Bingxue Zheng

A novel coronavirus (SCoV) is the etiological agent of severe acute respiratory syndrome (SARS). SCoV-like viruses were isolated from Himalayan palm civets found in a live-animal market in Guangdong, China. Evidence of virus infection was also detected in other animals (including a raccoon dog, Nyctereutes procyonoides) and in humans working at the same market. All the animal isolates retain a 29-nucleotide sequence that is not found in most human isolates. The detection of SCoV-like viruses in small, live wild mammals in a retail market indicates a route of interspecies transmission, although the natural reservoir is not known.

Stroke is the second leading cause of death for all human beings and poses a serious threat to human health. Environmental exposure to a mixture of metals may be associated with the occurrence and development of stroke, but the evidence in the Chinese population is not yet conclusive. This study evaluated the association between stroke risk and 13 metals Metal concentrations in whole blood samples from 100 stroke cases and 100 controls were measured by ICP-MS. The cumulative impact of mixed metal on stroke risk was investigated by using three statistical models, BKMR, WQS and QGC. The case group had higher concentrations of Mg, Mn, Zn, Se, Sn, and Pb than the control group (p<0.05). BKMR model indicated a correlation between the risk of stroke and exposure to mixed metals. WQS model showed that Mg (27.2 %), Se (25.1 %) and Sn (14.8 %) were positively correlated with stroke risk (OR=1.53; 95 %Cl: 1.03–2.37, p=0.013). The QGC model showed that Mg (49.2 %) was positively correlated with stroke risk, while Ti (31.7 %) was negatively correlated with stroke risk. Mg may be the largest contributor to the cumulative effect of mixed metal exposure on stroke risk, and the interaction between metals requires more attention. These findings could provide scientific basis for effectively preventing stroke by managing metals in the environment.

Lead is a potent toxicant that exerts deleterious effects on multiple organ systems within the human body. Existing evidence suggests that lead exposure may contribute to the progression of amyotrophic lateral sclerosis (ALS). However, the precise mechanism remains unclear and the experimental evidence is currently lacking. This study establishes an ALS cell model exposed to lead to investigate the potential relationship between lead exposure and ALS, and targets ferroptosis to elucidate the possible mechanism of lead exposure in ALS pathogenesis. Our findings demonstrate that lead exposure results in the accumulation of ROS and MDA in hSOD1 G93A cells, accompanied by increased iron content, reduced GSH levels, mitochondrial vacuolization, and disruption of the cristae structure, upregulationation of ACSL4 protein levels, and inactivation of SLC7A11 and GPX4, ultimately triggering ferroptosis. The bioinformatics analyses and cellular experiments of the present study suggest that activation of the MAPK/ERK signaling pathway plays a crucial role in the ferroptosis process of ALS cells induced by lead exposure. This study not only provides new experimental evidence of the link between lead exposure and ALS but also elucidates the possible mechanism by which lead exposure contributes to the pathogenesis of ALS, demonstrating that the prevention of ferroptosis through targeting the MAPK/ERK signaling pathway may offer a promising intervention strategy for addressing lead-related ALS pathogenesis issues. • Transfecting NSC34 cells with the mutant gene hSOD1 G93A is established as an ALS cell model. • Transcriptome sequencing revealed significant enrichment of the MAPK pathway in lead-treated ALS cell models. • The activation of the MAPK/ERK pathway is critical for lead-induced ferroptosis in an ALS cell model. • Targeting ferroptosis and the MAPK/ERK pathway may offer a novel perspective for lead-related ALS pathogenesis.