Objective: To monitor severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA contamination in samples linked to imported cold-chain food and assess the situation from the implementation of a centralized supervision warehouse system in Guangzhou, Guangdong Province, China. Methods: Swabs of workers and frozen-food-related samples were collected between July 2020 and December 2023 in Guangzhou, Guangdong Province. SARS-CoV-2 RNA was extracted and analyzed by a real-time quantitative polymerase chain reaction using the commercially available SARS-CoV-2 nucleic acid test kit. The risk level and food source were monitored simultaneously. Results: A total of 283 positive cold-chain events were found in Guangzhou since the first cold-chain-related event of the coronavirus disease 2019 pandemic was identified in July 2020. Most positive samples were a low-to-medium risk, and the cycle threshold value was >30. No live virus was detected, and no staff came into direct contact with a live virus. In total, 87.63% of positive events were identified through sampling and testing at the centralized food warehouse. Conclusion: Cold-chain food has a relatively low risk of transmitting SARS-CoV-2. Centralized food storage can be used as an effective method to control this risk, and this measure can also be used for other food-related, contact-transmitted diseases.

Cadmium (Cd), an environmental toxin, may cause neurological disorders. We studied the role and activation mechanism of FoxO3a in Cd-induced oxidative stress. In addition to oxidative stress, Cd activated the antioxidant defense system in neuronal cells. Furthermore, by using Western blot and confocal microscopy, we found that Cd induced nuclear expression of FoxO3a. Importantly, knockdown of FoxO3a significantly suppressed its target SOD2 protein expression and elevated the level of intracellular ROS, ultimately reducing cell viability in Cd-exposed neuronal cells. These results suggest the protective effect of FoxO3a is associated with oxidative stress resistance. Then, we investigated the activation mechanism of FoxO3a. Our results indicate that the nuclear expression of FoxO3a by Cd may be independent of Akt, which is generally regarded as an important negative regulator of FoxO3a. Furthermore, we found that p38 regulated the nuclear expression of FoxO3a in Cd-exposed cells. Finally, we demonstrate that the p38-FoxO3a pathway inhibits Cd-induced oxidative stress. These signaling molecules may be used as a novel biological marker of Cd-induced oxidative stress and provide potential therapeutic approaches for it.