Controlled atmosphere (CA) has been demonstrated to maintain the shelf-life quality of fruits, but its effect on the antioxidant activities and phenolic content of yellow peach is not comprehensive. This study analyzed the role of CA on the quality of shelf period, phenolic content and antioxidant activity of “Jinxiu” yellow peach. Yellow peach was left under specific aeration conditions (3.5–4% CO2, 2–3% O2, 92–95.5% N2, 1 ± 0.5 °C) and the control (1 ± 0.5 °C) for 21 d, to observe changes in physiological parameters of the fruit during 10 d of the shelf life (25 ± 1 °C). The result showed that CA reduced the weight loss rate (WLR), decay rate (DR), and browning index (BI) of yellow peaches. Furthermore, the CA held a high level of total flavonoid content (TFC), total phenol content (TPC) and phenolic content in the fruit. Antioxidant analysis showed that polyphenol oxidase (PPO) enzyme activity was lower and free radical scavenging capacity (DPPH, ABTS, and FRAP) and antioxidant enzyme activities (POD and PAL) were higher in the CA group. Combining the results of significance analysis, correlation analysis, principal component analysis (PCA) and hierarchical cluster analysis (HCA) clearly identified the differences between the CA group and the control group. The results showed that the CA could maintain higher phenolic content and reduce the oxidation of yellow peach fruit and enhance fruit quality by affecting the antioxidant activities of yellow peach.
In addition to the direct tumor cell cytotoxicity, chemotherapy also plays roles in modulating immune response. However, the underlying mechanism is not fully understood. Here we found that chemotherapy enhanced tumor cell antigen presentation to facilitate CD8+ T cell cytotoxic function. Cancer cell-autonomous type I IFN induction stimulated by chemotherapy was critical for CD8+ T cell cytotoxicity. Mechanistically, chemotherapy impaired mitochondrial function and anti-oxidant capacity, which increased reactive oxygen species (ROS) production. ROS triggered oxidized mtDNA accumulation in the cytosol of tumor cells and subsequently activated cGAS-STING signaling to drive type I IFN induction. cGAS-STING-IFN axis increased PD-L1 expression and predicted effective clinical responses to chemoimmunotherapy. Our findings highlight that a suitable dose of chemotherapy activates CD8+ T cell immunity instead of directly inducing intense tumor cell toxicity, which may alleviate the side effects of chemotherapy and potentiate the sensitivity to immune checkpoint inhibitors (ICIs). Screening chemotherapeutic drugs or developing new drugs which can stimulate type I IFN production in the tumor cells efficiently promote anti-tumor immunity and will be beneficial for chemoimmunotherapy. Conversely, antioxidants like N-acetylcysteine which impede type I IFN induction, attenuate the therapeutic efficacy and will be unfavorable for patients that are receiving chemoimmunotherapy.
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