• 대한수의학회지
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• 제55권4호
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• pp.263-266
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• 2015

A 13-year-old, spayed, female Chihuahua dog was referred for evaluation of fever, lethargy, and dyspnea. Hematologic evaluation revealed severe neutropenia, thrombocytopenia, and mild anemia. The dog had been undergoing phenobarbital therapy for the past 7 weeks because of generalized seizures due to meningoencephalomyelitis of unknown etiology. After ruling out other possible causes of cytopenias, a tentative diagnosis was made of drug-induced blood cell dyscrasia. The neutropenia and thrombocytopenia resolved after discontinuation of phenobarbital (8 days and 15 days after discontinuation, respectively). This is the first case report in Korea to demonstrate blood dyscrasia associated with idiosyncratic adverse effects of phenobarbital.

• Biomolecules & Therapeutics
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• 제16권3호
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• pp.215-218
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• 2008

To investigate the possible interaction between rutaecarpine and phenobarbital in rats, phenobarbital in saline at 80 mg/kg was given ip to male SD rats for 3 consecutive days. Saline was given to control animals. One day after phenobarbital pre-treatment, rutaecarpine at 16 mg/kg was administered through penile vein. Blood was collected and analyzed by using HPLC. The pharmacokinetic parameters were determined with the non-compartmental model. Pre-treatment with phenobarbital significantly altered the pharmacokinetic profiles of rutaecarpine and its metabolite, 10-hydroxyrutaecarpine. The AUC of rutaecarpine was reduced to approximately 50% of control and the plasma half-life of rutaecarpine was significantly shortened when compared with control. In addition, the Cmax of 10-hydroxyrutaecarpine was increased approximately 160% of control. The AUC and the plasma half-life of 10-hydroxyrutaecarpine were decreased to 76.9% of control and to 82.7 min from 175.9 min, respectively. The results suggested that phenobarbital might accelerate the metabolism of rutaecarpine, thereby changing the pharmacokinetic parameters of rutaecarpine in male SD rats.

• 한국동물위생학회지
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• 제40권2호
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• pp.143-147
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• 2017

A Korean domestic short hair (1-year-old, male) presented with 2 to 3 weeks of seizures, aggressive behavior, vomiting, anorexia, and lethargy. The frequency of seizure had gradually increased from once a week to once every 3 hours. Physical and neurologic examination, diagnostic screening tests, including complete blood count (CBC), serum chemistry, electrolyte, coagulation test, X-ray, ultrasonography, and urinalysis were performed. Feline Leukemia Virus (FeLV), Feline Immunodeficiency Virus (FIV) and Toxoplasma spp. All tested negative, but the Feline Corona Virus (FCoV) kit revealed a positive result. To determine the exact diagnosis, magnetic resonance imaging (MRI) was performed but yielded no specific findings. The patient was then diagnosed with idiopathic epilepsy and treatment of phenobarbital was initiated. A month's treatment with phenobarbital proved ineffective as symptoms worsened. Zonisamide was then selected as an additional anticonvulsant. After adding zonisamide, symptoms improved, and seizures abated for 15 months. This is the first case report in South Korea describing the use of phenobarbital and zonisamide in the treatment of a cat with idiopathic epilepsy.

• 약학회지
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• 제25권4호
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• pp.167-173
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• 1981

Spectroscopic investigation has been carried out to know the binding mechanism of riboflavin with barbiturates, such as phenobarbital and amobarbital in chloroform solution by using infrared and nuclear magnetic resonance spectra. Phenobarbital and isoalloxazine form a 1:1 cyclic hydrogen bonded dimer through the 3-N imino and the 2-C carbonyl groups of the isoalloxazine ring of the latter, and the 1-N (or 3-N) imino and the 2-C carbonyl groups of the pyrimidine ring of the former. Amobarbital and riboflavin form a 1:1 cyclic hydrogen bonded dimer by the same mode of phenobarbital.

• 대한약리학회지
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• 제8권2호
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• pp.27-34
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• 1972

The present study is concerned with the demonstration of the influence of long term treatment with caffeine and phenobarbital on pentobarbital sleeping time, gastric secretion, increase rate of body weight and brain and liver weight in rats. The experimental subjects were rats weighing about 140 to 150 g, each of them was isolated in a separate cage. Each group was given 1 ml normal saline solution as control, caffeine 10 mg/kg and phenobarbital 30 mg/kg as experimental groups. All drugs were injected intraperitoneally, daily for 4 weeks. The results obtained are summarized as follows; 1. There was significant difference between before and after injection of drugs (caffeine citrate 10 mg/kg and phenobarbital 30 mg/kg) on pentobarbital sleeping time. The sleeping time of caffeine treated group was delayed (22.4%, p<0.01) significantly compared with that of before injection. The sleeping time of phenobarbital treated group was markedly shortened (93.6%, p<0.001) compared with that of before injection of drugs. 2. The volume, free and total acidity and pH of gastric juice determined five hours after pyloric ligation in fasting rats were not significantly changed in experimental groups compared with control group. However the volume of gastric juice was increased 25% in both caffeine and phenobardital treated group. 3. The increased ratio of body weight revealed no remarkable difference compared with intial body weight. However, caffeine treated group showed markedly increased body weight after first and second week of injection. 4. The brain and liver weight in experimental group showed no significant difference compared with control group (as percentage of body weight).

• 대한약리학회지
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• 제21권2호
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• pp.128-141
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• 1985

실험적으로 명암에 적응시킨 백서의 뇌내 specific opiate binding과 ${\beta}-endorphin$ 함량 일중변동에 미치는 지속적인 암적응, phenobarbital 장기처리의 영향을 관찰하고 opiate recptor binding과 ${\beta}-endorphin$ 함량 양자간의 관계를 추구하여 다음과 같은 성적을 얻었다. 1. L : D, 12 : 12 주기에 적응시킨 대조군에서 maximum $(^3H)$-morphine binding과 뇌내 ${\beta}-endorphin$ 함량은 각각 22시 및 06시에 최고에 달하는 매우 특이한 일중변동을 보였고 24시간 평균 $(^3H)$-morphine binding 및 뇌내 ${\beta}-endorphin$ 함량은 각각 0.45+0.03 pmol/mg protein과 46.7+3.6 fmol/mg protein이었다. 2. D : D, 12 : 12 주기에 적응시킨 표본에서 maximum $(^3H)$-morphine binding과 뇌내 ${\beta}-endorphin$ 함량은 대조군에서와는 달리 02시 및 14시에 최고에 달하는 유의한 일증변동을 보였고, 24시간 평균 maximum $(^3H)$-morphine binding치는 0.36+0.03 pmol/mg protein으로 대조군에 비하여 유의하게 감소를 하였으며, 24시간 정균 뇌내 ${\beta}-endorphin$치는 35.9+3.1 fmol/mg protein으로 대조군에 비하여 유의한 감소를 보였다. 3. Phenobarbital처리 표본에서 maximum $(^3H)$-morphine binding과 뇌내 ${\beta}-endorphin$ 함량은 각각 02시 및 14시에 최고 그리고 14시 및 02시에 최저에 달하는 대조군과는 다른 일중변동을 보였고, 24시간 평균 maximum $(^3H)$-morphine binding치는 0.33+0.03 pmol/mg protein으로 대조군에 비하여 현저한 감소를 보였다. 4. 전 실험군에서 opiate receptor binding의 Kd치는 변동하지 않았다. 5. 전 실험군에서 maximum $(^3H)$-morphine binding은 ${\beta}-endorphin$ 함량과 유의한 역상관관계가 있었다. 이상의 실험성적은 phenobarbital이 뇌내 ${\beta}-endorphin$ 함량과 opiate수용체의 숫적변동을 일으켜 morphine의 약리적 작용을 변동시킬 수 있으며, 이와 더불어 opiate 수용체와 ${\beta}-endorphin$ 함량 일중변동을 변화시킬 수 있음을 보여준다.

• 한국환경생물학회:학술대회논문집
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• 한국환경생물학회 2001년도 학술대회
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• pp.105-106
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• 2001

• 한국잡초학회지
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• 제17권1호
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• pp.59-65
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• 1997

Bentazon이 첫 분해대사물질인 6-hydroxy bentazon으로 변화하는데 관련하는 cytochrome P-450 활성을 증진시키는 방법을 모색하기 위하여 벼 microsome에서 hydroxylase 효소 유기물질을 처리하여 bentazon 6-hydroxylase(B6H)와 식물에서 흔히 볼 수 있는 cinnamic acid 4-hydroxylase(CA4H) 효소를 대조하여 효소활성을 검정하였다. 1,8-naphthalic anhydride 0.5-2% 농도를 벼 종자에 분의처리하거나 fenclorim 5, 10${\mu}M$을 벼종자에 침지처리함에 따라 B6H와 CA4H 효소 활성이 증대되었다. Ethanol 2.5%를 벼 유묘에 처리함으로써 B6H와 CA4H 활성이 증대되었으며, phenobarbital 12mM 처리에서 B6H 활성이 증대되었고 phenobarbital 2mM 처리에서는 CA4H 활성이 증대되었다. B6H 효소활성은 ethanol 2.5, 5%와 phenobarbital 8, 12mM 혼합 처리 또는 1,8-naphthalic anhydride 0.5, 1%와 phenobarbital 8, 12mM 혼합처리에서 상승적으로 증가하였으며, CA4H 효소는 혼합처리에 의하여 활성이 저하되었다. 한편 벼 5 일묘에서는 B6H와 CA4H 활성 이 가장 높았으며 묘령이 진전될수록 효소활성은 현저히 감소되는 경향을 나타냈다.

• 한국잡초학회지
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• 제15권3호
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• pp.214-223
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• 1995

본 실험은 경엽처리 제초제로 널리 사용되고 있는 Bentazon에 의한 옥수수의 생장저해량을 측정하여 옥수수 품종간의 내성 차이를 구명하고, 선발된 내성 및 감수성 옥수수 품종을 공시하여 효소활성 유기화합물 1,8-naphthalic anhydride, Ethanol, Phenobarbital로 처리한 후 Microsome을 얻은 다음, $^{14}C$-bentazon을 공시하여 TLC(Chloroform : Methanol : Amonium hydroxide = 13 : 7 : 1)와 LSC를 이용하여 Bentazon 불활성 분해효소 Bentazon 6-hydroxylase(B6H)를 측정하여 옥수수 품종간 내성기작를 밝히고자 수행되었다. 1. 생장반응에 의한 품종간 Bentazon의 내성정도는 GA 209, IK 2, DB 544, 수원 19호에서 강하게 나타났으며, KSS 3, KSS 4, KS 5, 만옥 2호에서는 감수성을 나타냈는데, 특히 3엽보다 4엽에서 더욱 뚜렷하였다. 2. 내성 품종인 수원 19호와 GA 209는 Bentazon 6-hydroxylase 활성이 감수성 품종인 단옥 2호와 KS 5에 비해 비교적 높은 경향을 보였다. 3. 내성 품종인 수원 19호와 GA 209 에서는 1,8-NA 0.5% 이상, Ethanol 2.5% 이상에서 B6H 활성이 높은 경향을 보인 반면, 감수성 품종인 단옥 2호와 KS 5에서는 1,8-NA 0.25% 이상, Ethanol 1.0, 2.5% 이상에서 B6H 활성이 낮은 경향을 보였다. 그리고, Phenobarbital은 2mM 에서 B6H 활성이 가장 높았으며, 내성 품종은 전반적으로 감수성 품종보다 약 2배정도 높은 활성을 나타냈다. 4. 내성 품종인 수원 19호와 GA 209에서는 1,8-NA, Ethanol, Phenobarbital 처리에서 모두 B6H효소 활성이 감수성 품종인 단옥 2호와 KS 5보다 높은 경향이므로 B6H효소에 의한 Bentazon의 히드록시 반응 불활성 대사가 빨리 일어나기 때문에 Bentazon에 내성을 나타낸 것으로 사료된다.

• Toxicological Research
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• 제13권1_2호
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• pp.95-101
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• 1997

Ethyl carbamate (EC) is a potent teratogen in rodents and is present at low concentration in fermented foods and alcohol beverages. It has been well hypothesized that some metabolic products are responsible for the teratogenic effects of the compound. In the present study, the effects of phenobarbital (PB) on EC-induced embryotoxicity were investigated in SD rats. Six groups were constructed: EC 300 (EC 300 mg/kg/day), EC 600 (EC 600 mg/kg/day), EC 600+PB (EC 600 mg/kg/day and PB 80 mg/kg/day), PB (PB 80 mg/kg/day), DR (dietary restriction, 8 g/day/rat) and a control group. Rats of the EC 600+PB group were pretreated with phenobarbital intraperitoneally for three days to induce cytochrome P450 enzymes, followed by oral administration of EC for two consecutive days. The incidence of fetal deaths in the EC 600+PB group was higher than that of the EC 600 group(42.7 vs. 14.3%). The incidence of fetal realformations in the EC 600+PB group was higher than that of the EC 600 group (external; 7.0 vs. 4.1%, visceral; 31.4 vs. 11.3%, skeletal; 11.1 vs. 6.5%). There was no embryotoxicity in the control, EC 300, PB and DR groups. These results show that the pretreatment with phenobarbital augments EC-induced embryotoxicity in rats, indicating an evidence that metabolic activation by cytochrome P450 may be the major pathway of EC to its embryotoxic forms.