The oxidation of a number of thio ethers to Soxides (sulphoxidation) has been observed in biological systems. Compounds metabolized by mammals to the sulphoxide include chlorpromazine (Salzman & Brodie, 1956), 1,2-diphenyl-4-(phenylthioethyl)pyrazolidine-3,5-dione (Bums et al. 1957) and promazine (Walkenstein & Seifter, 1959). The oxidation occurs in microorganisms: (-)-biotin sulphoxide is produced by A8pergillu8 niger (Wright, Cresson, Valiant, Wolf & Folkers, 1954) and 17flacetoxy-7oc-methylthioandrost-4-en-3-one is converted by Catonectria decora into 17fi-hydroxy-7ctmethylsulphinylandrost-4-en-3-one (Holmlund et al. 1962). Several examples of the occurrence of sulphoxides in plants are known. They are principally S-alkyl-L-cysteine S-oxides, their derivatives and w-methylsulphinylalkyl isothiocyanate glucosides, and they have been reviewed recently by Virtanen (1962). The sulphoxidation of 4,4'-diaminodiphenyl sulphide has been observed in vitro with a preparation of guinea-pig-liver microsomes which required 1964
Cell cholesterol is believed to be confined mainly to the plasma membrane. Treatment here of human peripheral blood lymphocytes with cholesterol-free and cholesterol-containing liposomes to effect, respectively, decreases or increases in cholesterol content measureable by chemical analysis, markedly altered effector functions of the cells. Depletion of cholesterol evoked inhibition of spontaneous and phytohemagglutinin-dependent lymphocyte cytotoxicity against allogeneic target cells. Opposite effects resulted from cholesterol enrichment, with PHA-dependent and antibody-dependent cytotoxicities increasing significantly. Treatment, instead, with the known inhibitor of cholesterol biosynthesis, 25-hydroxycholesterol, had suppressive effects like those resulting from lowering the cholesterol level physically by liposome treatment. Our data suggest that the plasma membrane cholesterol content of different categories of lymphocytes in man is both essential and regulatory for their cytotoxic function.
The first evidence for the metabolic formation of an alkylmercapturic acid was obtained by Roberts & Warwick (1957, 1958), who showed by radiochromatographic methods that the administration of 14C-labelled ethyl methanesulphonate, CH3* S02 *°O C2H5 to rats is followed by the excretion of ethylmercapturic acid, N-acetyl-S-ethyl-L-cysteine. By the 10 Bioch. 1963, 86
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