• Korean Journal of Pharmacognosy
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• v.31 no.2
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• pp.216-223
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• 2000

The anti-inflammatory activity of SEO-KYONG-TANG extract(SKTWE) was examined by using carrageenin- and acetic acid-induced edema, croton oil-induced granuloma pouch, and adjuvant arthritis in rats. In addition, the acute toxicity, analgesic and antipyretic effects of SKTWE were investigated by using general experimental methods in mice. SKTWE did not show acute toxicity at 2400 mg/kg(p.o.) nor 1200 mg/kg(i.p.). After oral administration of the SKTWE to rats, significant anti-inflammatory activity was observed on 1% carrageenin- and 5% acetic acid-induced edema. Also, it significantly inhibited granuloma and exudation in these. In the adjuvant arthritis experiment, the SKTWE decreased the hind paw edema after 3 days of oral administration. In addition, it inhibited the writhing syndromes induced by 0.7% acetic acid in mice. The antipyretic activity of SKTWE was also observed through the typhoid vaccine experiment. These results suggest that SKTWE has analgesic, anti-inflammatory and antipyretic action.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.11b
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• pp.193-193
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• 2002

The subacute toxicities and toxicokinetics of a new fluoroquinolone antibiotics, DW-224a, were evaluated after single (at the 1st day) and 4-week (at the 28th day) oral administration of the drug, in doses of 0 (to serve as a control), 10, 30 and 90 mg/kg/day, to male and female dogs (n = 3 for male and female dogs for each dose).(omitted)

• Journal of The Korean Society of Clinical Toxicology
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• v.10 no.2
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• pp.97-102
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• 2012

Purpose: Serious acetaminophen (AAP) poisoning causes hepatotoxicity. N-acetylcysteine (NAC) is the most effective therapy for AAP poisoning and can be administered orally and intravenously (IV). Several studies have compared the efficacy of these two routes of administration and the results have been controversial. The purpose of this study was to compare the efficacy of oral and IV NAC for the prevention of hepatic toxicity in Korean patients whose serum AAP levels were higher than normal. Methods: A retrospective before/after study was performed, in which the patients presented to the emergency department with an AAP overdose from February 1995 to March 2012. A 3-day oral NAC regimen was used in the beginning, and a 20-hr intravenous regimen was then used from 2007. This study assessed the complications of an AAP overdose, such as hepatotoxicity, hepatic failure and renal failure as well as the side effects of the treatment regimen. Results: A total of 41patients was enrolled in this study. The median ALT and AST were 63 (IU/L) and 57 (IU/L) for the oral NAC treated patients, and 14 (IU/L) and 20 (IU/L) for the IV NAC treated patients (p=0.004 and p=0.001, respectively). The incidence of complications was similar in the treatment groups (p=0.399). Among the patients, 7 patients developed hepatotoxicity and were treated successfully with oral or IV NAC. Conclusion: This study suggests that IV NAC and oral NAC can prevent and successfully treat hepatic toxicity in patients whose serum AAP levels are higher than normal.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.28 no.6
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• pp.413-420
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• 2002

Mercury is one of the most frequently used heavy metal in dental clinic. Mercury poisoning rises up when someone is exposed to mercury chronically. In 1818, Amalgam was used for dental restorative procedure, and after then study about mercury toxicity has begun. Clinical signs of mercury toxicity in oral & maxillofacial area were increases of salivation, metallic taste, swelling and pain of tongue, redness and ulceration of oral mucosa, and increased mobility and loss of teeth. After we injected mercury($HgCl_{2}$) into intraperitoneum of rat, studied about histopathological changes of submandibular gland cell. Experimental group was divided into two groups by amount of mercury. (Group 1 was 0.5mg/Kg of mercury injection, group 2 was 1.0mg/Kg of mercury injection.) 1. After 3days of intraperitoneal injection, black granules were observed at macrophage cell in both group. In group 2, author found hyperchromatism of nucleus, and vacuolization of cellular matrix and nucleus of acinar cell. 2. After 1week of intraperitoneal injection, author found severe vacuolization of nucleus and cellular matrix, and irregular granules around nuclear membrane at mucous cell and serous cell in both group. Vacuolization of nucleus and cellular matrix was seen at duct cell in group 2. 3. After 2weeks of intraperitoneal injection, author could found severe vacuolization of cellular matrix, and sometimes nucleus was positioned in central area of cellular matrix at mucous and serous cell in both group. Vacuolization of nucleus and cellular matrix was found at vascular endothelial cell in group 2. 4. After 4weeks of intraperitoneal injection, destruction and distortion of gland cells were distinct. Vacuolization and destruction of nucleus and cellular matrix was found at duct cell in group 2. After intraperitoneal injection of mercury, we found equanimity of mercury and destruction of cellular matrix at serous cell, mucous cell, and duct cell of submandibular gland. So, we thought that metallic taste of mercury poisoning patient would be due to excretion of saliva containing mercury.

• The Korean Journal of Pesticide Science
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• v.12 no.3
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• pp.229-235
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• 2008

Lack of honey bee toxicity data for most pesticide products used for strawberry restricts to predict the adverse effects to foraging honey bee after treatment of pesticide in plastic house. This study was conducted to evaluate the actual risk of worker honey bees (Apis mellifera L.) through acute contact toxicity test, acute oral toxicity test and toxicity of residues on foliage test with 21 pesticide products. The mortality of honeybee sprayed with 6 pesticides including dichlofluanid WP showed significantly different from control at recommended application rate in acute contact toxicity test at 24 hours after treatment. Fenpropathrin EC and milbemectin EC treatment groups showed more than 25% mortalities at recommended application rate in acute oral toxicity test. In toxicity of residues on foliage test, only fenpropathrin EC treatment group showed more than 25% mortalities at 10 days after treatment at recommended application rate. It was concluded that the most toxic route to exposure for honey bee is direct contact exposure to sprayed pesticides. Safety interval for honey bee was established by concerning the results of these tests.

• The Korea Journal of Herbology
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• v.23 no.2
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• pp.81-85
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• 2008

Objectives : The aim of this study is to collect data for toxicity and safety of Mud chrysanthemum indicum. Methods : In this study, we investigated the acute toxicity for buthanol-extracted Mud schrysanthemum indicum, 25 male and 25 female mice were observed for 14days after one day oral administration of Mud chrysanthemum indicum at the respective doses of 0(control group), 1024, 1280, 1600 and 2000mg/kg. Results : We observed survival rates, general toxicity, change of body weight and autopsy. No abnormality was found for all cases. Conclusions : The data confirmed that Mud chrysanthemum indicum is free from, the toxicity and safety problems. Compared with the control group, we could not find any toxic alteration in all treated groups (1024, 1280, 1600 and 2000mg/kg), In conclusion, LD50 of Mud chrysanthemum indicum was over 2000 mg/kg and it is very safe to mice.

• The Korean Journal of Pesticide Science
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• v.15 no.4
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• pp.383-388
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• 2011

We investigated methiozolin acute toxicity using with Sprague-Dawley rats. The results of acute oral toxicity using rats showed $LD_{50}$ value of over 2,000 mg/kg bw for methiozolin. The calculate acute dermal $LD_{50}$ value of methiozolin was over 4,000 mg/kg. The skin irritation test showed moderately irritation and weak response of eye irritation test was observed in this experimental condition. According to these results, We concluded that methiozolin was Category IV in GHS chemical classification for acute toxicity. Future, we need more chronic toxicity test for safety.

• Proceedings of the PSK Conference
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• 2001.10a
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• pp.154.1-154.1
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• 2001

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.11a
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• pp.193-193
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• 2002

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2004.05a
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• pp.96-96
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• 2004