Environmentally persistent free radicals in PM_(2.5)from a typical Chinese industrial city during COVID-19 lockdown:The unexpected contamination level variation

The outbreak of COVID-19 has caused concerns globally.To reduce the rapid transmission of the virus,strict city lockdown measures were conducted in different regions.China is the country that takes the earliest home-based quarantine for people.Although normal industrial and social activities were suspended,the spread of virus was efficiently controlled.Simultaneously,another merit of the city lockdown measure was noticed,which is the improvement of the air quality.Contamination levels of multiple atmospheric pollutants were decreased.However,in this work,24 and 14 air fine particulate matter(PM_(2.5))samples were continuously collected before and during COVID-19 city lockdown in Linfen(a typical heavy industrial city in China),and intriguingly,the unreduced concentration was found for environmentally persistent free radicals(EPFRs)in PM_(2.5)after normal life suspension.The primary non-stopped coal combustion source and secondary Cu-related atmospheric reaction may have impacts on this phenomenon.The cigarette-based assessment model also indicated possible exposure risks of PM_(2.5)-bound EPFRs during lockdown of Linfen.This study revealed not all the contaminants in the atmosphere had an apparent concentration decrease during city lockdown,suggesting the pollutants with complicated sources and formation mechanisms,like EPFRs in PM_(2.5),still should not be ignored.

Inhibiting autophagy enhances sulforaphane-induced apoptosis via targeting NRF2 in esophageal squamous cell carcinoma

Sulforaphane(SFN), a natural anti-tumor compound from cruciferous vegetables, has been reported to induce protective autophagy to cancer cells, which might impair the anti-tumor efficiency of SFN. However, the accurate function and mechanism of SFN inducing autophagy in cancers are still obscure, especially in esophageal squamous cell carcinoma(ESCC), one of malignancies with high incidence in North China. Here, we mainly explored the potential function of autophagy upon SFN treatment in ESCC and molecular mechanism. We demonstrated that SFN could inhibit cell proliferation and induce apoptosis by activating caspase pathway. Moreover, we found activation of NRF2 pathway by SFN was responsible for the induction of autophagy and also a disadvantage element to the anti-tumor effects of SFN on ESCC, indicating that SFN might induce protective autophagy in ESCC. We, therefore,investigated effects of autophagy inhibition on sensitivity of ESCC cells to SFN and found that chloroquine(CQ) could neutralize the activation of SFN on NRF2 and enhance the activation of SFN on caspase pathway, thus improved the anti-tumor efficiency of SFN on ESCC in vitro and in vivo. Our study provides a preclinical rationale for development of SFN and its analogs to the future treatment of ESCC.