Waste-to-energy facilities are a key component of circular economy strategies, but their potential impact on air quality remains a public concern. This study evaluated whether the start-up of an energy recovery plant in northern Spain affected airborne levels of dioxins, furans (PCDD/Fs), and dioxin-like PCBs (dl-PCBs). Air samples were collected from 2017 to 2023 in two urban–industrial areas, one potentially affected by the plant and a control area. Concentrations before and after plant commissioning were compared using a before–after control–impact approach. Although pollutant levels were initially higher in the impact area, both sites showed a significant decline over time, with concentrations converging by the end of the study period. No statistically significant changes attributable to the plant start-up were observed. Similar congener profiles before and after commissioning suggest that regional industrial activities, rather than the energy recovery plant, are the main drivers of atmospheric PCDD/F and dl-PCB levels.
Mitochondrial function is reliant on interactions with other cell compartments, particularly the endoplasmic reticulum, via endoplasmic reticulum-mitochondrial contact sites (ERMCS). In this seminar, I will unravel how the ER influences mitochondrial DNA (mtDNA) replication, an essential process for cellular energy production and survival.
The research, conducted using both fibroblast and neuronal cell models, demonstrated a direct correlation between ERMCS abundance and mtDNA synthesis. Besides, I found that disrupting ERMCS via gene silencing (RTN4, ERLIN2, GRP75) significantly represses mtDNA replication. In addition, I identified manganese as a key ER-mitochondria signalling molecule that stimulates mtDNA replication and proposed a model which involves mitochondrial calcium uniporter transport and regulation. This work contributes significantly to the understanding of ER-mitochondria communication mechanisms, and suggests potential therapeutic avenues for stimulating mtDNA replication in cases of neurodegenerative disorders with ERMCS dysfunction.