Changes in the Levels of Short-Chain Acids and Tryptophan Metabolites in Mouse Intestine during Experimental Colitis.

The optimal balance of the intestinal microbiota is considered to be an essential part of the human body that affects many metabolic processes. However, the exact role of the gut microbiota in metabolism is still not fully understood. To investigate the metabolic role of gut microbiota, the content of short-chain fatty acids and tryptophan metabolites was studied in mice with sodium dextran sulfate-induced colitis.

Adaptations of Biofilms to Oxidative Stress Induced by Copper(II) Oxide Nanoparticles.

Copper(II) oxide nanoparticles (CuO NPs) are used in different industries and agriculture, thus leading to their release to the environment, which raises concerns about their ecotoxicity and biosafety. The main toxicity mechanism of nanometals is oxidative stress as a result of the formation of reactive oxygen species caused by metal ions released from nanoparticles. Bacterial biofilms are more resistant to physical and chemical factors than are planktonic cells due to the extracellular polymeric matrix (EPM), which performs a protective function.

Free radical fragmentation and oxidation in the polar part of lysophospholipids: Results of the study of blood serum of healthy donors and patients with acute surgical pathology.

The interaction of reactive oxygen species with cell membrane lipids is usually considered in the context of lipid peroxidation in the nonpolar component of the membrane. In this work, for the first time, data were obtained indicating that damage to human cell membranes can occur in the polar part of lysophospholipids at the interface with the aqueous environment due to free radical fragmentation (FRF) processes. FRF products, namely 1-hexadecanoyloxyacetone (PAc) and 1-octadecanoyloxyacetone (SAc), were identified in human serum, and a GC-MS method was developed to quantify PAc and SAc.

ALDH2 polymorphism and myocardial infarction: From alcohol metabolism to redox regulation.

Acute myocardial infarction (AMI) remains a leading cause of death worldwide. Increased formation of reactive oxygen species (ROS) during the early reperfusion phase is thought to trigger lipid peroxidation and disrupt redox homeostasis, leading to myocardial injury. Whilst the mitochondrial enzyme aldehyde dehydrogenase 2 (ALDH2) is chiefly recognised for its central role in ethanol metabolism, substantial experimental evidence suggests an additional cardioprotective role for ALDH2 independent of alcohol intake, which mitigates myocardial injury by detoxifying breakdown products of lipid peroxidation including the reactive aldehydes, malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE).