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The effect of hepatic glutathione (GSH) depletion and enzymes Induction on hepatic glutathione S-transferase (GST’s) activity, biliary excretion of GSH cadmium, zinc was studied in rats.The GSH depletor Methyl Iodide did not Influence hepatic GST activity but depending on the substrate used , Phenobarbital benzopyeren increased it by 50-60% , 20-30% respectively GSH depletor decreased (60%) , benzopyrene did not effect Phenobarbital increase(90%) the transport of GSH into bile.The biliary excretion of cadmium and zinc was reduced by methyl iodide depletor (52-65%) and enhanced by Phenobarbital (99- 110)% . treatment with benzopyrene did not affect the excretion of zinc into bile ,but decreased that of cadmium, these result do not provide evidence for the role of hepatic GST but support the importance of biliary GSH excretion in the hepatobiliary transport of cadmium & zinc . It is assumed that Phenobarbital enhance the biliary excretion of metals by increasing the transport of GSH as a chemical complexation (cadmium-glutathione, zinc-glutathion) while the benzopyrene was less effect .

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The aim of this study was to develop convulsion by giving pentylenetetrazol and to observe the interaction of this drug with diphenhydramine and phenobarbital in chickens with an evaluation of the interaction of these drugs and their effect on the biochemical parameters. The chicks were divided into five groups, each group containing six birds, control group injected with normal saline at 2ml/kg, second group injected with PTZ at56.5 mg/kg I.P., third group injected with diphenhydramine at dose 2.5 mg/kg I.M., before 20 minutes from injected of PTZ at dose 56.5 mg/kg I.P., forth group injected with phenobarbital at dose 10 mg /kg I.M., before 20 minutes from injected of PTZ at dose 56.5 mg/kg I.P., fifth group injected with diphenhydramineat dose 2.5 mg/kgI.M. and phenobarbital at dose 10 mg /kg I.M. before 20 minutes from injection of PTZ at dose 56.5 mg/kgI.P. The results showed that group which was treated with PTZ alone showed a significant decrease in glutathione concentration in plasma and brain compare with the control group. All groups except the group treated with PTZ diphenhydramine and phenobarbital showed a significantly increased in malondialdehyde concentration in plasma and brain compare with control group, as well as, all groups except the group treated with PTZ and phenobarbital appeared significantly increased in glucose concentration in plasma compared with the control group. In conclusion, the study appeared oxidative stress result in the lipid peroxidation which main reasons for decreasing of glutathione concentration and increasing of malondialdehyde concentration in chicks.

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Background: previous researches showed that the hepatoprotective effect of silymarin was through inhibition of cytochrome p450- system (e.g. protection against Amanita toxin), in addition to protection from free radicals generated by this enzymatic system. In contrast to that, many evidences clarified that silymarin may increase first pass metabolism of e.g. cyclosporine and benzodiazepenes. Objective: Our aim from this animal experiment was to relieve this confusion and detect that this herbal extract is absolutely hepatoprotective or induce hepatotoxicity in other conditions.
Materials and Methods: this study was performed on 15 healthy male rats randomized into two treatment groups; first group (5 rats) pretreated with phenobarbital (I.P) then given acetaminophen (I.P) and the second group (5 rats) pretreated with silymarin (orally) then given acetaminophen (I.P.); while the last five rats were considered as control group for comparison . Activities of SGOT, SGPT and histopathological sections were detected for both groups and compared with that of control.
Results: for both treatment groups, the activities of transaminase enzymes were significantly higher than control group. Meanwhile; activity of these enzymes and severity of hepatic damage were significantly higher for Phenobarbital group compared with silymarin.
Conclusion: we can conclude from this experimental study that, even though silymarin act as hepatoprotective by multifactorial mechanisms (antioxidant, increase glutathione level, antifibrotic, anti-inflammatory and enzyme inhibitor), it may act as enhancer for some hepatotoxic agents (like acetaminophen) by cytochrome P-450 induction mechanism.

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The present study was design to observe the effect of Phenobarbital sodium on the thyroid gland of rabbits. A dose of(75mg/kg) was injected intramuscularly to the rabbits for (17) days. The study revealed a histological changes include decrease in follicular size and a major decrease in size of the follicular lumen.

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Background: Prolonged jaundice is a type of neonatal jaundice, which occurs in infants with high bilirubin levels (>10 mg/dl) persisting beyond day 14 of life in term neonates, and beyond day 21 in preterm neonates. Prolonged jaundice may be caused by predominantly conjugated or unconjugated hyperbilirubinemia. Distinguishing between these types of jaundice helps to determine the risk for pathological causes of prolonged jaundice.Phenobarbital has been used to treat neonatal jaundice since the 1960s. Numerous clinical trials have shown that both administration of phenobarbital to pregnant mothers before delivery and phenobarbital administration to neonates after delivery limit the severity of unconjugated hyperbilirubinemia, reduce the peak serum total bilirubin concentrations caused by physiologic jaundice by 50%, and the need for exchange transfusion. Objective: The aim of this study was to evaluate the role of phenobarbital in reducing the total serum bilirubin(TSB) in neonates with prolonged unconjugated hyperbilirubinemia. Methods: This is a prospective clinical trial study that was performed in Karbala teaching hospital for children from 18th of December 2017 to the end of December 2018. A total of 101 neonate with prolonged unconjugated hyperbilirubinemia were included in this study. All neonates who included in this study received phenobarbital tablet (5 mg /kg/day) twice a day for 10 days and some of them need phototherapy according to American Academy Of Pediatrics Guidelines for phototherapy, Results: There was a highly statistically significant decrease in TSB for the patients who were treated with phenobarbital compared to the baseline level, mean baseline TSB 14.57± 2.31 mg/dl versus TSB after phenobarbital 6.79±1.62 mg/dl (P value <0.001). There was a highly statistically significant decrease in TSB for the patients who were treated with phototherapy in addition to phenobarbital compared to the baseline level, mean baseline TSB 19.94±1.36 mg/dl versus TSB after phototherapy and phenobarbital 6.33±1.37 mg/dl (P value <0.001). Conclusions: 1. Oral phenobarbital supplementation in the neonates with prolonged unconjugated hyperbilirubinemia can significantly accelerate reduction in serum bilirubin levels. 2. Phenobarbital was safe, tolerable and no obvious adverse effects had been reported. 3. No need for cessation of breast feeding in cases of presumed breast milk jaundice.

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