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1.  Communication: Synthesis of a Novel Triphenyltin(IV) Derivative of 2- Mercaptonicotinic Acid with Potent Cytotoxicity in vitro  
A novel triphenyltin(IV) derivative of 2-mercaptonicotinic acid (H2mna) of formula {[(C6H5)3Sn]2(mna).[(CH3)2CO]} (1) has been synthesized and characterized by elemental analysis and 1H, 13C-NMR, and FT-IR spectroscopic techniques. The crystal structure of complex (1) has been determined by single crystal X-ray diffraction analysis at 173(1) K. Compound (1) contains two triphenyltin moieties linked by a doubly de-protonated 2,mercaptonicotinic acid (H>2mna). It is an example of a pentacoordinated Ph3SnXY system with an axial-equatorial arrangement of the phenyl groups at Sn(1). Compound (1), exhibits potent, in vitro, cytotoxicity against sarcoma cancer cells (mesenchymal tissue) from the Wistar rat, polycyclic aromatic hydrocarbons (PAH, benzo[a]pyrene) carcinogenesis.
PMCID: PMC2267064  PMID: 18365056
2.  Platelet activating factor levels and metabolism in tangier disease: a case study 
Tangier disease (TD) is a phenotypic expression of rare familial syndrome with mutations in the ABCA1 transporter. The risk of coronary artery disease in patients with TD is variable. On the other hand the pivotal role of Platelet-Activating Factor (PAF) mediator in atheromatosis was found. Plasma lipoproteins are transporters of the PAF acetylhydrolase (PAF-AH) in cells and known as lipoprotein-phospholipase A2 (Lp-PLA2) in plasma and regulators of PAF levels in blood. In addition, PAF can be biosynthesized from the remodeling and the de novo pathways in which Lyso-platelet activating factor-acetyltransferase (Lyso-PAF-AT) and platelet activating factor-cholinephosphotransferase (PAF-CPT) are the regulatory enzymes. The aim of this study is to investigate in a TD patient with a unique mutation (C2033A), the concentration of PAF in blood, the Equivalent Concentration for 50% aggregation (EC50) values of platelet rich plasma (PRP) toward PAF, adenosine diphosphate (ADP) and thrombin, and the activities of PAF metabolic enzymes Lp-PLA2, PAF-AH, Lyso-PAF-AT and PAF-CPT.
The EC50 value of PRP was measured by an aggregometer. The determination of the specific activity of PAF-CPT and Lyso-PAF-AT was made after in vitro enzymatic assay, chromatographic separation and measurement of the produced PAF in a biological assay with washed rabbit platelets. The determination of PAF-AH and Lp-PLA2 was made after an in vitro enzymatic assay from the decay of radioactive PAF.
The TD patient had lower bound-PAF values in blood, decreased specific activity of PAF-CPT and Lyso-PAF-AT, increased specific activity of PAF-AH in platelets and leukocytes and Lp-PLA2 activity in plasma compared to healthy women. The EC50 of PAF and Thrombin were higher compared to healthy women.
The increased Lp-PLA2 activity, as well as, the decreased activities of PAF-CPT and Lyso-PAF-AT, explain the decreased bound-PAF level in TD patient and the EC50 of PAF. However, total PAF is in a normal range and this probably can explain one of the reasons this TD patient has no CAD.
PMCID: PMC3499335  PMID: 22769014
PAF; Tangier Disease; Atherosclerosis; Lp-PLA2; PAF-AH; Lyso-PAF-AT; PAF-CPT

Results 1-2 (2)