Molecular insights into the response of Acidithiobacillus caldus to leached metal toxicity during bioleaching of spent FCC catalyst.

Acidithiobacillus caldus, a thermoacidophilic sulfur-oxidizing bacterium, is utilized in bioleaching owing to its robust metabolic capabilities. This study explored the roles of A. caldus in metal bioleaching, the mechanisms of metal toxicity resistance, and the concentration-dependent strategies, aiming to provide insights for process optimization. In this study, an integrated approach was employed, encompassing dynamic monitoring of metal release, enzymatic activity assays, and de novo transcriptome sequencing. The integrated mechanism of "bioleaching promotion-toxicity response-resistance regulation" in A. caldus under SFCCC-induced stress was systematically revealed. The bacterium demonstrated high bioleaching efficiency of heavy metals from SFCCC. Under metal-induced stress, it employed defense mechanisms primarily through a glutathione peroxidase (GSH-Px) mediated antioxidant system. This response was sustained by the continuous activation of H⁺-ATPase and NADPH-generating metabolic pathways to maintain energy supply and reducing power. The bacterial response exhibited concentration dependence. Under low-concentration stress, A. caldus prioritized basal metabolic maintenance alongside initiation of defensive measures. However, under high-concentration stress, it employed a comprehensive survival strategy involving metabolic reprogramming to sacrifice non-essential functions in favor of critical survival processes. The transition reflects a strategic shift from a growth-oriented to a survival-oriented mode. These findings enhance the theoretical framework for understanding concentration-dependent strategic transitions in microbe-metal interactions and offer a molecular biology basis for improving the practical application of bioleaching technologies.