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Pharmacokinetic studies of amino acid analogues of 2-nitroimidazole, new hypoxic cell radiosensitizers.

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A series of new analogues of 2-nitroimidazole has been synthesized by inserting various amino acids at 1-position through an amide bond. The ethyl esters of N-alpha-[(2-nitro-1-imidazolyl)acetyl]-L-phenylalanine and N-alpha-[2-nitro-1-imidazolyl)acetyl]-L-tyrosine were found to be the most effective

New PET radiopharmaceuticals beyond FDG for brain tumor imaging.

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Brain tumors have a relatively high incidence (>14/100000 people/year) and represent a major cause of death in the population. The direct and indirect costs of brain tumors are high in the developed countries (5.2 bn EUR/year in the EU; 4.46 bn USD/year in the US). A combination of recent

Interaction of phosphatidylserine-phosphatidylcholine liposomes with sickle erythrocytes. Evidence for altered membrane surface properties.

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The sickle erythrocyte (RBC) is a pathologic RBC that contains multiple membrane abnormalities. Some of these abnormalities have been implicated in the pathophysiology of vasoocclusive crises characteristic of sickle cell disease; others have yet to be defined in terms of their clinical

4-Fluorobenzylamine and phenylalanine methyl ester conjugates of 2-nitroimidazole: evaluation as hypoxic cell radiosensitizers.

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We have synthesized two 2-nitroimidazole derivatives and evaluated their hypoxic radiosensitization properties. The first, a 4-fluorobenzylamine conjugate of 2-nitroimidazole (PK-110), was designed so that it could also be labeled with the F-18 and used for positron emission tomographic imaging of

Structural basis of mitochondrial dysfunction in response to cytochrome c phosphorylation at tyrosine 48.

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Regulation of mitochondrial activity allows cells to adapt to changing conditions and to control oxidative stress, and its dysfunction can lead to hypoxia-dependent pathologies such as ischemia and cancer. Although cytochrome c phosphorylation-in particular, at tyrosine 48-is a key modulator of

Oxidative stress is tightly regulated by cytochrome c phosphorylation and respirasome factors in mitochondria.

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Respiratory cytochrome c has been found to be phosphorylated at tyrosine 97 in the postischemic brain upon neuroprotective insulin treatment, but how such posttranslational modification affects mitochondrial metabolism is unclear. Here, we report the structural features and functional behavior of a

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