The protolysis equilibria of 2-hydroxybenzohydroxamic acid, H2SAX, have been studied at 25 degrees C in different ionic media by potentiometric titration with a glass electrode. The media were 0.513, 1.05, 2.21 and 3.5 mol/kg NaClO4. The constants beta(-p)(H2SAX<==>H(2-p)SAX(-p)+pH+), combined with salting effects of NaClO4 on H2SAX deduced from solubility determinations, were processed by the specific interaction theory, SIT, to give equilibrium constants at infinite dilution, log beta(-1)(o) = -7.655 +/- 0.013 and log beta(-2)(o) = -17.94 +/- 0.04, as well as specific interaction coefficients b(HSAX-,Na+) = 0.12 +/- 0.01 and b(SAX2-,Na+) = 0.17 +/- 0.02, molal(-1).

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Harzianic acid is a secondary metabolite of Trichoderma, structurally belonging to the dienyltetramic acid subgroup of the tetramic acids. Biological activities of harzianic acid are of great interest for its antimicrobial and plant growth-promoting activities, which might be related to its chelating properties. In the present work harzianic acid, isolated from cultures of a strain of Trichoderma pleuroticola associated to the gastropod Melarhaphe neritoides, was studied as a complexant agent of a number of biologically relevant transition metals (i.e., Zn2+, Fe2+, Cu2+, and Mn2+), using UV-VIS, potentiometry, MS and NMR techniques. Our findings show the coordination capacity of harzianic acid toward the above cations through the formation of neutral or charged complexes in a variable ratio depending on the metal and pH conditions.

The loop of Henle contributes to renal acidification by reabsorbing about 15% of ifitered bicarbonate. To study the effects on loop of Henle bicarbonate transport (JHC03) of acid-base disturbances and of several factors known to modulate sodium transport, these in vivo microperfusion studies were carried out in rats during: (a) acute and chronic metabolic acidosis, (b) acute and chronic (hypokalemic) metabolic alkalosis, (c) a control sodium diet, (d) a high-sodium diet, (e) angiotensin II (AU) intravenous infusion, (f) simultaneously intravenous infusion of both All and the AT1 receptor antagonist DuP 753, (g) acute ipsilateral mechanicochemical renal denervation. Acute and chronic metabolic acidosis increased JHCO3; acute metabolic alkalosis significantly reduced JHCO3, whereas chronic hypokalemic alkalosis did not alter JHCO3. Bicarbonate transport increased in animals on a high-sodium intake and following All administration, and the latter was inhibited by the AII (AT1) receptor antagonist DuP 753; acute renal denervation lowered bicarbonate transport. These data indicate that bicarbonate reabsorption along the loop of Henle in vivo is closely linked to systemic acid-base status and to several factors known to modulate sodium transport. (J. Clin. Invest. 1994. 94:830-838.) Key words: loop

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