Vanadium metabolism in wild type and respiratory‐deficient strains of S. cerevisiae

Abstract

Vanadium metabolism was studied in a wild type and respiratory-deficient strain of S. cerevisiae. Inhibition of growth by vanadate [V(+5)], vanadate accumulation, and conversion of medium vanadate [V(+5)] to both cell-associated and medium vanadyl [V(+4)] and vanadate [V(+5)] were compared. The growth of both the parental and respiratory-deficient strains was inhibited by vanadate at concentrations greater than or equal to 1 mM. Both parental and respiratory-deficient strains accumulated vanadate and converted medium vanadate to cellular vanadyl as detected using electron spin resonance (ESR). The accumulation of cell-associated vanadyl was correlated with the loss of medium vanadate in both strains using a chemical assay. In contrast, the respiratory-deficient strain showed a greater amount of a cell-associated vanadate compound, as detected with vanadium-51 nuclear magnetic resonance (51V-NMR), than the wild type strain or a representative respiratory-competent vanadate-resistant mutant. These data imply that mitochondrial function may be directly involved in vanadium metabolism.

Decavanadate (V10O286-) and oxovanadates: Oxometalates with many biological activities

“…This conclusion is in agreement with other vanadium compounds [16,46,47]. The response to decavanadate in vanadium accumulation, lipid peroxidation and oxidative stress markers [48] and yeast growth responses [26,27,49], is significantly different than that observed for the simple monomeric vanadate. In mitochondria, where the vanadium was found to accumulate most following decavanadate in vivo administration, nM concentration of decavanadate induces membrane depolarization in addition to the inhibition of oxygen consumption [50].…”

Vanadate Induces Necrotic Death in Neonatal Rat Cardiomyocytes Through Mitochondrial Membrane Depolarization

“…However, the ability of cardiac myocytes to attenuate the toxicity of vanadate by rapidly reducing vanadate to vanadyl before inducing irreversible effects remains speculative at present. Willsky and Dosch showed the relevance of mitochondrial function (oxidative phosphorylation) in vanadium metabolism, since yeast respiratory-deficient strains accumulated higher amounts of vanadate compounds. More recently, in previous works – , we have shown that the mitochondria of liver and heart tissues are the subcellular organelles with higher contents in vanadium in animals treated with in-blood injections of monovanadate or decavanadate solutions.…”

Electron paramagnetic resonance studies and effects of vanadium in Saccharomyces cerevisiae

“…An extensive study of vanadate uptake and metabolism in S. cerevisiae has been reported by Willsky (Willsky et al 1984, 1985, Willsky & Dosch 1986. They found that yeast cells absorbed vanadate and released vanadyl ions when VO43-was present at a concentration of less than 1 mM, and that 5 mM VO 3-was the toxic concentration for ceils grown in buffered synthetic medium containing yeast nitrogen base and tryptophan.…”