BPP-PTX

Citrus greening or huanglongbing is the most important disease of citrus and threatens citrus production worldwide. As nymphs of Diaphorina citri play a crucial role in the acquisition and transmission of the citrus greening bacterium, suppression of this life stage is particularly important. However, the lack of a tractable feeding assay for use with first instar D. citri nymphs has impeded assessment of the toxicity of bioactives. Of several bacterial pesticidal proteins (BPP) that are toxic to D. citri adults, Mpp51Aa1 and Cry1Ba1, which have LC₅₀ values of 110 and 120 µg/mL respectively in adults, were fed to 1st instar nymphs in a newly developed assay. For this new sandwich feeding assay, parafilm layers containing feeding solution were placed on top of two 35 mm Petri dishes, with a concave surface created on each. Fifty nymphs were transferred to the membrane on one Petri dish, and the second Petri dish placed on the top to create a "sandwich" with the 1st instar nymphs in the middle. Nymphs were fed for four days and the LC₅₀ values for Mpp51Aa1 and Cry1Ba1 were calculated at 6.7 and 41.6 µg/mL respectively. Bioassays with bioengineered plants expressing Cry1Ba1 confirmed that the majority of D. citri mortality occurs during the 1st instar nymph stage, while egg laying adults are much less susceptible. Taken together, these results confirm that 1st instar D. citri nymphs are more susceptible to BPP than adults and demonstrate the utility of the sandwich feeding assay for effective screening of BPPs prior to investment into production of transgenic plants.

Bisphenol P (BPP) has been detected in human biological samples; however studies on its nephrotoxicity are scarce. Given the susceptibility of kidneys to endocrine-disrupting chemicals, there is an urgent need to investigate the renal toxicity of BPP. This study aimed to evaluate the effects of different concentrations of BPPs on the kidneys of C57BL/6 mice and elucidate the underlying mechanisms of renal damage using a combination of mouse renal transcriptomic data and human renal proximal tubular epithelial cells (HK-2). Mice were exposed to BPP (0, 0.3, 30, 3000 μg/kg bw/d) via gavage for 5 weeks. Renal injury was assessed based on changes in body and kidney weights, serum renal function indices, and histopathological examination. Transcriptomic analysis identified differentially expressed genes and pathways, whereas cellular assays were used to measure cell viability, reactive oxygen species (ROS), apoptosis, and the expression of key genes and proteins. The results show that BPP exposure induces renal injury, as evidenced by increased body weight, abnormal renal function indices, and renal tissue damage. Transcriptomic analysis revealed alterations in genes and pathways related to oxidative stress, p53 signaling, autophagy, and apoptosis. Cellular experiments confirmed that BPP induces oxidative stress and apoptosis. Furthermore, BPP exposure significantly inhibits autophagy, potentially exacerbating apoptosis and contributing to kidney injury. Treatment with a ROS inhibitor (N-Acetylcysteine, NAC) mitigated BPP-induced autophagy inhibition and apoptosis, implicating oxidative stress as a key factor. BPP exposure may lead to renal injury through excessive ROS accumulation, oxidative stress, inflammatory responses, autophagy inhibition, and increased apoptosis. The effects of NAC highlight the role of oxidative stress in BPP-induced nephrotoxicity. These findings enhance our understanding of BPP-induced nephrotoxicity and underscore the need to control BPP exposure to prevent renal disease. This study emphasized the importance of evaluating the safety of new Bisphenol A analogs, including BPP, in environmental toxicology.