Biodegradation of Photocatalytic Degradation Products of Sulfonamides: Kinetics and Identification of Intermediates.

Sulfonamides can be effectively removed from wastewater through a photocatalytic process. However, the mineralization achieved by this method is a long-term and expensive process. The effect of shortening the photocatalytic process is the partial degradation and formation of intermediates. The purpose of this study was to evaluate the sensitivity and transformation of photocatalytic reaction intermediates in aerobic biological processes. Sulfadiazine and sulfamethoxazole solutions were used in the study, which were irradiated in the presence of a TiO2-P25 catalyst. The resulting solutions were then aerated after the addition of river water or activated sludge suspension from a commercial wastewater treatment plant. The reaction kinetics were determined and fifteen products of photocatalytic degradation of sulfonamides were identified. Most of these products were further transformed in the presence of activated sludge suspension or in water taken from the river. They may have been decomposed into other organic and inorganic compounds. The formation of biologically inactive acyl derivatives was observed in the biological process. However, compounds that are more toxic to aquatic organisms than the initial drugs can also be formed. After 28 days, the sulfamethoxazole concentration in the presence of activated sludge was reduced by 66 ± 7%. Sulfadiazine was practically non-biodegradable under the conditions used. The presented results confirm the advisability of using photocatalysis as a process preceding biodegradation.

Identification of functional microflora underlying the biodegradation of sulfadiazine-contaminated substrates by Hermetia illucens.

The increasing discharge of antibiotic residues into the natural environment, stemming from both human activities and animal farming, has detrimental effects on natural ecosystems and serves as a significant driving force for the spread of antibiotic resistance. Biodegradation is an important method for the elimination of antibiotics from contaminated substrates, but the identifying in situ microbial populations involved in antibiotic degradation is challenging. Here, DNA stable isotope probing (DNA-SIP) was employed to identify active sulfadiazine (SDZ) degrading microbes in the gut of black soldier fly larvae (BSFLs). At an initial SDZ concentration of 100 mg kg-1, the highest degradation efficiency reached 73.99% after 6 days at 28 °C. DNA-SIP revealed the incorporation of 13C6 from labeled SDZ in 9 genera, namely, Clostridum sensu stricto 1, Nesterenkonia, Bacillus, Halomonas, Dysgonomonas, Caldalkalibacillus, Enterococcus, g_unclassified_f_Xanthomonadaceae and g_unclassified_f_Micrococcaceae. Co-occurrence network analysis revealed that a significant positive correlation existed among SDZ degrading microbes in the gut microbiota, e.g., between Clostridium sensu stricto 1 and Nesterenkonia. Significant increases in carbohydrate metabolism, membrane transport and translation were crucial in the biodegradation of SDZ in the BSFL gut. These results elucidate the structure of SDZ-degrading microbial communities in the BSFL gut and in situ degradation mechanisms.

Pyrimidine salvage in Toxoplasma gondii as a target for new treatment.

Toxoplasmosis is a common protozoan infection that can have severe outcomes in the immunocompromised and during pregnancy, but treatment options are limited. Recently, nucleotide metabolism has received much attention as a target for new antiprotozoal agents and here we focus on pyrimidine salvage by Toxoplasma gondii as a drug target. Whereas uptake of [3H]-cytidine and particularly [3H]-thymidine was at most marginal, [3H]-uracil and [3H]-uridine were readily taken up. Kinetic analysis of uridine uptake was consistent with a single transporter with a Km of 3.3 ± 0.8 µM, which was inhibited by uracil with high affinity (Ki = 1.15 ± 0.07 µM) but not by thymidine or 5-methyluridine, showing that the 5-Me group is incompatible with uptake by T. gondii. Conversely, [3H]-uracil transport displayed a Km of 2.05 ± 0.40 µM, not significantly different from the uracil Ki on uridine transport, and was inhibited by uridine with a Ki of 2.44 ± 0.59 µM, also not significantly different from the experimental uridine Km. The reciprocal, complete inhibition, displaying Hill slopes of approximately -1, strongly suggest that uridine and uracil share a single transporter with similarly high affinity for both, and we designate it uridine/uracil transporter 1 (TgUUT1). While TgUUT1 excludes 5-methyl substitutions, the smaller 5F substitution was tolerated, as 5F-uracil inhibited uptake of [3H]-uracil with a Ki of 6.80 ± 2.12 µM (P > 0.05 compared to uracil Km). Indeed, we found that 5F-Uridine, 5F-uracil and 5F,2'-deoxyuridine were all potent antimetabolites against T. gondii with EC50 values well below that of the current first line treatment, sulfadiazine. In vivo evaluation also showed that 5F-uracil and 5F,2'-deoxyuridine were similarly effective as sulfadiazine against acute toxoplasmosis. Our preliminary conclusion is that TgUUT1 mediates potential new anti-toxoplasmosis drugs with activity superior to the current treatment.