Enhanced degradation of sulfamethazine by Achromobacter via oxygenation through co-metabolism.

The addition of glucose as a readily biodegradable primary carbon source not only provides additional nutrients and energy but also minimizes the production of toxic intermediates of sulfamethazine (SM2), such as benzoquinone, thereby promoting the proliferation of the strain (with a 227.70 % increase in the OD600 value) and enhancing the SM2 removal rate by 64.45 %. Transcriptome sequencing revealed that co-metabolism induced strain JD417 to significantly upregulate the expression of genes encoding key oxidoreductases (such as sulfanilamide monooxygenase, catechol 1,2-dioxygenase, and acyl-CoA dehydrogenase) and transferases (including glutathione S-transferase and 3-oxoadipate CoA-transferase), which are crucial for organic degradation and metabolism. Furthermore, genes associated with the sulfonamide (SA) degradation pathways (sadA, sadB, sadC, catA, catB, pcaC, pcaJ) were upregulated, thereby enhancing SM2 degradation via sadABC-driven mineralization. In contrast, the stressed group without co-metabolism exhibited an upregulation of stress response genes in strain JD417, with enzymatic activity assays confirming significantly enhanced antioxidant defenses (CAT: +57.5 %, GST: +54.2 %, SOD: +58.9 % in CK group) to counteract oxidative stress from accumulated toxic intermediates. These findings demonstrate how strain JD417 dynamically allocates metabolic resources between stress response and degradation pathways depending on carbon availability, with glucose co-metabolism optimizing the balance between detoxification and SM2 mineralization. It provides novel insights into the molecular mechanisms underlying the bioremediation of SAs.