• Journal of Preventive Medicine and Public Health
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• v.15 no.1
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• pp.161-166
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• 1982

Cyanide poisoning is expected to be antagonized by the administration of oxygen, when it is administered in combination with the conventional cyanide antidote, sodium thiosulfate. However, the antidotal efficacy and its exact mechanism of oxygen in cyanide poisoning is still a controversial one. To test the effect of oxygen on the antidotal action of thiosulfate in cyanide poisoning, author designed this study on the dose-mortality patterns for potassium cyanide in mice. Potency ratios derived from $LD_{50}$ values were compared in groups of mice treated with sodium thiosulfate alone and sodium thiosulfate with oxygen. These results indicated that oxygen enhances the antidotal effect of sodium thiosulfate, effectively. This fact demonstrates that oxygen is of importance in the treatment of cyanide poisoning.

• YAKHAK HOEJI
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• v.29 no.4
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• pp.206-215
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• 1985

1) Puerariae Radix butanol ext. (100, 200, 400mg/kg, p.o. single treatment) alone partly showed blood pressure decreasing effect in SHRs and increasing effect of urinary volume in normal rats. 2) Cadmium nitrate (10mg/kg, s.c. single treatment) induced toxicity such as body weight decreasing effect, antidiuretic effect and muscle relaxant effect such as pull-up test, traction test and rota rod test in rats. However, Puerariae Radix butanol ext. (100, 200, 400mg/kg, p.o. single treatment) showed antidotal effects on the above and also in acute toxicity test when coadministered with both of them. 3) Cadmium nitrate (1mg/kg, s.c. 7 days consecutive treatment) did not showed toxicity in body weight change, blood pressure, change, serum biochemical parameters in rats. Puerariae Radix butanol ext. (100, 200, 400mg/kg, p.o. 7 days consecutive treatment) did not also showed any antidotal effects when coadministered with both of them for 7 days.

• Journal of the Korean Society of Food Science and Nutrition
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• v.34 no.3
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• pp.342-350
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• 2005

In the present work antidotal effect of dietary garlic was studied on lead-intoxicated rat. One of 5 groups of young Wistar sp. male rat, aged 4 weeks for control were fed only normal diet. Lead (25 ㎎/㎏.bw/week) was administered to other four groups for plumbism model over 4 weeks, of which three groups were supplemented with one of the following raw garlic juice: 1.10 (1% diet), 2.21 (2%) and 3.31 (3%) ㎎/㎏.bw/day respectively. Body weight gain rates in all garlic group significantly increased, especially in 2% garlic group that showed 9.8% net gain, as compared with only-lead treated group but lower values than control. The fecal and urinary lead excretion in all garlic groups significantly increased in a dose dependent fashion with highest value of 9.59% net gain in 3% garlic group as compared to lead treated control group. In comparison with lead treated control group, all garlic groups showed significantly increased hemoglobin contents, hematocrit values (Hct), red blood cell (RBC) count, mean corpuscular volume (MCV), and δ-amino levulinic acid dehydratase (δ-ALAD) activities. The values of 2% and 3% garlic groups remarkably increased while no significant difference between the values of 2% and 3% garlic groups was observed. The ALT activities, blood urea nitrogen (BUN) and creatinine (CR) in all garlic groups significantly decreased as compared with lead-treated control group. The values of 2% garlic group were the lowest and significantly different from the values of 1% and 3% garlic groups. The results showed that 2%-3% garlic juice in diet had obviously antidotal effects in lead-poisoned rats by promoting lead excretion. However, mega dose garlic such as in 3% garlic group might have some adverse effects on hepatic and renal functions in rats. In conclusion, the dietary habit to take ordinary garlic sauce in appropriate amount, may be helpful for preventing lead or other heavy metal intoxication.

• Korean Journal of Pharmacognosy
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• v.15 no.2
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• pp.108-113
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• 1984

The structure of tuguaconitine, MP $196{\sim}198^{\circ}C$, a new diterpene alkaloid isolated from the roots of Aconitum sibiricum P., was studied. Its empirical formula is $C_{23}H_{35}NO_7$ and spectroscopic evidence shows that the base contains three methoxyl, three hydroxyl and one N-ethyl groups. The acute toxicities of most of Aconitum species were strong and the acute toxicity of the alkaloid fraction of A. sibiricum was decreased by Glycyrrhizae, black bean or Zingiberis extract.

• Toxicological Research
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• v.16 no.3
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• pp.195-200
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• 2000

Antidotal efficacy of physostigmine plus procyclidine, the combinational prophylactics for organophosphate poisoning, was evaluated in rats and guinea pigs. To assess the dose-response relation-ship in rats, various doses (0.3-6.0mg/kg) of procyclidine in combination with a fixed dose (0.1mg/kg) of physostigmine were pretreated subcutaneously 30 min prior to subcutaneous exposure to nerve-agents. Physostigmine alone exerted protection ratios of 2.44, 1.20, 1.50, 1.50 and 2.20 folds for tabun, sarin, soman, cyclosarin and V-agent, respectively. Interestingly, coadmnistration of procyclidine with physostigmine exhibited remarkable synergistic effects in a dose-dependent manner, leading to 4.00~8.00 folds for tabun, 2.15-8.50 folds for sarin, 1.92~507 folds for so man, 2.15~2.90 folds for cyclosarin, and 2.71~10.50 folds for V-agent. On the contrary, a low effect (l.65 fold) was achieved with the traditional antidotes atropine (17.4 mg/kg) plus 2-pralidoxime (30 mg/kg) treated immediately after soman poisoning. Noteworthy, the combinational prophylactics markedly potentiated the effect of atropine plus 2-pralidoxime to 6.13 and 12.27 folds with 1.0 and 3.0 mg/kg of procyclidine, respectively, against soman poisoning. In guinea pigs, the physostigmine plus procyclidine prophylactics exerted protective effects of 3.00~4.70 folds against soman intoxcation, which were much higher at low doses (0.3~1.0 mg/kg) of procyclidine than those in rats. Taken together, it is proposed that the combinational prophylactics composed oj physostigmine and procyclidine could be a promising antidote regimen for the poisoning with organophosphates possessing diverse properties.

• Toxicological Research
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• v.16 no.3
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• pp.187-193
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• 2000

The antidotal, anticonvulsant and neuroprotective effects of physostigmine and procyclidine. the combinational prophylactics for organophosphate poisoning, were evaluated in rats. In comparison with a low protective effect (1.6 fold) of atropine (15 mg/kg) and 2-pralidoxime (30 mg/kg), the traditional antidotes regimen, a marked protection ratio of 7.3 fold was achieved by combinational pretreatment with physostigmine (0.05 mg/kg) and procyclidine (10 mg/kg), which was superior to that (3.5 fold) with pyri-dostigmine (0.1 mg/kg) and atropine (15 mg/kg). Rats exposed to a high dose (10 mg/kg. 2 X $LD_{50}$) of diisopropylfluorophosphate showed severe epileptiform seizures on electroencephalography, resulting in necrotic and apoptotic brain injuries in discrete brain regions under histopathological and TUNEL immuno-histochemical examinations in 24 hr. Such seizures and excitotoxic brain injuries were fully prevented by pretreatment with physostigmine (0.05 mg/kg) and procyclidine (10 mg/kg). in contrast to a negligible effect of pyridostigmine (0.1 mg/kg) and atropine (15 mg/kg). Taken together, it is proposed that the prophylactics composed of physostigmine and procyclidine could be a promising regimen for the prevention of lethality, seizures and brain injuries induced by organophosphate poisoning.

• Journal of The Korean Society of Clinical Toxicology
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• v.15 no.2
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• pp.107-115
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• 2017

Purpose: Glehnia littoralis has been used to treat ischemic stroke, phlegm, cough, systemic paralysis, antipyretics and neuralgia. The pharmacological mechanisms of Glehnia littoralis include calcium channel block, coumarin derivatives, anticoagulation, anti-convulsive effect, as well as anti-oxidant and anti-inflammatory effects. Alpha-amanitin (${\alpha}$-amanitin) is a major toxin from extremely poisonous Amanita fungi. Oxidative stress, which may contribute to severe hepatotoxicity was induced by ${\alpha}$-amanitin. The aim of this study was to investigate whether Glehnia littoralis ethyl acetate extract (GLEA) has the protective antioxidant effects on ${\alpha}$-amanitin -induced hepatotoxicity. Methods: Human hepatoma cell line HepG2 cells were pretreated in the presence or absence of GLEA (50, 100 and $200{\mu}g/ml$) for 4 hours, then exposed to $60{\mu}mol/L$ of${\alpha}$-amanitin for an additional 4 hours. Cell viability was evaluated using the MTT method. AST, ALT, and LDH production in a culture medium and intracellular MDA, GSH, and SOD levels were determined. Results: GLEA (50, 100 and $200{\mu}g/ml$) significantly increased the relative cell viability by 7.11, 9.87, and 14.39%, respectively, and reduced the level of ALT by 10.39%, 34.27%, and 52.14%, AST by 9.89%, 15.16%, and 32.84%, as well as LDH by 15.86%, 22.98%, and 24.32% in culture medium, respectively. GLEA could also remarkably decrease the level of MDA and increase the content of GSH and SOD in the HepG2 cells. Conclusion: In the in vitro model, Glehnia littoralis was effective in limiting hepatic injury after ${\alpha}$-amanitin poisoning. Its antioxidant effect is attenuated by antidotal therapy.

• Journal of The Korean Society of Clinical Toxicology
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• v.16 no.2
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• pp.108-115
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• 2018

Purpose: Glehnia littoralis has been reported to have several pharmacological properties but no in vivo reports describing the protective effects of this plant on${\alpha}$-amanitin-induced hepatotoxicity have been published. ${\alpha}$-Amanitin is a peptide found in several mushroom species that accounts for the majority of severe mushroom poisonings leading to severe hepatonecrosis. In our previous in vitro study, we found that ${\alpha}$-amanitin induced oxidative stress, which may contribute to its severe hepatotoxicity. The aim of this study was to investigate whether Glehnia littoralis acetate extract (GLEA) has protective antioxidant effects on ${\alpha}$-amanitin-induced hepatotoxicity in a murine model. Methods: Swiss mice (n=40 in all groups) were divided into four groups (n=10/group). Three hours after giving ${\alpha}$-amanitin (0.6 mg/kg, i.p.) to the mice, they were administered silibinin (50 mg/kg/d, i.p.) or Glehnia littoralis ethyl acetate extract (100 mg/kg/d, oral) therapies once a day for 3 days. After 72 hours of treatment, each subject was killed, cardiac blood was aspirated for hepatic aminotransferase measurement, and liver specimens were harvested to evaluate the extent of hepatonecrosis. The degree of hepatonecrosis was assessed by a pathologist blinded to the treatment group and divided into 4 categories according to the grade of hepatonecrosis. Results: GLEA significantly improved the beneficial functional parameters in ${\alpha}$-amanitin-induced hepatotoxicity. In the histopathological evaluation, the toxicity that was generated with ${\alpha}$-amanitin was significantly reduced by GLEA, showing a possible hepatoprotective effect. Conclusion: In this murine model, Glehnia littoralis was effective in limiting hepatic injury after ${\alpha}$-amanitin poisoning. Increases of aminotransferases and degrees of hepatonecrosis were attenuated by this antidotal therapy.

• Journal of Environmental Health Sciences
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• v.12 no.2
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• pp.1-9
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• 1986

The purpose of this study is to determine the antidotal effects of thiamine in phenylmercury poisoning rats. Sixty-six rats were divided into six groups the control group, the $40{\gamma}$ thiamine-only-dosed group, the 6 ppm phenylmercury-only-dosed group, the simultaneously-dosed-group with 6 ppm mercury & $20{\gamma}$ thiamine, and with 6 ppm mercury & $40{\gamma}$ thiamine, and with 6 ppm mercury & $80{\gamma}$ thiamine. The thiamine was put into pellet by various concentrations, and phenylmercury was mixed in drinking water by 6 ppm concentration. The rats were sacrificed for observing the histopathological changes of brain, liver and kidney. The remits summarized are as follows 1. In the group dosed with only $40{\gamma}$ thiamine, the tissues of brain, liver and kidney did not show any abnormal architecture. 2. The phenyhnercury-only-dosed group and the simultaneoulsy-dosed group with mercury and $20{\gamma}$ thiamine showed remarkable degenerative or necrotic hepatic cells. In addition, a remarkable swelling and necrosis on epithelium of proximal tubules in kidney were found. 3. The simultaneously-dosed group with mercury and $40{\gamma}$ thiamine showed moderate degeneration and necrosis of Purkinje cells in cerebellum. A moderate necrosis and swelling on epithelium of proximal tubules and a large amount of tubular casts were found as well. 4. The simultaneously-dosed group with mercury and $80{\gamma}$ thiamine showed a slight degenerative change of Purkinje cells. A slight degenerative change on epithelium of proximal tubules and a small amount of tubular casts were also found.

• The Journal of Korean Medicine
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• v.19 no.2
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• pp.485-501
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• 1998

Cortex Mori (Moros alba L.), the root bark of mulberry tree has been used as an autiphlogistic, diuretic and expectorant in herval medicine. Recently, a few papers reported that phenolic extract of Cortex Mori had the hypotensive, hypoglycemic, antiviral and anticancer effects, and hot water extract of Cortex Mori(CM) had inhibitory effect on the degranulation and histamine release from activated mast cells. These previous studies suggest a possibility that CM has an antidotal activity against inflammation which was mediated mainly by macrophage-secreting inflammatory factors. This study was performed to evaluate the influences of CM on carrageenan-induced edema in vivo and release of inflammatory mediators such as NO, TNF and IL-1 by macrophages stimulated with LPS or $IFN-{\gamma}$ in vitro. Subcutaneous injections of carrageenan into the mouse paw rapidly induced local edema by increasing vascular permeability, but single intraperitoneal injection of CM extract at 30 minutes before carrageenan suppressed the development of edema. NO and TNF production from macrophage stimulated by LPS or $IFN-{\gamma}$ were significantly suppressed, especially TNF secretion by up to 3-4 folds. LPS stimulated IL-1 production was also inhibited, but not significantly. Cell viability assay verified that the inhibition was not due to general cell toxicity. These results suggest that reduction of NO, TNF and IL-1 production may be one of the means by which CM prevent inflammation associated diseases.