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REFERENCE LINKING PLATFORM OF KOREA S&T JOURNALS
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Journal DOI :
The Korean Society of Toxicology
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Volume & Issues
Volume 22, Issue 4 - Dec 2006
Volume 22, Issue 3 - Sep 2006
Volume 22, Issue 2 - Jun 2006
Volume 22, Issue 1 - Mar 2006
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Terminology of Developmental Abnormalities in Common Laboratory Animals
Kim, Jong-Choon ; Yang, Young-Su ; Ahn, Tai-Hwan ; Kim, Sung-Ho ; Chung, Soo-Youn ; Rhee, Gyu-Seek ; Chung, Na-Young ; Chung, Moon-Koo ;
Toxicological Research, volume 22, issue 3, 2006, Pages 157~220
This paper presents the first version of a Korean glossary of terms for structural developmental abnormalities in common laboratory animals, mainly rats, mice and rabbits. This is a translation of the glossary entitled Terminology and Developmental Abnormalities in Common Laboratory Mammals that was edited by the International Federation of Teratology Societies(IFTS) Committee on International Harmonization of Nomenclature in Developmental Toxicology. The purpose of the Korean glossary is to provide a common vocabulary that will reduce confusion and ambiguity in the description of developmental effects, particularly in submissions to regulatory agencies worldwide. The glossary contains a primary term or phrase, a definition of the abnormality, and notes, where appropriate. Selected synonyms or related terms, which reflect a similar or closely related concept, are noted. Non-preferred terms are indicated where their usage may be incorrect. Modifying terms used repeatedly in the glossary(e.g., absent, branched) are listed in Appendix A, and syndrome names are generally excluded from the glossary, but are listed separately in Appendix B. The glossary is organized into broad sections for external, visceral, and skeletal observations, then subdivided into regions, structures, or organs in a general overall head to tail sequence. Numbering is sequential, and not in any regional or hierarchical order, Uses and misuses of the glossary are discussed. Updates of the Korean glossary are planned based on the comments received.
Hair Growth Promotion Effect of a Bio-Active Shampoo, Bonogen in C57BL/6 Mice
Hong, Jin-Tae ; Lee, Se-Ra ; Kim, Hwan-Hee ; Jo, Young-Kwang ; Baek, In-Jeoung ; Yon, Jung-Min ; Nahm, Sang-Seop ; Kwack, Dong-Hoon ; Lee, Jung-Eun ; Lee, Beom-Jun ; Yun, Young-Won ; Kim, Cheol-Jung ; Nam, Sang-Yoon ;
Toxicological Research, volume 22, issue 3, 2006, Pages 221~228
Bonogen shampoo is composed of several plant extracts which are known to be used in oriental medicine. This study was carried out to investigate the effects of Bonogen shampoo on hair growth in an alopecia model of C57BL/6 mice. There were eight male and female experimental groups including distilled water(DW: negative control), a commercial shampoo[M], 3% minoxidil (MXD) and Bonogen shampoo(BNG). Dorsal skin hair of six-week-old mice was trimmed with an electric clipper carefully not to damage the skin. The next day, mice without skin scratch were selected, randomized and separated in 10 mice per group. The test compounds were topically treated with 0.15 ml per mouse or dorsal skin for 21 days daily and then washed thoroughly with DW. The hair regrowth was determined photographically at 0, 4, 7, 10, 15, 18, and 21 days and histologically at day 21. No clinical signs were observed in all mice. Although body weight was slightly increased in 3% MXD group than other groups, it was not significant. Hair regrowth began to be promoted after 14 days and appeared a distinct regrowth pattern in all animals by topical treatment of test compounds at 18 days. In particular, the topical treatment of bonogen shampoo or 3% MXD for 21 days to dorsal skin accelerated hair regrowth faster than DW or M shampoo. At 21 days, the hair regrowth promotion speed was in order of 3% MXD>BNG>M>DW. The bonogen shampoo or 3% MXD also promoted hair follicle elongation compared to the negative control. These results suggest that bonogen shampoo has hair growth promoting activities and may be useful for treatment of bald or alopecia.
Anti-oxidative, Nitric Oxide Inhibitory Activities and Irritation Test of the Fermented Opuntia humifusa Cladodes
Chang, Zhi-Qiang ; Hwang, Mi-Hyun ; Oh, Byung-Chul ; Lee, Sam-Pin ; Rhee, Man-Hee ; Kim, Kil-Soo ; Jeong, Kyu-Shik ; Kim, Jong-Choon ; Park, Seung-Chun ;
Toxicological Research, volume 22, issue 3, 2006, Pages 229~235
Opuntia humifusa is a member of the Cactaceae family. In the present study, the antioxidant, nitric oxide(NO) inhibitory activities and potential irritation response of the fermented Opuntia humifusa cladodes(FOH) were investigated for cosmetic use. Antioxidant activities were tested using 1,1-diphenyl-2-picrylhydrazyl(DPPH) and xanthine oxidase assay, we found that FOH could scavenge DPPH free radicals and inhibit xanthine oxidase activity in a dose dependent manner, with
, respectively. To investigate the possible anti-inflammatory effects of FOH, RAW 264.7 macrophages were pretreated with FOH(
) for 30 min and then treated with LPS for 24 h. We found that cell number did not vary significantly with the treatment of FOH, and FOH did not show any inhibitory effects on LPS-induced NO production. After application of FOH to rabbits for skin and eye irritation test, the experimental sites did not show any response compared to the control. FOH were considered to be a non-irritant to the skin and eye. Based on the above information, we suggest that FOH can be considered to be a non-irritant base cosmetic material for safely use.
A Respiratory Toxicity Study of Sepiolite in Sprague-Dawley Rats
Chung, Yong-Hyun ; Han, Jeong-Hee ; Sung, Jae-Hyuck ; Yu, Il-Je ;
Toxicological Research, volume 22, issue 3, 2006, Pages 237~244
Two kinds of sepiolite, a
heat-treated sepiolite, and a
heat-treated sepiolite were analyzed for their physicochemical properties. After these sepiolites were instilled into rat lungs, the effects of the substances on lung pathological changes were evaluated. The lungs instilled with sepiolite increased their weight compared with the unexposed control. The pathological examination further showed increased legions of granuloma with early fibrosis. The heat treated sepiolites, however, did not show any toxicological differences from the untreated sepiolites. Thus chronic experiments are needed to evaluate the durability of mineral fibers, which is an essential experiment for evaluating biopersistence of fibers in lungs.
Regulation of LPS-induced Nitric Oxide Synthase Activity by Cigarette Smoke in Mouse Brain
Moon, Ja-Young ; Lim, Heung-Bin ; Sohn, Hyung-Ok ; Lee, Young-Gu ; Hyun, Hak-Chul ; Shin, Hantae ; Lee, Dong-Wook ;
Toxicological Research, volume 22, issue 3, 2006, Pages 245~251
Nitric oxide(nitrogen monoxide, NO) plays important physiological roles, but excessive generation can be toxic. NO is present in cigarette smoke at up to 1,000 ppm, and probably represents one of the greatest exogenous sources of NO to which humans are exposed. We investigated whether cigarette smoking reduces the production of endogenous NO and whether it influences the action of lipopolysaccharide(LPS) to induce nitric oxide synthase activity in mouse brain. Mice(C57BL6/J) were exposed to cigarette smoke for 8 weeks. LPS was injected intraperitoneally in single or combination with the exposure to cigarette smoke. Six hours after the injection of LPS, mice were sacrificed and sera and brains were collected. Serum concentrations of nitrate and nitrite were not charged by 4-week smoke exposure, but were significantly increased by 6 and 8 weeks of smoke exposure. Interestingly, cigarette smoke reduced the elevation in serum nitrate and nitrite concentrations produced by LPS after 4-week smoking exposure. NO synthase(NOS) activity in brain was upregulated by LPS-administration. However, cigarette smoke exposure remarkably and consistently decreased the LPS-induced activity in mouse brain. This result suggests that cigarette smoking may affect against overproduction of the endogenous NO by LPS through the inhibition of NOS activity induced by LPS in brain or by modulation of the LPS action for the induction of NOS activity. We also suggest the possibility that the exogenous NO evolved in cigarette smoke enables feedback inhibition of NOS activity or other possibility that it attenuates the toxicity of endotoxin LPS in vivo by unknown mechanisms, which should be further studied.
Effects of Estrogen, Aging and Oxidative Stress on Bone Remodelling in a View of Molecular Mechanisms
Park, Yeong-Chul ; Koh, Young-Do ; Han, Jung-Ho ; Kim, Mi-Kyung ;
Toxicological Research, volume 22, issue 3, 2006, Pages 253~266
Bone is a dynamic tissue that is constantly being remodelled. Resolution of bone and formation of new bone are closely linked, so that bone mass remains constant. With age, this process becomes unlinked with an imbalance in bore resorption and formation that results in a net loss of bone. Especially, osteoporosis is a disease characterized by low bone mass with age. One form of aging-related primary osteoporosis is postulated with the reduction of circulating estrogen, rapid bone loss occurs as a result of enhanced bore remodelling with an excess of resorption over bore formation. The oxidative stress is also involved in the pathogenesis of osteoporosis. Oxidative stress by cytokines, such as IL-a and TNF-
, inhibits osteoblast function in vitro and stimulates osteoblast apoptosis resulting in an imbalance in bore remodelling. The present article reviews the current perspectives on the interaction between bone remodelling and factors such as estrogen and oxidative stress, providing an interpretation of bone diseases in a view of molecular mechanisms
Tungtungmadic Acid Isolated from Salicornia herbacea Suppresses the Progress of Carbon Tetrachloride-induced Hepatic Fibrosis in Mice
Chung, Young-Chul ; Choi, Jae-Ho ; Oh, Kyo-Nyeo ; Chun, Hyo-Kon ; Jeong, Hye-Gwang ;
Toxicological Research, volume 22, issue 3, 2006, Pages 267~273
Tungtungmadic acid(3-caffeoyl, 4-dihydrocaffeoyl quinic acid: CDCQ) is a new chlorogenic acid derivative isolated from the Salicornia herbacea. The suppressive effects of CDCQ on the progress of acute carbon tetrachloride(
)-induced hepatic fibrosis were investigated in mice. CDCQ significantly suppressed
-induced hepatic necrosis and inflammation, as determined by serum enzymatic activities of alanine and aspartate aminotransferase and serum TNF-
levels in a dose-dependent manner. In addition, increased hepatic lipid peroxidation and fibrosis after acute
treatment were suppressed by the administration of CDCQ. CDCQ also significantly prevented the elevation of hepatic hydroxyproline and collagen content and
-smooth muscle actin(
-SMA) expression in the liver of
-intoxicated mice. These results suggest that the suppressive effects of CDCQ against the acute
-induced hepatic fibrosis possibly related to its ability to block both hepatic inflammation and the activation of hepatic stellate cells.
Eugenol Inhibits Excitotoxins-Induced Delayed Neurotoxicity, Oxidative Injury and Convulsion
Wie, Myung-Bok ; Cheon, Byung-Hwa ; Lee, Seon-Young ; Son, Kun-Ho ; Song, Dong-Keun ; Shin, Tae-Kyun ; Kim, Hyoung-Chun ;
Toxicological Research, volume 22, issue 3, 2006, Pages 275~282
In previous our studies, we have reported that eugenol derived from Eugenia caryophyllata(Myrtaceace) exhibits acute N-methyl-D-aspartate(NMDA)- and oxygen/glucose deprivation-induced neurotoxicity in primary cortical cultures and protects hippocampal neurons from global ischemia. In this study, we investigated whether the extracts and fractions of E. caryophyllata or eugenol shows the neuroprotective effects against delayed neuronal injury evoked by NMDA or
-amino-3-hydroxy-5-methylisoxazole propionate(AMPA), and oxidative damage induced by arachidonic acid-, hydrogen peroxide-,
/ascorbic acid-, and buthionine sulfoximine(BSO) in primary cortical cultures. We examined the neurotoxicity of eugenol itself in cultures and inhibitory effect of eugenol on NMDA- or kainate(KA)-induced convulsion in BALB/c mice. Each water, methanol extract and methanol fraction of E. caryophyllata was significantly attenuated NMDA-induced delayed neurotoxicity, respectively. Eugenol exhibited a significant inhibitory action against the convulsion evoked by NMDA and KA, and reduced delayed or brief neurotoxicity induced by NMDA, AMPA, and various oxidative injuries. These results suggest that eugenol derived from E. caryophyllata may contribute the neuroprotection against delayed-type excitotoxicity and excitotoxins-mediated convulsion through the amelioration of oxidative stress.
Calcium-induced Human Keratinocytes(HaCaT) Differentiation Requires Protein Kinase B Activation in Phosphatidylinositol 3-Kinase-dependent Manner
Piao, Longzhen ; Shin, Sang-Hee ; Yang, Keum-Jin ; Park, Ji-Soo ; Shin, Eul-Soon ; Li, Yu-Wen ; Park, Kyung-Ah ; Byun, Hee-Sun ; Won, Min-Ho ; Lee, Choong-Jae ; Hur, Gang-Min ; Seok, Jeong-Ho ; Kim, Ju-Duck ;
Toxicological Research, volume 22, issue 3, 2006, Pages 283~291
The survival and growth of epithelial cells depends on adhesion to the extracellular matrix. An adhesion signal may regulate the initiation of differentiation, since epidermal keratinocytes differentiate as they leave the basement membrane. A metabolically dead cornified cell envelope is the end point of epidermal differentiation so that this process may be viewed as a specialized form of programmed cell death. In order to investigate the precise cellular signaling events loading to terminal differentiation of keratinocytes, we have utilized HaCaT cells to monitor the biological consequences of
stimulation and numerous downstream signaling pathways, including activation of the extracellular signal-regulated protein kinase(ERK) pathway and activation of phosphatidylinositol 3-kinase(PI3K). The results presented in this study show that
function as potent agents for the differentiation of HaCaT keratinocytes, and this differentiation depends or the activation of ERK, Protein kinase B(PKB) and p70 ribosomal protein S6 kinase(p70S6K). Finally, the results show that the expression of Activator protein 1(AP-1; c-Jun and c-Fos) increased following
-mediated differentiation of HaCaT cells, suggesting that ERK-mediated AP-1 expression is critical for initiating the terminal differentiation of keratinocytes.
Magnolol Inhibits iNOS, p38 Kinase, and NF-κB/Rel in Murine Macrophages
Li Mei Hong ; Chang In-Youp ; Youn Ho-Jin ; Jang Dae-Sik ; Kim Jin-Sook ; Jeon Young-Jin ;
Toxicological Research, volume 22, issue 3, 2006, Pages 293~299
We demonstrate that magnolol, a hydroxylated biphenyl compound isolated from Magnolia officinalis, inhibits LPS-induced expression of iNOS gene in RAW 264.7 cells(murine macrophage cell line). Treatment of RAW 264.7 cells with magnolol inhibited LPS-stimulated nitric oxide production in a dose-related manner. RT-PCR analysis showed that the decrease of NO was due to the inhibition of iNOS gene expression. Western immunoblot analysis of phosphorylate p38 kinase showed magnolol significantly inhibited the phosphorylation of p38 kinase which is important in the regulation of iNOS gene expression. The specific p38 inhibiter SB203580 abrogated the LPS-induced NO generation and iNOS expression, whereas the selective MEK-1 inhibitor PD98059 did not affect the NO induction. Immunostaining of p65 and reporter gene assay showed that magnolol inhibited NF-
nuclear translocation and transcriptional activation, respectively. Collectively, this series of experiments indicates that magnolol inhibits iNOS gene expression by blocking NF-k/Rel and p38 kinase signaling. Due to the critical role that NO release plays in mediating inflammatory responses, the inhibitory effects of magnolol or iNOS suggest that magnolol may represent a useful anti-inflammatory agent.
Morphologic Changes in Microcystin-LR Treated Hepatocytes In vitro
Rhee, Seong-Hee ; Kim, Bum-Seok ; Lim, Chae-Woong ;
Toxicological Research, volume 22, issue 3, 2006, Pages 301~306
Microcystin-LR(MC-LR), a cyanobacterial toxin produced by Microcystis aeruginosa, causes severe hepatotoxicity. Here we investigated the morphologic changes of rat hepatocyte spheroid induced by exposure of MC-LR(
) in vitro. In addition, to determine the effects of such toxin in the process of hepatocyte spheroid formation, primarily isolated hepatocytes were incubated with MC-LR and the process of spheroid formation was observed. In both hepatocyte spheroid and suspension culture systems, the morphologic changes caused by MC-LR were noticible at 5 min post exposure and were characterized by the loss of microvilli, cytoplasmic vacuolation, the accumulation of lipid droplets, and blob formation. Especially, the size and numbers of blob on the cell surface were increased as the incubation time prolonged and the appearance of electron dense bodies were observed in the cytoplasm of hepatocyte at 20 min post exposure. Furthermore, bile canaliculi-like structures in the hepatocyte spheroids were slightly widened and the process of spheroids formation was inhibited in the isolated hepatocytes incubated with MC-LR. These results indicate that morphologic changes in. the hepatocyte membrane and organelles seem to be typical events in showing the MC-LR induced hepatotoxic effects and the spheroid culture method might be a useful experimental tool to evaluate hepatoxicity since it reflects the in vivo status of hepatocytes.