A pronounced catalytic effect of sodium dodecyl sulfate (SDS) was observed on the in situ production of S-alkylisothiouronium salts via the reaction of primary, allyl and benzyl halides with thiourea in SDS droplets .Hydrolysis of the generated Salkylisothiouronium salts in the palisade layer of the droplets produces the corresponding thiol moieties which are immediately added to the electron-deficient olefins that are present in the micellar core to produce the thia-Michael adducts. The entire route is an almost odorless process. The yields of the products are good to excellent and the method is applicable to large-scale operation without any problem.

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This article is available online at http://www.jlr.org Myeloperoxidase (MPO), an abundant heme protein released by activated leukocytes, catalyzes the oxidation of chloride ions by hydrogen peroxide (H 2 O 2 ) to yield hypochlorous acid (HOCl). MPO has been identifi ed as a biomarker for pathological conditions including sepsis, ischemic injury and atherosclerosis ( 1-4 ). Increased circulating levels of MPO are associated with increased coronary risk, and MPO colocalizes with macrophages in human atherosclerotic lesions ( 1, 2 ). HOCl is a potent oxidant whose cellular targets of action include thiols, amines, nucleotides, unsaturated fatty acids and lipoproteins ( 5 ). With respect to lipoprotein metabolism, HOCl impairs both LDL and HDL function. HOCl oxidizes apolipoprotein (apo) B100 and lipid components of LDL particles, resulting in increased scavenger receptor uptake of LDL by macrophages and the development of fatty lesions ( 6, 7 ). The HOCl-dependent oxidation of HDL converts it to a form that is proatherogenic (8)(9)(10)(11). Dysfunctional HDL particles demonstrate a reduced capacity to mediate ATPbinding cassette transporter A1 (ABCA1)-dependent cholesterol effl ux and are resistant to metabolism by hepatic enzyme systems ( 12-17 ). MPO and HOCl also inhibit the activity of the HDL-associated enzyme lecithin cholesterol acyl transferase (LCAT), thus attenuating the formation of mature ␣ -HDL particles ( 18 ). The MPO-catalyzed oxidation of HDL also attenuates anti-apoptotic and anti-infl ammatory effects of the lipoprotein ( 11 ). These changes are associated with reduced binding of HDL to scavenger receptor class B1 (SR-B1).Data suggest that the formation of dysfunctional HDL by MPO and HOCl is due principally to changes in the protein components of the particle (whereas higher concentrations may induce changes in the lipid composition

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