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Pharmacological, toxicological, and therapeutic evaluation in mice of doxorubicin entrapped in cardiolipin liposomes 总被引:4,自引:0,他引:4
Doxorubicin possesses high affinity for binding to cardiolipin. We have utilized these properties in preparing stable liposomes of doxorubicin and cardiolipin with a net positive charge. Doxorubicin liposomes were formed by using 11.2 mumol of drug, 5.6 mumol of cardiolipin, 28.5 mumol of phosphatidylcholine, 19.5 mumol of cholesterol, and 11.1 mumol of stearylamine. These liposomes were sonicated for 90 min at 37 degrees followed by extensive dialysis against buffer. The pharmacological, toxicological, and therapeutic effects of doxorubicin entrapped in cardiolipin liposomes were compared with those of free doxorubicin in mice. At a dose of 4 mg/kg i.v., the peak cardiac concentration was achieved in 30 min following free doxorubicin administration, the value being 8.1 micrograms/g. The peak cardiac concentration with doxorubicin in cardiolipin liposomes was obtained at 5 min with a value of 2.8 micrograms/g of tissue. The cardiac concentration X time values for free doxorubicin for the 24-hr period of observation were 55.1 micrograms X hr/g, whereas it was only 7.8 micrograms X hr/g with the drug entrapped in cardiolipin liposomes. Compared to free drug, the liposomal entrapped doxorubicin significantly reduced the histopathological lesions in cardiac tissue of mice at a dose of 15 mg/kg as determined by electron microscopy. The nadir of peripheral white blood cell counts in mice with free drug, 6 mg/kg, was observed on Day 3 which was 50% of control, whereas with liposomal encapsulated drug it was reduced only 23% on Day 7. Doxorubicin in cardiolipin liposomes demonstrated enhanced chemotherapeutic potential against murine ascitic P388 leukemia with a 144% increased life span compared to 55% increased life span with free drug at a dose of 7.5 mg/kg on Days 1, 3, and 7. We conclude that doxorubicin liposomes developed in these studies possess improved therapeutic action as demonstrated by their ability to reduce the toxicity of the drug substantially. 相似文献
994.
Mucinous pancreatic duct ectasia in the body of the pancreas 总被引:2,自引:0,他引:2
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Death occurs in the homozygous mutant mouse weaver among several classes of neuron in cerebellum and ventral midbrain, because these neurons carry a mutation in the G protein-gated inwardly rectifying potassium channel, Girk2. GIRK2 is expressed in all neuronal types killed by wv in cerebellum and midbrain as well as in neurons elsewhere that suffer lesser consequences. GIRK2(wv) affects neurons postnatally, after proliferation, at the time of final differentiation. To assess the impact of GIRK2(wv) on neuronal development and viability, we introduced cDNA encoding wild-type and mutant channels into a variant of a CNS derived catecholamine cell line (Cath.a) known as Cath.a-differentiated. When cultured in serum-free medium, Cath.a-differentiated cells cease proliferation and undergo morphological differentiation, growing long neurites. Cath.a-differentiated cells do not express endogenous Girk channels. Transfection of GIRK2(wv) resulted in the death of Cath.a-differentiated cells, in a cDNA-concentration dependent manner. The highest concentration of Girk2(wv) cDNA caused loss of about half the cells, the next highest concentration one-third, and the least had no effect on viability. However, even the lowest concentration resulted in disruption of neurite outgrowth and reduced the protein products of co-transfected genes. High concentrations of MK801, which prevent Na(+) influx through the mutant channel, prevented death induced by GIRK2(wv). Cell death and disruption of neurite outgrowth were counteracted in GIRK2(wv)-expressing cells by the presence of an unrelated inwardly rectifying potassium channel, Kir2.3. These results are consistent with wv being a gain-of-function mutation, causing disruption of cellular homeostasis by mechanisms such as increased Na(+) influx and chronic depolarization which may in turn result in an excessive metabolic burden on the cell. 相似文献
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J. S. Macdonald M. E. Lippman P. V. Woolley P. P. Petrucci P. S. Schein 《Cancer chemotherapy and pharmacology》1978,1(3):135-138
Summary A patient with a benign hepatic neoplasm developing after treatment with estrogenic hormones is described. After excision, the neoplastic tissue was analyzed for the presence of cycosol estrogen and progeterone binding proteins. The noeplasm was classified as focal nodular hyperplasia of the liver and was demonstrated to contain high-affinity cytosol estrogen and progesterone hormone receptors. The estrogen0binding affinity of the neoplasm was three times greater than that of normal liver.Further investigation of cytosol hormone receptors in estrogen associated hepatic neoplasms will be required to define the role of these binding proteins in the possible etiology of certain liver tumors.This work was supported in part by contracts NCI # OD 3323863, and NCI # NOLCM 67110 相似文献
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