A computer model of blood plasma which has allowed the effect of Gd(III) contrast agents to be simulated has been developed. Initial binding of Gd(III) is to transferrin. At high concentration the metal ion binds to citrate and salicylate. At a concentrate of 10(-3) M, GdCl3 is predicted to effect a redistribution of the in vivo Zn(II), Ca(II), and Fe(II) complexes present in blood plasma. There is little effect on the Cu(II) distribution. At a concentration below 10(-5) M EDTA and DTPA have little effect on the free Gd(III) metal ion concentration. Above this concentration though, the metal ion is bound almost exclusively to the EDTA or DTPA. An attempt is made to relate the toxicity of GdCl3, [Gd(EDTA)]-, and [Gd(DTPA)]2- to the thermodynamic stability of these complexes. The effect of substitution kinetics is also discussed.

The complete assignment of the natural abundance 3C n.m.r. spectrum of citreoviridin, a mycotoxin produced by PeniciMum pulvillorum CSI R 1406, allowed a study of its biosynthetic origin using 13C-labelled precursors. The results show that citreoviridin is derived from a C18-polyketide formed from an acetate chain-starter unit and eight malonate units. The five remaining carbon atoms, i.e. the five methyl groups, are derived from (2s)-methionine.CITREOVIRIDIN (1), a potent neurotoxic mycotoxin produced by Penicillium citreoviride and P. @&k?lorum is reputed to be the causative agent of the epidemic-like occurrence of cardiac beri-beri in man in parts of East-Asia.l The compound's acute toxicity, like that of the related fungal metabolites, the aurovertins and asteltoxin is due to its inhibition of ATP-synthesis and ATPhydrolysis catalysed by mitochrondrial enzyme systems2The participation of propionate as a starter unit in the biosynthesis of aurovertin B(2) prompted us to investigate the biosynthesis of citreoviridin by 13C n.m.r. spectroscopy using 13C-labelled precursors. In previous studies with l*C-labelled precursors only a few positions of incorporation in citreoviridin could be determined by chemical degradation. The results, however led to the conclusion that the metabolite is derived from a Clspolyketide formed from acetylcoenzyme A as a starter unit and eight malonylcoenzyme A units.The assignment of the lH n.m.r. spectrum of citreoviridin (1) as presented in Table 1 is based on proton-proton 19

The complete assignments of the 'H and '"CNMR spectra for (@)-trishomocuban-4-01 (3) and (4)-trishomocubanone (4) are reported. The difference between the 'H and "C chemical shifts of 3 and 4 and those of the hydrocarbon (Q)-trishomocubane, and the substituent effect of the hydroxy group, can be adequately explained by the unique stereochemistry of these compounds.

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