Dissipation behavior, residue dynamics, and dietary risk assessment of forchlorfenuron in postharvest kiwifruits during simulated cold chain logistics and store shelf life.

Forchlorfenuron (CPPU) is often applied during the cultivation of kiwifruit to produce larger fruit. To address degradation patterns of CPPU during simulated cold chain logistics and simulated shelf life of the fruit after harvest, appropriate storage methods and safe consumption behavior can be investigated. In this study, an ultra-high-performance liquid chromatography-tandem mass spectrometry method was adopted to detect CPPU residues under different conditions. CPPU in kiwifruit stored at 6 °C had a half-life of 40.8-77.0 days. However, when kiwifruit was stored at 0 °C under simulated cold chain storage conditions, the half-life of CPPU was 63.0-115.5 days, implying that lower storage temperatures can reduce the degradation rate of CPPU. The residues of CPPU in kiwifruit pulp declined with time, and the reduction followed the first-order kinetics equation. More CPPU residues were present in the pulp of postharvest kiwifruit treated with exogenous ethylene than in the pulp of untreated kiwifruit. Thus, using exogenous ethylene for artificial ripening after harvest is not recommended. We determined that the appropriate cold chain storage temperature is 6 °C. It is recommended that the public select kiwifruit stored for at least 2 weeks. The estimated chronic and acute dietary risk quotients of CPPU are ≤ 0.79% and ≤ 0.11%, respectively. Therefore, it is highly unlikely that consumers will be poisoned by CPPU due to kiwifruit consumption. Our results provide scientific evidence regarding the adoption of appropriate kiwifruit storage methods and consumption behavior to enhance consumption safety.

Enhanced proliferation inhibition and apoptosis in glioma cells elicited by combination of irinotecan and imatinib.

Glioma is a kind of lethal malignant tumor, and lacks efficient therapies. Combination therapy has been claimed to be a promising approach to combat cancer, due to its increased anti-cancer effects and reduced side effects. This study aimed to investigate the anti-cancer effect and mechanism of combining imatinib with irinotecan or its active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38). First, we found that this drug combination exerted synergistic antitumor effects against glioma in vitro and in vivo. In addition, flow cytometry results proved that the SN-38-induced apoptosis was further enhanced by imatinib, and similar results were observed by determining the protein expression levels of apoptosis biomarkers. Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53. Meanwhile, the markedly elevated p21 expression was observed only in the combination group, instead of the mono-treated groups. According to the results of p21 knockdown, we found that p21 was also required for the synergistic inhibitory effects. Moreover, we explored and ruled out the possibility of imatinib enhancing the sensitivity of irinotecan by inhibiting drug efflux pumps. Thus, our findings collectively suggest that combining irinotecan with imatinib could be a promising new strategy to fight against glioma.