Synthesis of platinum complexes from N-benzyl ethylenediamine derivatives

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Abstract

N-benzylethylenediamine derivatives have been prepared in good yields using methodology diferent than that described in the literature. ¹H and 13C NMR spectra were used to characterize those compounds. Nine new platinum(II) complexes, analogs of cisplatin and carboplatin, containing these ligands have been prepared and characterized. Preliminary in vitro tests against buccal human carcinoma cell lines (KB cells) showed that the complexes are cytotoxic.

Translated abstract

O ligante N-benziletilenodiamina e derivados foram preparados em bons rendimentos utilizando-se metodologia diferente da descrita na literatura. Espectros de RMN de ¹H e de 13C foram empregados para a caracterização destes compostos. Nove novos complexos de platina(II) com estes ligantes, análogos da cisplatina e da carboplatina, foram preparados e caracterizados. Testes preliminares in vitro em linhagens celulares de carcinoma bucal humano (células KB) indicam que estes complexos são citotóxicos.

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Oscillations of cyclic AMP in hormone-stimulated insulin-secreting beta-cells.

Oleg Dyachok, Yegor Isakov, Jenny Sågetorp … (2006)

Cyclic AMP is a ubiquitous second messenger that transduces signals from a variety of cell surface receptors to regulate diverse cellular functions, including secretion, metabolism and gene transcription. In pancreatic beta-cells, cAMP potentiates Ca2+-dependent exocytosis and mediates the stimulation of insulin release exerted by the hormones glucagon and glucagon-like peptide-1 (GLP-1) (refs 4, 5-6). Whereas Ca2+ signals have been extensively characterized and shown to involve oscillations important for the temporal control of insulin secretion, the kinetics of receptor-triggered cAMP signals is unknown. Here we introduce a new ratiometric evanescent-wave-microscopy approach to measure cAMP concentration beneath the plasma membrane, and show that insulin-secreting beta-cells respond to glucagon and GLP-1 with marked cAMP oscillations. Simultaneous measurements of intracellular Ca2+ concentration revealed that the two messengers are interlinked and reinforce each other. Moreover, cAMP oscillations are capable of inducing rapid on-off Ca2+ responses, but only sustained elevation of cAMP concentration induces nuclear translocation of the catalytic subunit of the cAMP-dependent protein kinase. Our results establish a new signalling mode for cAMP and indicate that temporal encoding of cAMP signals might constitute a basis for differential regulation of downstream cellular targets.

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An inherited disorder of lymphocyte apoptosis: the autoimmune lymphoproliferative syndrome.

M Lenardo, M Sneller, Stephen E Straus … (1999)

The autoimmune lymphoproliferative syndrome (ALPS) affords novel insights into the mechanisms that regulate lymphocyte homeostasis and underlie the development of autoimmunity. This syndrome arises early in childhood in persons who inherit mutations in genes that mediate apoptosis, or programmed cell death. The timely deletion of lymphocytes is a way to prevent their accumulation and the persistence of cells that can react against the body's own antigens. In ALPS, defective lymphocyte apoptosis permits chronic, nonmalignant adenopathy and splenomegaly; the survival of normally uncommon "double-negative" CD3+ CD4- CD8- T cells; and the development of autoimmune disease. Most cases of ALPS involve heterozygous mutations in the lymphocyte surface protein Fas that impair a major apoptotic pathway. Detailed immunologic investigations of the cellular and cytokine profiles in ALPS show a prominent skewing toward a T-helper 2 phenotype; this provides a rational explanation for the humoral autoimmunity typical of patients with ALPS. Prospective evaluations of 26 patients and their families show an ever-expanding spectrum of ALPS and its major complications: hypersplenism, autoimmune hemolytic anemia, thrombocytopenia, and neutropenia. Defective apoptosis may also contribute to a heightened risk for lymphoma.