Polyethylene terephthalate nanoplastics cause oxidative stress induced cell death in Saccharomyces cerevisiae.

Polyethylene terephthalate (PET) is a common plastic widely used in food and beverage packaging that poses a serious risk to human health and the environment due to the continual rise in its production and usage. After being produced and used, PET accumulates in the environment and breaks down into nanoplastics (NPs), which are then consumed by humans through water and food sources. The threats to human health and the environment posed by PET-NPs are of great concern worldwide, yet little is known about their biological impacts. Herein, the smallest sized PET-NPs so far (56 nm) with an unperturbed PET structure were produced by a modified dilution-precipitation method and their potential cytotoxicity was evaluated in Saccharomyces cerevisiae. Exposure to PET-NPs decreased cell viability due to oxidative stress induction revealed by the increased expression levels of stress response related-genes as well as increased lipid peroxidation. Cell death induced by PET-NP exposure was mainly through apoptosis, while autophagy had a protective role.

SLX5 deletion confers tolerance to oxidative stress in Saccharomyces cerevisiae.

Slx5, a subunit of a SUMO-targeted ubiquitin ligase (STUbL) in yeast, has been implicated in maintenance of genomic stability. SUMOylation is an important post-translational modification involved in the regulation of several important cellular processes and cellular response to various environmental stressors. Oxidative stress occurs when production of reactive oxygen species (ROS) exceeds the antioxidant defense capacity of the cell. Elevated ROS levels cause oxidative damage to important cellular macromolecules such as DNA, lipids, and proteins, which is associated with several diseases. Herein, we investigated the role of Slx5 in oxidative stress tolerance in Saccharomyces cerevisiae. We show that deletion of SLX5 increases survival of yeast cells in response to H2O2-induced oxidative stress in a cell cycle independent manner. Accumulation of intracellular ROS as well as DNA and lipid damages were reduced; expressions of antioxidant defense mechanism-related genes were increased in slx5Δ cells compared to wild type (WT) under oxidative stress. We also show that slx5Δ cells have increased intracellular ROS levels and oxidative damage to DNA and lipids compared to WT in the absence of oxidative stress. Thus, our data together suggest that an adaptive stress induced by SLX5 deletion increases tolerance to oxidative stress in slx5∆ cells.