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Since milk whey is an abundant dairy by-product and a significant threat to the environment, its utilization is of great interest. The study compares valorization of lactose and lactates—the main carbon sources of whey—by fermentation—an environmentally friendly process. Antimicrobials released during fermentation by food-grade bacteria can help increase the microbiological safety of food. Propionic acid—a strong antimicrobial—is obtained mainly by the petrochemical route, yet there is increasing interest in its synthesis in biotechnological pathway. Five strains of propionic acid bacteria (Acidipropionibacterium acidipropionici, Propionibacterium cyclohexanicum, Propionibacterium freudenreichii, Acidipropionibacterium jensenii and Acidipropionibacterium thoenii) were investigated for their ability to produce organic acids and biomass using Na lactate or lactose as carbon sources. Selected fermentates were investigated for their antimicrobial efficacy during in vitro studies with foodborne pathogens: Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Bacillus subtilis and Staphylococcus aureus. Results confirm that the production of acids and biomass is considerably influenced by the added carbon source. The tested fermentates have strong and specific antimicrobial activity against Pseudomonas aeruginosa, Bacillus subtilis and Staphylococcus aureus. In addition, inhibition of Staphylococcus aureus and Klebsiella pneumonia depends on the activity of produced bacteriocins. The article also discusses the possibility of increasing the antimicrobial activity of fermentates by acidification. [ABSTRACT FROM AUTHOR]

The accumulation of long-chain fatty acids (FAs) and their CoA and carnitine esters is observed in the ischaemic myocardium after acute ischaemia/reperfusion. The aim of the present study was to identify harmful FA intermediates and their detrimental mechanisms of action in mitochondria and the ischaemic myocardium. In the present study, we found that the long-chain acyl-CoA and acylcarnitine content is increased in mitochondria isolated from an ischaemic area of themyocardium. In analysing the FA derivative content, we discovered that long-chain acylcarnitines, but not acyl-CoAs, accumulate at concentrations that are harmful to mitochondria. Acylcarnitine accumulation in the mitochondrial intermembrane space is a result of increased carnitine palmitoyltransferase 1 (CPT1) and decreased carnitine palmitoyltransferase 2 (CPT2) activity in ischaemic myocardium and it leads to inhibition of oxidative phosphorylation, which in turn induces mitochondrial membrane hyperpolarization and stimulates the production of reactive oxygen species (ROS) in cardiac mitochondria. Thanks to protection mediated by acyl-CoA-binding protein (ACBP), the heart is much better guarded against the damaging effects of acyl- CoAs than against acylcarnitines. Supplementation of perfusion buffer with palmitoylcarnitine (PC) before occlusion resulted in a 2-fold increase in the acylcarnitine content of the heart and increased the infarct size (IS) by 33%. A pharmacologically induced decrease in the mitochondrial acylcarnitine content reduced the IS by 44%. Long-chain acylcarnitines are harmful FA intermediates, accumulating in ischaemic heart mitochondria and inducing inhibition of oxidative phosphorylation. Therefore, decreasing the acylcarnitine content via cardioprotective drugs may represent a novel treatment strategy. [ABSTRACT FROM AUTHOR]

Increased plasma concentration of trimethylamine N -oxide (TMAO), a proatherogenic metabolite, has been linked to adverse cardiovascular outcomes; however, it remains unclear whether TMAO is a biomarker or whether it induces direct detrimental cardiovascular effects. Because altered cardiac energy metabolism and mitochondrial dysfunction play crucial roles in the development of cardiovascular diseases, we hypothesized that increased TMAO concentration may alter mitochondrial energy metabolism. The aim of the present study was to determine the effects of TMAO on cardiac mitochondrial energy metabolism. Acute exposure of cardiac fibers to TMAO decreased LEAK (substrate-dependent) and OXPHOS (oxidative phosphorylation-dependent) mitochondrial respiration with pyruvate and impaired substrate flux via pyruvate dehydrogenase. The administration of TMAO at a dose of 120 mg/kg for 8 weeks increased TMAO concentration in plasma and cardiac tissues 22–23 times to about 15 μM and 11 nmol/g, respectively. Long-term TMAO administration decreased mitochondrial LEAK state respiration with pyruvate by 30% without affecting OXPHOS state respiration. However, no significant changes in mitochondrial reactive oxygen species production were observed after acute exposure of cardiac fibers to TMAO under physiological conditions. In addition, both long-term TMAO administration and acute exposure to TMAO decreased respiration with palmitoyl-CoA indicating impaired β-oxidation. Taken together, our results demonstrate that increased TMAO concentration impairs pyruvate and fatty acid oxidation in cardiac mitochondria. Thus, the accumulation of TMAO in cardiac tissues leads to disturbances in energy metabolism that can increase the severity of cardiovascular events. [ABSTRACT FROM AUTHOR]