Changes in the Activities of Antioxidant Enzymes in the Fat Body and Hemolymph of L. Due to Pollen Monodiets.

The increasing prevalence of monocultures has reduced floral diversity, diminishing pollen diet variety for bees. This study examines the impact of monofloral pollen diets (hazel, rapeseed, pine, buckwheat, , goldenrod) on the antioxidant enzyme activities in the fat body from tergite 3, tergite 5, sternite, and hemolymph of honey bees. We show that pollen from plants such as rapeseed, , buckwheat, and goldenrod (rich in phenolic compounds and flavonoids) increases the activities of SOD, CAT, GST, and GPx in the fat body and hemolymph compared to the control group.

E-Cigarette and Vaping Perspectives: Recommendations for Occupational Health Nurses.

Background: Statistics from the Centers for Disease Control indicate that the use of e-cigarettes, vaping, and other electronic nicotine delivery systems (ENDS) are increasing although data on their safety is limited. While most employers ban smoking in the workplace, tobacco-free policies do not always extend specifically to e-cigarette products.

Methods: An IRB approved exploratory, cross-sectional study was conducted to investigate occupational health professionals' (OHPs) knowledge of e-cigarettes, vaping and ENDS and the ability to create change in tobacco-free workplace policies.

How does adulteration of wax foundation affect phenoloxidase and lysozyme activities as selected parameters of immunity in ?

Introduction: The adulteration of wax foundation is, for many reasons, a growing problem of modern beekeeping not only in Europe but also around the world. Wax foundation contaminated with stearin addition leads to a brood die-off, while paraffin addition negatively affects the strength of combs. It is tenable that such adulterated wax foundation reduces bees' immunity.

Concurrent loss of LKB1 and KEAP1 enhances SHMT-mediated antioxidant defence in KRAS-mutant lung cancer.

Non-small-cell lung cancer (NSCLC) with concurrent mutations in KRAS and the tumour suppressor LKB1 (KL NSCLC) is refractory to most therapies and has one of the worst predicted outcomes. Here we describe a KL-induced metabolic vulnerability associated with serine-glycine-one-carbon (SGOC) metabolism. Using RNA-seq and metabolomics data from human NSCLC, we uncovered that LKB1 loss enhanced SGOC metabolism via serine hydroxymethyltransferase (SHMT).

Unraveling ETC complex I function in ferroptosis reveals a potential ferroptosis-inducing therapeutic strategy for LKB1-deficient cancers.

The role of the mitochondrial electron transport chain (ETC) in regulating ferroptosis is not fully elucidated. Here, we reveal that pharmacological inhibition of the ETC complex I reduces ubiquinol levels while decreasing ATP levels and activating AMP-activated protein kinase (AMPK), the two effects known for their roles in promoting and suppressing ferroptosis, respectively. Consequently, the impact of complex I inhibitors on ferroptosis induced by glutathione peroxidase 4 (GPX4) inhibition is limited.