Abstract
Acidithiobacillus thiooxidans A01 is widely used in bioleaching processes and commonly thrives in most metal-rich environments. However, interactions between different heavy metals remain obscure. In this study, we elaborated the effect of ferric iron on the growth and gene expression of At. thiooxidans A01 under the stress of nickel. The results showed that 600 mM Ni2+ completely inhibited the growth and sulfur metabolism of At. thiooxidans A01. However, trace amounts of Fe3+ (0.5 mM) facilitated the growth of At. thiooxidans A01 in the presence of 600 mM Ni2+. With the addition of 5 mM Fe3+, the maximum cell density reached 1.84 × 108 cell/mL, and pH value was 0.95. In addition, metal resistance-related and sulfur metabolism genes were significantly up regulated with extra ferric iron. Taking the whole process into account, the promoting effect of Fe3+ addition can be attributed to the following: (1) alleviation of the effects of Ni2+ toxicity and restoring the growth of At. thiooxidans A01, (2) a choice of multiple pathways to export nickel ion and producing precursor of chelators of heavy metals. This can suggest that microorganisms may widely exhibit metabolic activity in iron-rich environments with heavy metals. Our study will facilitate the technique development for the processing of ore bodies with highly challenging ore compositions.
Highlights
Biohydrometallurgy is widely used in industrial bioleaching of ores to extract metals such as copper, nickel, gold, uranium
Microorganisms have evolved in the presence of this metal, which is necessary in trace amounts for a variety of metabolic processes but toxic in high concentrations, causing oxidative stress in the cell [3]
We investigated the effect of ferric iron on the growth and sulfur metabolism of At. thiooxidans A01 in the presence of Ni 2+ to clarify the mechanism at transcription level
Summary
Biohydrometallurgy is widely used in industrial bioleaching of ores to extract metals such as copper, nickel, gold, uranium. It is done mainly by acidophilic microorganisms [1]. Nickel has been identified as a component in a number of enzymes, participating in important metabolic reactions such as ureolysis, hydrogen metabolism, methane biogenesis and acitogenesis [2]. In this way, microorganisms have evolved in the presence of this metal, which is necessary in trace amounts for a variety of metabolic processes but toxic in high concentrations, causing oxidative stress in the cell [3]. The toxicity of nickel is attributed to its replacement of metals in metalloproteins, to its binding to catalytic residues in sulfur dioxygenase, sulfite oxidase and the plasma membrane, and indirectly to its exertion of oxidative stress [4]
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