Are photocatalytic processes effective for removal of airborne viruses from indoor air? A narrative review

A wide variety of methods have been applied in indoor air to reduce the microbial load and reduce the transmission rate of acute respiratory diseases to personnel in healthcare sittings. In recent months, with the occurrence of COVID-19 pandemic, the role of portable ventilation systems in reducing the load of virus in indoor air has received much attention. The present study delineates a comprehensive up-to-date overview of the available photocatalysis technologies that have been applied for inactivating and removing airborne viruses. The detection methods for identifying viral particles in air and the main mechanisms involving in virus inactivation during photocatalysis are described and discussed. The photocatalytic processes could effectively decrease the load of viruses in indoor air. However, a constant viral model may not be generalizable to other airborne viruses. In photocatalytic processes, temperature and humidity play a distinct role in the inactivation of viruses through changing photocatalytic rate. The main mechanisms for inactivation of airborne viruses in the photocatalytic processes included chemical oxidation by the reactive oxygen species (ROS), the toxicity of metal ions released from metal-containing photocatalysts, and morphological damage of viruses.

     

Toxicity of 4-methylimidazole on isolated brain mitochondria: using both in vivo and in vitro methods

4-methylimidazole (4MI) is a compound widely used in various industrial and consumer applications. The most important sources of exposure include chemical caramel coloring, ammoniated molasses, dyes and pigments, rube, cleaning and agricultural chemicals. Toxicity attributed to 4MI in foods has recently become a focus of research. Recent studies showed that 4MI induced adverse changes in various target tissues. Brain is known to be a target organ for 4MI-induced toxicity but its cytotoxic mechanisms have not yet been elucidated. In this study, experiments were divided into two parts: (1) using in vivo methodology, doses of 4MI at 100, 200, or 300 mg/kg were administered orally to mice daily for 14 to obtain brain mitochondria; and (2) utilizing in vitro methodology, brain mitochondria were incubated with 4MI at 400, 800, or 1600 μM concentrations. Subsequently, the neurotoxicity of 4MI was assessed using mitochondrial dysfunction tests, including reactive oxygen species (ROS) formation, mitochondrial membrane potential (MMP) collapse, mitochondrial swelling, and cytochrome c release. Our results from both in vivo and in vitro experiments on isolated brain mitochondria showed a significant decrease in complex II activity and also marked elevation in the ROS formation, MMP collapse, mitochondrial swelling, and enhanced release of cytochrome c. Data indicated that 4MI induced neurotoxicity through the impairment of electron transfer chain especially at complex II and elevated ROS formation leading to subsequent oxidative stress events including mitochondrial membrane depolarization, mitochondrial swelling, and release of cytochrome c, which is the starting point of mitochondrial-mediated apoptosis signaling and neurodegeneration.