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The present investigation was undertaken to assess the effects of aflatoxin (AF) on the exocrine pancreas in quails by means of light and electron microscopy. A total of 30 quails were divided into three groups, each composed of ten animals. Total AF was incorporated into the diet of these groups, at doses of 0, 2.5, and 5.0 mg of AF/kg feed, ppm, respectively. The quails were raised in cages with electrical heating and 24-h lighting for a period of 3 weeks. Ad libitum access was provided to feed and drinking water. Pancreas samples were taken for light and electron microscopic examination from animals that were killed by means of cervical dislocation at the end of the study. Light microscopic examination demonstrated mild mononuclear cell infiltration of exocrine tissue and vacuolisation of acinar cells in the group fed on AF at 2.5 ppm. On the other hand, electron microscopic examination demonstrated degranulation of the rough endoplasmic reticulum (rER) of acinar cells, decrease in the number of zymogen granules and free ribosomes and polisomes, and dilatation of capillaries in the group fed on AF at a dose of 2.5 ppm. Numerous degenerative acinar cells were determined in the group fed a diet containing 5.0 ppm AF, in addition to the findings common with the other group exposed to the toxin.

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The aim of this study was to determine the transportations of rivastigmine containing from various liposome formulations through Madin Darby Canine Kidney (MDCK) cells monolayer and to compare the in vitro test results with in vivo. There is no other liposome formulation of rivastigmine and the transportations of rivastigmine through MDCK cell monolayers or related study available in the literature. Cytotoxicity (MTT) test was used to determine cell viabilities. The effect of sodium-taurocholate or dimethyl-beta-cyclodextrine as penetration enhancer was also investigated. Characterization and stability studies for liposome formulations were performed. Permeation experiments of rivastigmine were performed through MDCK cells and dialysis membrane. The kinetic of release from liposomes was also investigated. The highest apparent permeability coefficient (log. values) was obtained with sodium-taurocholate liposomes for -1.15 ± 0.16 for MDCK cell. Rivastigmine liposomes and solutions were also administered to mice orally and intraperitonally. Acetylcholinesterase (AChE) activity was determined by Ellman method. AChE% inhibition values were calculated for both blood and brain after administration of rivastigmine solution and liposomes. The highest AChE inhibition was observed for rivastigmine-sodium-taurocholate liposomes. Histological observations of the mice' brains were performed under transmission electron microscope (TEM). The histological results were also indicated and supported all these findings.

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