“Google:Suggestsubtypes”:[[7][“Metabolism C”

Nearly to of orally administered curcumin is eliminated unabsorbed by feaces.Difficulty is also associated with its topical application due to less permeability through skin.Finally we conclude that transfersome entrapped curcumin gel gives better permeation as compare to plain drug gel.Transdermal delivery requires higher permeability because dose of the drug is very high.By this fact transfersomal formulation is better delivery system for transdermal delivery for the curcumin., article. ViewpublViewpublicaticationst atsionstats The user has requested enhancement of the downloaded file.Oxidative stress has been implicated in the mechanism of naphthaleneinduced cataract. during the present studies, we have examined whether low levels of dietary curcumin could prevent naphthaleneinduced opacication of rat lens.Naphthalene cataractogenesis in rats has been used as a valuable animal model to study the etiology of senile cataractogenesis in human because the morphology of naphthalene cataractogenesis is reported to be similar to that of agerelated cataract. Toxic manifestations of naphthalene have been suggested to be due to the oxidative stress caused by generation of reactive oxygen species during its phase I metabolism by cytochrome P and by the redox cycling of its metabolite, naphthoquinone. Naphthoquinone metabolites generated during cytochrome P mediated metabolism of naphthalene have markedly higher cataractogenic potential than the parent compound. Cytochrome P inhibitors prevent naphthaleneinitiated cataract while cytochrome P inducers augment cataractogenic potential of naphthalene.Naphthaleneinitiated cataractogenesis could be attenuated by antioxidants such as caffeic acid, vitamin E, and the free radical spin such as aphenylN tbutylnitrapping agents trone. Naphthalene causes DNA damage and lipid peroxidation in cells, which is also consistent with the idea of ROS involvement in mechanisms of its toxicity.Prevention of naphthalene cataractogenesis by procysteine drugs and depletion of lenticular glutathione during naphthaleneinitiated cataracts also support the idea that oxidative stress is perhaps the major causative factor in naphthalene cataractogenesis. Antiinammatory activity of curcumin has been reported and it has been shown to inhibit enzymes of the cyclooxygenase and lipoxygenase pathways. Recently, curcumin has attracted a great deal of interest because of its cancer preventative properties in rodent models against different chemical carcinogens. Lipid peroxidation has been linked to cataractogenesis in animal models, a toxic product of lipid peroxidation, induces cataractogenesis in rat lens and that pretreatment of rats with curcumin provides protection against the cataractogenic effect of HNE. Furthermore, we have shown that galactosemic cataractogenesis in rats can also be attenuated by a diet supplemented with curcumin. Since the involvement of ROS is suggested to be a common factor in the etiology of galactosemic cataractogenesis and naphthalene cataractogenesis, the present studies were designed to examine whether or not curcumin could provide protection against naphthaleneinitiated cataractogenesis in rats.Experiments were designed to compare naphthaleneinitiated cataract in rats kept on AIN diet and those kept on AIN diet supplemented with low levels of curcumin.During cataractogenesis caused by ROS, the lens epithelial cells have been reported to undergo apoptosis. Therefore, we have also examined if the naphthaleneinitiated cataract is accompanied by apoptosis of lens epithelial cells and whether or not curcumin could prevent this effect of naphthalene.The animals were housed in hanging steel wire cages with free access to AIN diet and tap water and kept on xed length of light:dark cycle.

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