Thesis (M.S.)--Ball State University, 2009. / Title from PDF t.p. (viewed on June 08, 2010). Includes bibliographical references (p. 75-80).

Stability studies were undertaken at ambient (25ºC/60%RH) and accelerated conditions (40ºC/75%RH) to determine the effect of changing of hard gelatin capsule supplier on a phenytoin sodium (100 mg) capsule formulation. Three hard gelatin capsule suppliers: RP Scherer (Supplier A), Capsugel (supplier B) and Associated Caps (Supplier C) were used in the study. Capsules were analyzed just after filling of the capsules (T0), after 1 month (T1), after 2 months (T2) and after 3 months (T3) after being stored in securitainers under the above-mentioned conditions. The moisture content of the empty shells as well as the capsule contents were analysed at each time-point. The capsule disintegration time was recorded at each time point. Multi-point dissolution testing was performed at each time point to determine the release of the active substance in each case. Based on the achieved results, the best capsule shell supplier was recommended, and other suggestions were made to improve the capsule formulation.

No description available.

Thesis (M.S.)--University of Michigan, 1964.

Thesis (M.S.)--University of Michigan, 1964.

Cerebral ischaemia, traumatic injury to the brain, inflammatory neurological disorders and HIV infections are amongst the most prevalent causes of neurodegeneration. Neuroprotective strategies are usually to limit the progressive secondary injury that generally occurs, thus limiting overall tissue damage. Neuroprotective strategies are usually to limit the progressive secondary injury that generally occurs, thus limiting overall tissue damage. Sodium channel blockers have been often used for this matter as they prevent the cascade of events culminating in free radical generation and eventually neuronal apoptosis. Newer compounds, such as antiperoxidants and free radical scavengers, show encouraging experimental results, but their clinical use is still very limited. Phenytoin being a popular drug in the treatment of epilepsy has also been used as a neuroprotectant during certain neurological emergencies and in pharmacological prophylaxis of post-traumatic epilepsy. Furthermore this agent functions by prolonging inactivation of voltage gated sodium channels. In these sets of experiment the neuroprotective properties of phenytoin were examined. The histological study revealed that phenytoin confers protection to the CA1 and CA3 regions of the hippocampus under the insult of QUIN. Cells maintain their characteristic shape and minimal tissue necrosis occurs in the presence of this agent. The in vitro effect of this antiepileptic drug on free radicals generation shows that phenytoin does not reduce or prevent the formation of these reactive species. Lipid peroxidation was induced using QUIN and iron (II), two known neurotoxins. The study reveals that only lipid peroxidation induced using iron (II) is reduced by phenytoin. These experiments were carried out in whole rat brain homogenate. These studies show that phenytoin possesses poor free radical scavenging properties. However, the dose-related reduction of iron-induced lipid peroxidation allows for speculation that phenytoin interacts with iron in order to reduce neuronal damage. Metal binding studies were performed using UV, IR and electrochemical analysis to examine the interaction of phenytoin with iron (II) and iron (III). Phenytoin, when added to iron (II) in solution, first oxidises the latter to iron (III) and maintains it in that form. A shift in the peak was observed in the UV spectrum when iron was added to phenytoin. Moreover, electrochemical studies indicate that the interaction between the metal and the ligand is very weak. The IR analysis it shows that phenytoin may be coordinating with iron through the Nitrogen atom on the phenytoin molecule. These studies show that phenytoin maintains iron in its oxidised form, which is a good property to possess as a neuroprotectants. Pineal organ culture showed that phenytoin does not increase melatonin production but slightly and non-significantly reduces the levels of this pineal hormone. However there is a significant rise in precursor NAS levels. As melatonin is known to possess antioxidant and free radical scavenging properties, this could mean that this drug can cause the CNS to become more susceptible to attacks by reactive oxygen species.

A study was made of the effects of diphenylhydantoin (DPH) and the carrier solution on the spleen, lymph node, and thymus. DPH was injected i.p. at concentrations of 5 and 10 mg./100 gm. for 30 and 60 days. Hematologic effects observed were leucocytosis, neutrophilia, eosinophilia, and lymphopenia. Respiratory measurements of lymph node tissue slices were made using the oxygen electrode method. The carrier solution was found to cause a marked increase in oxygen consumption. A DPH effect on lymph tissue respiration was not observed. The carrier alone caused an atrophy of the lymph nodes and thymus, as well as an increase in the total body weight. Histological examination revealed that the 5 mg./100 gm. DPH injected for 60 days and the 10 mg./100 gm. DPH injected for 30 or 60 days produced a histiocytic cell type lymphoma, resembling Hodgkin's disease in the lymph node, thymus, and spleen in rats. The data indicated that DPH may not be a direct carcinogen, but it may interfere with the normal immune mechanism to produce the changes observed.

No description available.

The hypothesis of this study was that dietary n-3 fatty acids protect against phenytoin (P) teratogenicity by inhibiting embryonic prostaglandin H synthase bioactivation of P and/or by delaying embryonic development. Female caesarian-derived (CD-1) mice were fed a safflower (SAFF)- or a cod liver/linseed oil (CLO/LO)-based diet for three weeks prior to impregnation and throughout pregnancy. The CLO/LO diet, compared to the SAFF diet, reduced malformations and fetal growth retardation due to P. Open eye defect was the only anomaly induced by P in CLO/LO fetuses while P produced cleft palates only in SAFF fetuses. Since the period of maximal susceptibility to open eye defect occurs before palatal closure, this result suggests that the CLO/LO diet delayed development relative to the SAFF diet. In Exp 2, dietary n-6/n-3 fatty acid ratios were reflected in maternal hepatic phospholipids. Lipid peroxidation (LPO) was induced in maternal hepatic tissues by the SAFF diet while LPO was induced by P only in CLO/LO embryos.

Class of 2005 Abstract / Objectives: To determine whether the quantity of active ingredient and content uniformity of lorazepam and phenytoin manufactured in Mexico is comparable with those manufactured in the United States. Methods: A high-performance liquid chromatography (HPLC) assay based on slightly modified United States Pharmacopoeia- National Formulary (USP-NF) guidelines was used. Relative quantification of the active ingredient was accomplished using the US products as standards. The US products were assumed to contain 100% of the active ingredient. Lorazepam 1mg tablets and phenytoin 100mg capsules were tested using the assays. Results: The quantity of active ingredient in the Mexican lorazepam 1mg tablets were within the acceptable range of the USP-NF guidelines at 100%. The content uniformity was also within the acceptable range of the USP-NF guidelines at 104.6%. The quantity of active ingredient in the Mexican phenytoin 100mg capsules as well as content uniformity were also within the acceptable range of the USP-NF guidelines at 101.6% and 98.2%, respectively. Implications: The results of this study showed that lorazepam and phenytoin manufactured in Mexico were comparable to those manufactured in the US with no significant differences regarding amount of active ingredient and content uniformity.