The aim of this study was to determine the effect of blanching and frying on selected properties of potato crisps of yellow- and purple-fleshed cultivars. The material used was yellow flesh cv. Ismena and purple flesh cv. Provita. Potato slices were blanched (1–5 min at 80–90 °C) and then fried (155–175 °C). The control sample was comprised of crisps that were not blanched. The fat content and color parameters were determined in crisps, while in defatted samples, the following were determined: the content of total polyphenols; antioxidant capacity, measured by the ability to scavenge the ABTS^•+ radical cations (TEAC ABTS) and by the FRAP method; and the level of fluorescent intermediary compounds (FICs) and browning index (BI), as indicators of the progress of the Maillard reaction. The content of kynurenic acid (KYNA) was examined in the raw material, in slices, in the water after blanching and in the crisps. Blanching affected the fat absorption, with time being more critical than temperature. The color of crisps from yellow flesh potatoes after blanching lightened, while the color in the purple samples darkened. The content of total polyphenols was higher in purple crisps. Increasing the temperature and shortening the time of blanching increased the polyphenol content and the antioxidant capacity. Blanching decreased the level of FICs, while frying increased FICs. Higher BI values characterized the crisps from cv. Provita. Blanching reduced BI values by 50%, while frying at highest temperature increased these values. The content of KYNA in purple potatoes was almost three times higher than in yellow ones. Blanching and frying decreased the KYNA content in potatoes and fried crisps.

This review focuses on four unusual thin-layer chromatography (TLC) approaches for the determination of lipophilicity: (1) the use of medium-polar stationary phases: CN, NH₂, and DIOL instead of RP plates, together with water-based mobile phase; (2) the use of silica gel in a typical normal-phase manner and treating extrapolated retention indices as the “reversed lipophilicity”; (3) the use of oil impregnated silica gel in the reversed-phase manner; and (4) the use of salting-out mobile phases. The chromatographic indices obtained in these systems are numerously reported as well correlated with lipophilicity and they are an interesting alternative to classical RP systems approaches.

Kynurenic acid (KYNA) is a metabolite of tryptophan formed on the kynurenine pathway. Its pharmacological effects are relatively well characterized in mammals, whereas its role in fish is poorly understood. Therefore, the aim of the study was to expand the knowledge of KYNA’s presence inside a fish’s body and its impact on fish development and function. The study was performed on zebrafish larvae and adult rainbow trout. We provide evidence that KYNA is present in the embryo, larva and mature fish and that its distribution in organs varies considerably. A study of KYNA’s effect on early larval development suggests that it can accelerate larval maturation, especially under conditions that are suboptimal for fish growth. Moreover, KYNA in concentrations over 1 mM caused morphological impairment and death of larvae. However, long-lasting exposure of larvae to subtoxic concentrations of KYNA does not affect the behavior of 5-day-old larvae kept under standard optimal conditions. We also show that ingestion of KYNA-supplemented feed can lead to KYNA accumulation, particularly in the pyloric caeca of mature trout. These results shed new light on the relevance of KYNA and provide new impulse for further research on the importance of the kynurenine pathway in fish.

Neurodegenerative diseases, such as Parkinson’s and Alzheimer’s, are becoming an increasingly serious challenge for modern medicine because of the significant increase in incidence and the narrow range of effective therapeutic strategies. In recent years, the kynurenine pathway, which is one of the main pathways of tryptophan metabolism, responsible for the synthesis of products that act oppositely in the CNS including neurotoxic (quinolinic acid) and neuroprotective products, has gained increasing recognition as a potential therapeutic target. Abnormalities in the production of these metabolites, causing a disruption of homeostasis in the CNS, often lead to the development of inflammation, which can cause oxidative stress or neuronal death. This paper aims to discuss strategies useful in modulation of the kynurenine pathway, based on increasing the production of neuroprotective metabolites and reducing the synthesis of neurotoxic compounds, as well as to outline the progress in preclinical and clinical studies and the challenges encountered in these studies, among others, in the search for new KP inhibitors. The pharmacological (IDO and KMO inhibitors) and non-pharmacological (physical activity, diet) strategies are discussed, as well as new approaches from combination and targeted therapies. Together with the results of preclinical studies, they demonstrate the high utility of this target in the treatment of neurodegeneration. Despite its promising activity, further key studies are needed to fully understand the mechanisms involved in metabolism, which may translate into increased efficacy of developed therapies in the future.

Cognitive impairments, particularly in the context of neurodegenerative diseases, are associated with disruptions in mitochondrial function and key metabolic pathways. This study investigates the impact of short-term scopolamine exposure on mitochondrial DNA (mtDNA) stability and the kynurenine pathway (KP) in the hippocampus, a brain region central to learning and memory. We analyzed the mitochondrial D-loop region for mutations and heteroplasmy levels in hippocampal tissue from rats exposed to scopolamine (1 mg/kg/0.4 mL/cc i.p. x 14 days). Additionally, the expression of the KP enzymes kynurenine aminotransferase (KAT I, KAT II) and kynurenine 3-monooxygenase (KMO) and receptors aryl hydrocarbon receptor (Ahr) and G protein-coupled receptor 35 (GPR35) was evaluated using quantitative PCR. Neither significant mutation nor heteroplasmy changes were observed in the mtDNA D-loop region between the scopolamine-treated and control groups. Similarly, the hippocampal expression levels of the kat I, kat II, kmo and ahr and gpr35 genes remained unchanged, indicating no activation of this metabolic pathway under short-term scopolamine exposure. These findings suggest that the mitochondrial genome in the hippocampus remains stable under acute pharmacological stress induced by scopolamine, with no significant activation of the KP. These results underline the distinction between transient, reversible cognitive deficits and chronic neurodegenerative processes, providing insights for therapeutic approaches targeting specific stages of cognitive change.

Chronic kidney disease (CKD) and kidney failure significantly reduce patients’ quality of life and markedly increase cardiovascular risk and overall mortality. Disturbed metabolism of tryptophan (Trp) through kynurenine (KYN) pathway was implicated as an important factor in kidney damage and its complications. However, the expression of genes coding crucial enzymes of KYN pathway was not examined so far. The goal of the present study was to analyze the expression of Ido (indoleamine-2,3-dioxygenase), Kat1 (kynurenine aminotransferase 1), Kat2 (kynurenine aminotransferase 2), and Kmo (kynurenine-3-monooxygenase) genes in patients undergoing kidney failure with kidney replacement therapy (KFRT) treatment with either hemodiafiltration (HDF) or hemodialysis (HD) in relation to selected clinical and dialysis parameters. Our data imply that Ido, Kat1, and Kmo gene expression does not differ between KFRT patients with analyzed comorbidities, vascular access types, or diuresis occurrence. However, Ido and Kmo gene expression correlated with pre-dialysis concentration or reduction ratio (RR) of selected metabolites. Interestingly, patients treated with HDF manifested lower Kmo gene expression in comparison with patients treated by HD. Our study suggests that epigenetic factors do not exert noticeable impact on the KYN pathway enzymes expression in patients with KFRT. The advantageous effect of HDF vs. HD towards the KYN pathway genes expression has potential therapeutic implications, as it may reflect superiority of the former method in KFRT patients.