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.

Effects of Different Calorie Restriction Protocols on Oxidative Stress Parameters in a Transgenic Mouse Model of Breast Cancer.

Aging and diseases related to aging, such as cancer, have been linked to oxidative stress. On the other hand, calorie restriction (CR) is one of the most effective interventions to slow down aging and prevent a variety of diseases such as cancer in preclinical models. CR has also been reported to modify oxidative stress. The aim of this study was to investigate the effects of different CR protocols and aging on oxidative stress parameters in the MMTV-TGF-α breast cancer mouse model in a cross-sectional study. Female mice were randomly enrolled in three groups: ad libitum (AL), chronic calorie restriction (CCR, 15% CR) or intermittent calorie restriction (ICR, three weeks AL followed by one week 60% CR in cyclic periods) starting at the age of 10 weeks until 81/82 weeks of age. Liver samples were analyzed for malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GSH-Px) levels. At week 49/50, the GSH level increased significantly in the CCR group compared to the AL and ICR-R groups which had higher mammary tumor (MT) incidence rates. Additionally, liver MDA levels in ICR groups were significantly increased, while aging led to decreased CAT and SOD activities in all CR groups. The application of different CR protocols did not have any significant effect on MDA, CAT, and SOD parameters in the liver at week 81/82. These results suggest that although GSH may interfere with MT development at the systemic level, many of the oxidative stress parameters may have more local effects on tumor development than the systemic effects.

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.

Noncoding RNAs in age-related cardiovascular diseases.

Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality in the adult population worldwide and represent a severe economic burden and public health concern. The majority of human genes do not code for proteins. However, noncoding transcripts play important roles in ageing that significantly increases the risk for CVDs. Noncoding RNAs (ncRNAs) are critical regulators of multiple biological processes related to ageing such as oxidative stress, mitochondrial dysfunction and chronic inflammation. NcRNAs are also involved in pathophysiological developments within the cardiovascular system including arrhythmias, cardiac hypertrophy, fibrosis, myocardial infarction and heart failure. In this review article, we cover the roles of ncRNAs in cardiovascular ageing and disease as well as their potential therapeutic applications in CVDs.

LEPTIN RECEPTORS EXPRESSION IN MAMMARY TUMORS AND MAMMARY FAT PAD OF TRANSGENIC MAMMARY CANCER MOUSE MODEL.

BACKGROUND: Leptin is an adipokine encoded by the Ob (obese) gene and predominantly produced by adipocytes. The roles of both leptin and leptin receptor (ObR) in numerous pathophysiological conditions including mammary tumor (MT) development have been reported. AIM: To examine protein expression levels of leptin and its receptors (ObR) including the long form, ObRb, in MT tissue and mammary fat pad of a transgenic mammary cancer mouse model. Further, we investigated whether the effects of leptin on MT development are systemic or local. MATERIALS AND METHODS: MMTV-TGF-α transgenic female mice were fed ad libitum from week 10 up to week 74. Protein expression levels of leptin, ObR, and ObRb were measured in the mammary tissue samples of 74-week old MMTV-TGF-α mice with and without MT (MT-positive/MT-negative) by Western blot analysis. Serum leptin levels were measured by using the mouse adipokine LINCOplex kit 96-well plate assay. RESULTS: Protein expression levels of ObRb were significantly lower in MT as compared to control tissue of mammary gland. In addition, protein expression levels of leptin were significantly higher in the MT tissue of MT-positive mice compared to control tissue of MT-negative mice. However, ObR protein expression levels in tissues of mice with and without MT were similar. Serum leptin levels at different ages were not significantly different between the two groups. CONCLUSION: Leptin and ObRb in the mammary tissue may play a critical role in the mammary cancer development, while contribution of short ObR isoform may be less important.