Sulfur oxidation kinetics of Acidithiobacillus caldus and its inhibition on exposure to thiocyanate present in cyanidation tailings wastewater

Abstract

The sulfur oxidation kinetics of an industrial strain of Acidithiobacillus caldus (At. caldus) cultured on elemental sulfur was explored in batch experiments in the absence and presence of thiocyanate (SCN⁻), a toxin inherent within cyanidation tailings wastewater. The Contois rate expression accurately described At. caldus sulfate generation (R² > 0.93) and microbial growth (R² > 0.87). For a culture maintained at 45 °C a maximum specific growth rate (${\mu }_{\max }$) of 0.105 h⁻¹, sulfate yield from biomass ($Y_{px}$) of 4.8 × 10⁻⁹ mg SO₄²⁻.cell⁻¹, and Contois affinity coefficient ($K_x$) of 1.56 × 10⁻⁸ mg S.cell⁻¹ were established. The presence of SCN⁻ (0 mg/L - 20 mg/L) in the bulk solution inhibited the microbial system competitively. Moreover, SCN⁻ impeded microbial growth differentially; the rate expression was therefore partitioned with respect to SCN⁻ concentration and inhibition constants ($K_i$) were determined for each region. Adaptation to discrete concentrations of SCN⁻ (1 mg/L and 20 mg/L) improved SCN⁻ tolerance in At. caldus; however, adapted strains exhibited reduced sulfur oxidation potential when cultured under thiocyanate-free conditions relative to the non-adapted control strain. To describe the adapted systems accurately, the Contois affinity coefficient ($K_x$) was revised to reflect the suspected metabolic decline. The derived $K_x$ values increased in magnitude and affirmed an innate reduction in microbial substrate affinity or substrate adsorption capacity. Inclusion of these updated $K_x$ constants within the rate equation suitably represented the experimental data for both adapted At. caldus strains with R² > 0.94. Furthermore, the impact of adaptation on the inhibition kinetics and inhibition mechanism associated with SCN⁻ exposure were reviewed. Thiocyanate inhibited sulfur oxidation non-competitively in the adapted strains, and the shift in inhibition mechanism may be attributed to the compromised metabolic state following adaptation.