Effect of yhfS gene on Bt LLP29 antioxidant and UV ray resistance.

BACKGROUND: Bacillus thuringiensis (Bt) is a widely used microbial insecticide. However, its persistence is limited because of ultraviolet (UV) rays or other environmental factors. The yhfS gene, which encodes acetyl-CoA acyltransferase, plays an important role in lipid transport and metabolism in many organisms. To explore whether it is related to the stress resistance of Bt LLP29, the yhfS gene knockout strain LLP29 Δ-yhfS and the complementary strain LLP29 R-yhfS were generated successfully by homologous recombination technology, and the related phenotypic changes were compared in this study. RESULTS: Gene yhfS was found to be functional in response to UV radiation in Bt by comparing the survival rates of Bt LLP29 harboring yhfS or not under UV light. Enzyme activity assays of key enzymes showed the the Embden-Meyerhof-Parnas pathway was enhanced yet the tricarboxylic acid cycle as well as butanoate synthesis were repressed when the gene was deleted. At the same time, the amino acid content was decreased, but reduced nicotinamide adenine dinucleotide (NADH) and reactive oxygen species (ROS) content were increased. Most noteworthy, antioxidase (such as superoxide dismutase and peroxidase) activities and contents of some potent antioxidants (such as pyruvate, carotenoids and NADPH) were lower in LLP29 Δ-yhfS than in LLP29. CONCLUSION: These tests revealed that the loss of the yhfS gene led to metabolic disorders and reduction of the antioxidant ability of Bt. Higher ROS level and lower anti-oxidative capacity might be responsible for the reduced UV resistance when the gene was deleted. These results not only greatly enrich understanding of the mechanism of Bt UV resistance, but also provide an important theoretical basis for Bt application. © 2023 Society of Chemical Industry.

The Sustainability of Energy Conversion Inhibition for Tumor Ferroptosis Therapy and Chemotherapy.

The hyperactive energy metabolism mostly contributes the tumor cells growth and proliferation. Herein, the intelligent nanoparticles (P-B-D NPs) obtained by loading BAY-876 and doxorubicin (Dox)-Duplex into nanoparticles composed of disulfide bond (SS) containing polymer are reported, which provide an efficient resistance of tumor cells energy metabolism and tumor growth to conquer malignant tumor. In response to the reducing microenvironment of tumor tissue, the SS bond can be disintegrated by intracellular glutathione to block the synthesis of lipid repair enzyme-glutathione peroxidase 4 for ferroptosis therapy. More importantly, the released BAY-876 can inhibit the functionality of glucose transporter 1, restricting the glucose uptake of tumor cells to a low energy metabolism status. Meanwhile, Dox-Duplex can interact with ATP to reduce intracellular ATP content and release Dox to kill tumor cells. Collectively, this work offers a new idea for restricting tumor cells energy metabolism to inhibit their proliferation.