• Korean Journal of Veterinary Research
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• v.55 no.4
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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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• v.16 no.3
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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.

• Korean Journal of Veterinary Service
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• v.40 no.2
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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.

• YAKHAK HOEJI
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• v.25 no.4
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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.

• The Korean Journal of Pharmacology
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• v.8 no.2
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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).

• The Korean Journal of Pharmacology
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• v.21 no.2
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• pp.128-141
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• 1985

To investigate the influence of phenobarbital sodium on the action of morphine and on the diurnal rhythms of both opiate receptor binding and ${\beta}-endorphin$ contents, the amount of specifically bound $(^3H)$-morphine and immunoreactive ${\beta}-endorphin$ were measured in the midbrain of phenobarbital-treated rats at 4h intervals in a day. Rats were housed and adapted to a controlled cycle of either 12 h light-12 h dark or 24 h constant dark. After 3 weeks of adaptation, 0.5 ml of physiological saline or phenobarbital sodium (20mg/kg/day, i.p.) were administered twice a day for 2 weeks. Highly significant diurnal rhythms of opiate receptor binding and ${\beta}-endorphin$ were present in rat midbrain. In control group, the peak of maximum $(^3H)$-morphine binding was observed at 22:00 h, whereas the peak of ${\beta}-endorphin$ content was found at 06:00 h. Even in the absence of time cues these diurnal rhythms persisted, but they were highly modified with respect to the wave form as well as differences in the timing of peak and nadir. In the phenobarbital-treated group, these diurnal rhythms were also modified in shape, phase and amplitude, as well as in timing of peak and nadir. In this group, 24 h mean of opiate receptor binding was significantly decreased, while the 24 h mean level of ${\beta}-endorphin$ content was highly increased. However, Kd values in all experimental groups did not change. This indicates that differences in binding were not due to changes in the affinity, but in the number of binding sites. Statistical analysis of regression line indicates that changes of receptor binding were closely correlated with the changes of ${\beta}-endorphin$ content. These results suggest that phenobarbital may influence the action of morphine by changing the number of opiate receptors and that the modification of diurnal rhythm of opiate receptor by the agent is possibly due to changes of ${\beta}-endorphin$ content.

• Proceedings of the Korea Society of Environmental Biology Conference
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• 2001.12a
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• pp.105-106
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• 2001

• Korean Journal of Weed Science
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• v.17 no.1
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• pp.59-65
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• 1997

Bentazon 6-hydroxylase (B6H) and cinnamic acid 4-hydroxylase (CA4H) activities were determined in rice (Oryza sativa L.) microsomes to study methods of enhancing cytochrome P-450 mediated aryl hydroxylation of bentazon by hydoxylase inducing compounds. Pretreating rice seeds with 1,8-naphthalic anhydride at 0.5-2% and fenclorim at 5 and 10 ${\mu}M$ increased B6H and CA4H activities. Treatments of rice seedling with ethanol 2.5% enhanced B6H and CA4H activities, and with phenobarbital at 12 mM enhanced B6H activity, and CA4H activity was enhanced at 2 mM. B6H activity was synergistically enhanced by combined treatments of ethanol 2.5 or 5% and phenobarbital 8 or 12mM and also that of 1,8-naphthalic anhydride 0.5 or 1% and phenobarbital 8 or 12 mM, but CA4H activity was decreased by combined treatment. Five-day-old rice seedlings showed higher B6H and CA4H activities which decreased with seedling age.

• Korean Journal of Weed Science
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• v.15 no.3
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• pp.214-223
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• 1995

Tolerant corn cultivars to bentazon were selected and tolerance mechanism of corn cultivars to bentazon was studied by determining bentazon 6-hydroxylase(B6H) activity which was known to detoxify bentazon to 6-hydroxy bentazon at induced enzyme conditions with treatments of 1,8-naphthalic anhydride, ethanol and phenobarbital. Tolerant cultivars to bentazon were selected by growth response of corn by foliar application of bentazon to corn cultivars. Kwanganok, GA 209, IK 2, DB 544, and Suwon 19 were tolerant to bentazon, but KSS 3, KSS 4, KS 5, and Danok 2 were susceptible. Pretreating corn seeds with 1,8-naphthalic anhydride increased B6H activity at all cultivars, but the tendencies were more remarkable at Suwon 19 and GA 209, tolerant cultivars, than at Danok 2 and KS 5, susceptible cultivars. Treating corn shoots with ethanol increased B6H activity at Suwon 19 and GA 209. B6H activity was enhanced by treatments of ethanol at 1.0 or 2.5%, but decreased at ethanol 2.5 or 5.0% at Danok 2 and KS 5. Treating corn shoots with phenobarbital increased B6H activity at Suwon 19, GA 209, Danok 2, and KS 5 by treatments of phenobarbital at 2.0mM, but decreased at 4.0 or 8.0mM at all cultivars. Therefore, the tolerant mechanism of corn cultivars to bentazon may be explained partially by the activity of bentazon 6-hydroxylase which detoxifies bentazon to 6-hydroxy bentazon.

• Toxicological Research
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• v.13 no.1_2
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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.