$\pm$0.21 mg/kg but ketoconazole had ED50, 8.00$\pm$0.73 mg/kg respectively. And administered RCK13 at the ED50 for 14 days improved survival rates as well as ketoconazole. Acute oral toxicity studies of RCK13 were carried out in ICR mice of both sexes. These acute oral toxicities of RCK13 were low and LD50 values were over 2,850 mg/kg in ICR mice. The genotoxicities of RCK13 had been evaluated. RCK13 was negative in Ames test with Salmonella typhimurium and chromosomal aberration test in CHL cells. The clastogenicity was tested on the RCK13 with in vivo mouse micronucleus assay. RCK13 did not show any clastogenic effect in mouse peripheral blood and was negative in mouse micronucleus assay. These results indicate that RCK13 has no genotoxic potential under these experimental conditions.

• Korean Journal of Oriental Medicine
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• v.9 no.1
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• pp.137-144
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• 2003

The objective on this study was to investigate medicinal protection with KH-19, which was composed of 9 kinds of oriental herbs tonifying the blood, against side effect of chemotherapy in mice and its mechanism through microarray. Not only WBC (white blood cell), and PLT (platelet) as a hematopoiesis toxicity indicator but also spleen weight as an immune toxicity indicator was reduced significantly 7 day after. 5-flurouracil (FU) treatment. However, reduction of WBC, PLT, and spleen weight after 5-FU treatment was significantly recovered by KH-19. For mechanic study on KH-19 action, gene expression in mouse spleen treated 5-FU was compared with gene expression in mouse treated 5-FU and KH-19. The result indicates that 23 genes were increased. in expression level over 2 fold and 41 genes were decreased in expression level more than 2 fold at mouse spleen by KH-19 treatment. KH-19 mechanism may be complicated more than other drug which of mechanism were composed of single compound because KH-19 was composed of various compounds.

• Journal of Food Hygiene and Safety
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• v.14 no.1
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• pp.55-59
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• 1999

6-(4-Iodophenyl)amino-7-chloro-5,8-quinolinedione (RCK9) was evaluated for antifungal activities. The MIC values of RCK9 were determined against A. flavus, c. albicans, C. neoformans and F. oxysporium. The RCK9 showed generally potent antifungal activities against the tested fungi. Acute oral toxicity studies of RCK9 were carried out in ICR mice of both sexes. These acute oral toxicities of RCK9 had been evaluated. RCK9 were low and LD50 values were over 2,850 mg/kg in ICR mice. The genotoxicities of RCK9 had been evaluated. RCK9 was negative in Ames test with Salmonella typhimurium and chromosomal aberration test in CHL cells. The clastogenicity was tested on the RCK9 with in vivo mouse micronucleus assay. RCK9 did not show any clastogenic effect in mouse peripheral blood and was negative in mouse micronucleus assay. The results indicate that RCK9 has no genotoxic potential under these experimental conditions.

• Molecules and Cells
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• v.44 no.8
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• pp.613-622
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• 2021

In vertebrate eyes, the retinal pigment epithelium (RPE) provides structural and functional homeostasis to the retina. The RPE takes up retinol (ROL) to be dehydrogenated and isomerized to 11-cis-retinaldehyde (11-cis-RAL), which is a functional photopigment in mammalian photoreceptors. As excessive ROL is toxic, the RPE must also establish mechanisms to protect against ROL toxicity. Here, we found that the levels of retinol dehydrogenases (RDHs) are commonly decreased in phosphatase tensin homolog (Pten)-deficient mouse RPE, which degenerates due to elevated ROL and that can be rescued by feeding a ROL-free diet. We also identified that RDH gene expression is regulated by forkhead box O (FOXO) transcription factors, which are inactivated by hyperactive Akt in the Pten-deficient mouse RPE. Together, our findings suggest that a homeostatic pathway comprising PTEN, FOXO, and RDH can protect the RPE from ROL toxicity.

• Microbiology and Biotechnology Letters
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• v.18 no.1
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• pp.18-25
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• 1990

Paralytic Shellfish Poison (PSP) is mainly produced by marine dinoflagellates such as Protogonyaulax sp. and Pyrodinium sp.. The PSP was known to be accumulated in digestive gland of shellfish as result of feeding toxic dinoflagellates. PSP illness when occurs when one eats PSP intoxicated shellfish. Therefore PSP is becoming as serious problem in food hygiene and shellfish cultivation industry. The purpose of this study was to develop detoxification method for utilization of PSP intoxicated sea mussel and prevent from PSP illness. The PSP was extracted with 0.1 N HCl solution from the submitted sea mussel, then the toxicity was measured by mouse assay according to Official Methods of Analysis of the Association of Official Analytical Chemists. No detoxification effect was observed by adding extracted juice of garlic and ginger. When the sea mussel homogenate was heated at various temperatures, the PSP toxicity was not changed significantly at below $70^{\circ}C$ for 60 minutes but it was decreased as the heating temperature was increased. For example, when the sea mussel homogenate was heated at 100, $121^{\circ}C$ for 10 minutes, the toxicity was decreased about 67 and 90%, respectively. When the sea mussel containing 645 $\mu$g PSP per 100g of edible meat was processed according to general shellfish canning procedure, the toxicity was decreased as the level of PSP undetected by mouse assay.

• 대한생식의학회:학술대회논문집
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• 1996.11a
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• pp.61.1-61.1
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• 1996