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The present study was performed to investigate the effects of dietary yeast β-1,3/1,6-D-glucans after 15-, 30-, and 45-day feeding periods on the development of oxidative stress, antioxidant defenses, and lysosomal functioning in gills and hepatic tissue of rainbow trout, Oncorhynchus mykiss (Walbaum). The fish were fed a control diet or an experimental diet containing the supplement Yestimun® at a dose of 1% in the basal feed (with 85% content of β-1,3/1,6-glucans). On days 15, 30, and 45 of the experiment, the following were analyzed in gills and hepatic tissue: oxidative stress biomarkers (2-thiobarbituric-acid-reacting substances [TBARS]); aldehydic and ketonic derivatives of oxidatively modified proteins; activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), and glutathione peroxidase (GPx); total antioxidant capacity (TAC); activities of lysosomal enzymes (alanyl aminopeptidase [AAP], leucyl aminopeptidase [LAP], acid phosphatase [AcP], β-N-acetylglucosaminidase [NAG]). The dietary β-glucans stimulated CAT, GPx, LAP, and AcP activities in gills and hepatic tissue compared to the control group; however, the opposite trend was observed in TAC levels in gills on days 30 and 45. The present study suggests that β-glucans can enhance immune response, antioxidant capacity, and lysosomal functioning effectively in rainbow trout.

Determination of morphological and biochemical blood indices facilitates assessment of the health and welfare of horses, their nutrient demand, the effects of training already undertaken, and the horses’ suitability for exercise. Identification of the season-dependent components and the effects of sex and exercise on changes in frequently referenced haematological and biochemical parameters was the main goal of the current study.

This study analyzed time-dependent effects of vaccination against Y. ruckeri on the oxidative mechanism underlying those effects by detecting relevant lipid peroxidation (2-thiobarbituric acid reactive substances, TBARS) and protein oxidation biomarkers [aldehydic and ketonic derivatives of oxidatively modified proteins (OMP)], antioxidant defenses [activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), total antioxidant capacity (TAC)], as well as activities of lysosomal functioning [alanyl aminopeptidase (AAP), leucyl aminopeptidase (LAP), acid phosphatase (AcP), and â-N-acetylglucosaminidase (NAG)] in hepatic tissue of rainbow trout, Oncorhynchus mykiss (Walbaum) following anti-Y. ruckeri vaccination in the first, second, and sixth months. A concentrated vaccine with Y. ruckeri strains was enclosed in fish feed and was administered three times every other day. Rainbow trout from each group were euthanized 31, 61, and 181 days following vaccination, and hepatic tissue was sampled for analysis. In the current study, vaccination against Y. ruckeri resulted in a no statistically significant change in TBARS levels, while aldehydic and ketonic derivatives of OMP in hepatic tissue decreased, especially after the first and second months following immunization. Moreover, the activities of glutathione-dependent enzymes increased, especially after the first and sixth months. The highest TAC levels were observed two and six months after vaccination. It has been shown that vaccination-related oxidative stress in hepatic tissue is involved in adaptive responses through the temporary mobilization of antioxidant and lysosomal enzymes in rainbow trout. The present study showed the effect of vaccination on lysosome membrane permeability for carbohydrate cleavage after the development of immunity against Yersinia, whereas antioxidant defence was reduced. Our results confirmed that the concept of preserving antioxidant enzyme function after vaccination was also evident when CAT, GR, and GPx activities either increased or were unchanged following vaccination.

The present study was performed to investigate the effects of dietary yeast β-1,3/1,6-D-glucans supplemented over a 14-day feeding period on liver and cardiac function and the oxidative mechanism underlying these effects. We assessed relevant lipid peroxidation and protein oxidation biomarkers, antioxidant defense indices [superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), total antioxidant capacity (TAC)], and biochemical alterations [activities of aminotransferases (AT), lactate dehydrogenase (LDH), and succinate dehydrogenase (SDH), and levels of lactate (L) and pyruvate (P)] in rainbow trout, European whitefish, and grayling. The fish received a control diet and an experimental diet containing yeast β-1,3/1,6-D-glucans at a dose of 1% in the basal feed for 14 days. The results demonstrated enhancement in the phagocytic activity and phagocytic index in the groups fed β-glucans, compared to the control groups. In the groups fed β-glucans, the oxidative stress parameters such as lipid peroxidation, oxidatively modified proteins, and TAC did not vary significantly. The dietary β-glucans stimulated CAT and GPx activities in hepatic and cardiac tissues in comparison to the control group; however, a reverse trend was observed in the GR activity in these tissues.

The current study assessed health risks posed by exposure to metals from the consumption of Baltic Sea trout (Salmo trutta L.). Concentrations of essential minerals in sea trout muscles were determined and compared with the physiological requirements of these minerals in Polish nutrition standards, recommended dietary allowances (RDA), and estimated average requirements (EAR). Chemical analyses indicated that sea trout was rich in phosphorus, calcium, magnesium, sodium, and potassium. The pattern significance gradation of the element concentrations was as follows: P>Ca>Mg>Na>K>Fe>Zn>Cu>Se>Mn>Co. Sea trout consumption can provide a considerable portion of the RDA of copper, magnesium, phosphorus, calcium, iron, and zinc. The ranking order of the mean toxic element concentrations in sea trout muscle tissues was As>Pb>Cd>Hg. Potential risk estimated with the hazard quotient (HQ) indicated that most metals posed no health risk because they did not exceed reference doses at HQ < 1. For carcinogenic and non-carcinogenic effects, the maximum allowable rates of sea trout consumption were sufficiently high to ensure human health. According to these data, the consumption of farmed sea trout from the Baltic Sea in the northern region of Pomerania, Poland did not pose a risk to human health.

Exposure to heavy metals and lifestyle factors like smoking contribute to the production of free oxygen radicals. This fact, combined with a lowered total antioxidant status, can induce even more damage in the development of ankylosing spondylitis (AS). Despite the fact that some researchers are looking for more genetic factors underlying AS, most studies focus on polymorphisms within the genes encoding the human leukocyte antigen (HLA) system. The biggest challenge is finding the effective treatment of the disease. Genetic factors and the influence of oxidative stress, mineral metabolism disorders, microbiota, and tobacco smoking seem to be of great importance for the development of AS. The data contained in this review constitute valuable information and encourage the initiation and development of research in this area, showing connections between inflammatory disorders leading to the pathogenesis of AS and selected environmental and genetic factors. [ABSTRACT FROM AUTHOR]

Age-related macular degeneration (AMD) is a chronic disease, which often develops in older people, but this is not the rule. AMD pathogenesis changes include the anatomical and functional complex. As a result of damage, it occurs, in the retina and macula, among other areas. These changes may lead to partial or total loss of vision. This disease can occur in two clinical forms, i.e., dry (progression is slowly and gradually) and exudative (wet, progression is acute and severe), which usually started as dry form. A coexistence of both forms is possible. AMD etiology is not fully understood. Extensive genetic studies have shown that this disease is multifactorial and that genetic determinants, along with environmental and metabolic-functional factors, are important risk factors. This article reviews the impact of heavy metals, macro- and microelements, and genetic factors on the development of AMD. We present the current state of knowledge about the influence of environmental factors and genetic determinants on the progression of AMD in the confrontation with our own research conducted on the Polish population from Kuyavian-Pomeranian and Lubusz Regions. Our research is concentrated on showing how polluted environments of large agglomerations affects the development of AMD. In addition to confirming heavy metal accumulation, the growth of risk of acute phase factors and polymorphism in the genetic material in AMD development, it will also help in the detection of new markers of this disease. This will lead to a better understanding of the etiology of AMD and will help to establish prevention and early treatment. [ABSTRACT FROM AUTHOR]

Ageing is a natural ontogenetic phenomenon that entails a decrease in the adaptive capacity of the organism, as a result of which the body becomes less adaptable to stressful conditions. Nitrate and nitrite enter the body from exogenous sources and from nitrification of ammonia nitrogen by intestinal microorganisms. This review considers the mechanisms of action of l -arginine, a known inducer of nitric oxide (NO) biosynthesis, and nitrates as supplements in the processes of ageing and aggravated stress states, in which mechanisms of individual physiological reactivity play an important role. This approach can be used as an element of individual therapy or prevention of premature ageing processes depending on the different levels of initial reactivity of the functional systems. A search was performed of the PubMed, Scopus, and Google Scholar databases (n = 181 articles) and the author's own research (n = 4) up to May 5, 2023. The review presents analyses of data on targeted treatment of NO generation by supplementation with l -arginine or nitrates, which is a promising means for prevention of hypoxic conditions frequently accompanying pathological processes in an ageing organism. The review clarifies the role of the individual state of physiological reactivity, using the example of individuals with a high predominance of cholinergic regulatory mechanisms who already have a significant reserve of adaptive capacity. In studies of the predominance of adrenergic influences, a poorly trained organism as well as an elderly organism correspond to low resistance, which is an additional factor of damage at increased energy expenditure. Conclusion It is suggested that the role of NO synthesis from supplementation of dietary nitrates and nitrites increases with age rather than from oxygen-dependent biosynthetic reactions from l -arginine supplementation. [ABSTRACT FROM AUTHOR]

The most frequently isolated bacteria in Polish aquaculture are of the Aeromonas genus; also pathogenic to human fish consumers, they cause substantial economic losses, and require antibiotic therapy to treat. Antibiotic residues in animal-derived food provoke concern. The aim of the study was to appraise the antimicrobial activity of ethanolic extracts of Ficus plant species against Aeromonas strains.

Background/Aims: Important benefits of intermittent hypoxic training (IHT) have emerged as an effective tool for enhancing adaptive potential in different pathological states, among which acute hypoxia dominates. Therefore, the aim of our study was to evaluate the mechanisms related to the effects of the nitric oxide system (nitrites, nitrates, carbamide, and total polyamine content) on ADP-stimulated oxygen consumption and oxidative phosphorylation in heart and liver mitochondria and biomarkers of oxidative stress in the blood, heart, and liver of rats exposed to the IHT method and acute hypoxia and treated with the amino acid L-arginine (600 mg/kg, 30 min) or the NO synthase inhibitor L-NNA (35 mg/kg, 30 min) prior to each IHT session. Methods: We analysed the modulation of the system of oxygendependent processes (mitochondrial respiration with the oxygraphic method, microsomal oxidation, and lipoperoxidation processes using biochemical methods) in tissues during IHT in the formation of short-term and long-term effects (30, 60, and 180 days after the last IHT session) with simultaneous administration of L-arginine. In particular, we investigated how mitochondrial functions are modulated during intermittent hypoxia with the use of oxidation substrates (succinate or α-ketoglutarate) in bioenergetic mechanisms of cellular stability and adaptation. Results: The IHT method is associated with a significant increase in the production of endogenous nitric oxide measured by the levels of its stable metabolite, nitrite anion, in both plasma (almost 7-fold) and erythrocytes (more than 7-fold) of rats. The intensification of in the heart and liver, accompanied by oscillatory mechanisms of adaptation in the interval mode, causes a probable decrease in the production of urea and polyamines in plasma and liver, but not in erythrocytes. The administration of L-arginine prior to the IHT sessions increased the level of the nitrite-reducing component of the nitric oxide cycle, which persisted for up to 180 days of the experiment. Conclusions: Thus, the efficacy of IHT and its nitritedependent component shown in this study is associated with the formation of long-term adaptive responses by preventing the intensification of lipoperoxidation processes in tissues due to pronounced changes in the main enzymes of antioxidant defence and stabilisation of erythrocyte membranes, which has a pronounced protective effect on the system of regulation of oxygen-dependent processes as a whole. [ABSTRACT FROM AUTHOR]

Anti-ageing biology and medicine programmes are a focus of genetics, molecular biology, immunology, endocrinology, nutrition, and therapy. This paper discusses metabolic therapies aimed at prolonging longevity and/or health. Individual components of these effects are postulated to be related to the energy supply by tricarboxylic acid (TCA) cycle intermediates and free radical production processes. This article presents several theories of ageing and clinical descriptions of the top markers of ageing, which define ageing in different categories; additionally, their interactions with age-related changes and diseases related to α-ketoglutarate (AKG) and succinate SC formation and metabolism in pathological states are explained. This review describes convincingly the differences in the mitochondrial characteristics of energy metabolism in animals, with different levels (high and low) of physiological reactivity of functional systems related to the state of different regulatory systems providing oxygen-dependent processes. Much attention is given to the crucial role of AKG and SC in the energy metabolism in cells related to amino acid synthesis, epigenetic regulation, cell stemness, and differentiation, as well as metabolism associated with the development of pathological conditions and, in particular, cancer cells. Another goal was to address the issue of ageing in terms of individual characteristics related to physiological reactivity. This review also demonstrated the role of the Krebs cycle as a key component of cellular energy and ageing, which is closely associated with the development of various age-related pathologies, such as cancer, type 2 diabetes, and cardiovascular or neurodegenerative diseases where the mTOR pathway plays a key role. This article provides postulates of postischaemic phenomena in an ageing organism and demonstrates the dependence of accelerated ageing and age-related pathology on the levels of AKG and SC in studies on different species (roundworm Caenorhabditis elegans, Drosophila, mice, and humans used as models). The findings suggest that this approach may also be useful to show that Krebs cycle metabolites may be involved in age-related abnormalities of the mitochondrial metabolism and may thus induce epigenetic reprogramming that contributes to the senile phenotype and degenerative diseases. The metabolism of these compounds is particularly important when considering ageing mechanisms connected with different levels of initial physiological reactivity and able to initiate individual programmed ageing, depending on the intensity of oxygen consumption, metabolic peculiarities, and behavioural reactions. [ABSTRACT FROM AUTHOR]

High-altitude intolerance and consequently high-altitude sickness, is difficult to predict. Liver is an essential organ in glucose and lipid metabolism, and may play key role in the adaptation to high altitude. In response to extreme high altitude, mitochondrial respiration exhibits changes in substrate metabolism, mitochondrial electron transport chain activity, and respiratory coupling. We determined the cobalt chloride (Co[Cl.sub.2]) effects on liver mitochondrial plasticity and oxygen uptake in rats with low resistance (LR) and high resistance (HR) to extreme hypobaric hypoxia. The polarographic method proposed by Chance and Williams was used as a simple and effective tool to trace mitochondrial functionality and oxygen consumption. HR rats had more efficient processes of NADH- and FAD-generated mitochondrial oxidation. Co[Cl.sub.2] promoted more efficient NADH-generated and diminished less efficient FAD-generated mitochondrial respiratory reactions in HR rats. Co[Cl.sub.2] diminished both aerobic and anaerobic processes in LR rats. Glutamate and pyruvate substrates of NADH-generated mitochondrial pathways were highly affected by Co[Cl.sub.2]. Red blood cells acted as cobalt depots in HR and LR rats. We have unveiled several mechanisms leading to differentiated mitochondrial respiratory responses to hypobaric hypoxia in LR and HR rats. Our study strongly supports the existence of adaptive liver mitochondrial plasticity to extreme hypoxia. Key words: hypobaric hypoxia, cobalt chloride, liver mitochondrial respiration, oxidative phosphorylation, anaerobic metabolic pathways. L'intolerance aux hautes altitudes, et consecutivement le mal des montagnes est difficile a predire. Or, le foie est un organe essentiel au metabolisme du glucose et des lipides, et il pourrait jouer un role cle dans l'adaptation aux hautes altitudes. En reaction aux hautes altitudes extremes, la respiration mitochondriale presente des variations dans le metabolisme des substrats, l'activite de la chaine de transport des electrons et le couplage de la respiration. Nous avons etabli les effets du chlorure de cobalt (Co[Cl.sub.2]) sur la plasticite mitochondriale hepatique et la captation de l'oxygene chez des rats presentant une resistance basse (RB) ou elevee (RE) a l'hypoxie hypobare extreme. Nous avons suivi le fonctionnement des mitochondries et la consommation d'oxygene a l'aide de la methode simple et efficace de polarographie mise de l'avant par Chance et Williams. Les rats RE disposaient de processus plus efficaces pour l'oxydation mitochondriale engendree par le NADH et le FAD. Chez les rats HR, le Co[Cl.sub.2] entrainait une amplification des reactions de respiration mitochondriale plus efficaces obtenues avec le NADH et une attenuation des reactions de respiration moins efficaces obtenues avec le FAD. Chez les rats RB, le Co[Cl.sub.2] entrainait une diminution des processus aerobies comme anaerobies. Les substrats glutamate et pyruvate des voies de signalisation mitochondriales portees par le NADH etaient tres affectes par le Co[Cl.sub.2]. Les globules rouges servaient de depots de cobalt chez les rats RE comme RB. Nous avons releve plusieurs modes d'action menant a des reactions differentielles de la respiration mitochondriale a l'hypoxie hypobare chez les rats RE et RB. Notre etude appuie fortement l'existence d'une plasticite mitochondriale hepatique adaptative dans l'hypoxie extreme. [Traduit par la Redaction] Mots-cles : hypoxie hypobare, chlorure de cobalt, respiration mitochondriale hepatique, phosphorylation oxydative, voies metaboliques anaerobies., Introduction In 2018, 2 rescuers from Polish K2 Winter Expedition 2018, Denis Urubko and Adam Bielecki, climbed more than 1000 m up Nanga Parbat, the ninth highest mountain in the [...]

Background/Aims: Currently, it is proven that the cellular metabolism of nitric oxide is necessary to maintain optimal health and adaptation of the organism to the impact of various environmental factors. The aim of this work was to reveal the biological role of nitric oxide, its metabolic changes, and its mechanism of action in tissues under hypoxia, as well as the possibility of tissue metabolism correction through NO-dependent systems under the influence of Krebs cycle intermediates. Methods: A systematic assessment of the effect of succinate (SC, 50 mg/kg b.w.) and α-ketoglutarate (KGL, 50 mg/kg b.w.) in the regulation of oxygen-dependent processes in rats (mitochondrial oxidative phosphorylation, microsomal oxidation, intensity of lipid peroxidation processes, and the state of the antioxidant defense system) depending on functional changes in nitric oxide production during hypoxia was evaluated. The state of the nitric oxide system was estimated spectrophotometrically by determination of the concentration of its stable nitrite anion metabolite (NO2-). The levels of catecholamines were estimated from the content of epinephrine and norepinephrine using the differentially fluorescent method. The activity of cytochrome P450-dependent aminopyrine-N-demethylase was determined with the Nash reagent. Results: Tissue hypoxia and metabolic disorders caused by this condition through changes in the content of catecholamines (epinephrine, norepinephrine, dopamine, DOPA) as well as the cholinesterase-related system (acetylcholine content and acetylcholinesterase activity) were the studied experimental parameters under acute hypoxia (AH, 7% O2 in N2, 30 min). The activation of lipid peroxidation and oxidatively modified proteins and an increase in the epinephrine content in AH are associated with an increased role of SC and a decrease in KGL as substrates of oxidation in mitochondria. A more pronounced effect of exogenous KGL, compared to SC, on the content of nitrite anion as a stable metabolite of nitric oxide in the liver under acute hypoxia against the background of a decrease in the intensity of lipid peroxidation processes was revealed. The activation of SC-dependent mitochondrial oxidative processes caused by AH was found to decrease in animals after an intermittent hypoxia training (IHT) course. IHT (7% O2 in N2, 15-min, 5 times daily, 14 days) prevented the activation of oxidative stress in tissues and blood after the AH impact and increased the efficiency of energy-related reactions in the functioning of hepatic mitochondria through increased oxidation of KGL. Conclusion: The studied effects of adaptation are mediated by an increase in the role of NO-dependent mechanisms, as assessed by changes in the pool of nitrates, nitrites, carbamides, and total polyamines. [ABSTRACT FROM AUTHOR]

Oxidative stress is involved in the development of various cancers. In the present study, the effect of long-term administration of peroral antidiabetic metformin and pineal hormone melatonin on liver antioxidant and aerobic status in female Sprague-Dawley rats carrying mammary tumors induced by N-methyl-N-nitrosourea was evaluated. Both substances were administered in a preventive and curative manner (12 days before and 16 weeks after the carcinogen application). Carcinogen administration induced oxidative stress: the level of thiobarbituric acid reactive substances (TBARS) considered as a marker of reactive oxygen species (ROS) generation in liver increased as well as the level of oxidatively modified protein content (OMP; aldehyde and ketone derivates). Metformin administration restored succinate dehydrogenase and lactate dehydrogenase activity and associated ROS production and OMP content to the level of intact rats, with predominant activation of superoxide dismutase (SOD) and glutathione reductase (GR). Melatonin alone and in combination with metformin also decreased TBARS content. OMP content decreased in all groups receiving chemoprevention. The rise in total antioxidant capacity after melatonin and particularly metformin and melatonin combination might result from the initiation of anaerobic metabolism and increasing SOD, GR, and glutathione peroxidase activity. Long-term administration of metformin and melatonin exerts antioxidant properties in liver, especially in combination. Key words: metformin, melatonin, liver, high-fat diet, oxidative stress, mammary carcinogenesis. Le stress oxydatif joue un role dans le developpement de divers cancers. Dans la presente etude, nous avons evalue l'effet de l'administration a long terme de metformine (un antidiabetique peroral) et de melatonine (une hormone pineale) sur l'etat d'antioxydation et aerobie du foie chez des rates Sprague-Dawley porteuses de tumeurs mammaires engendrees a l'aide de N-methyl-N-nitrosouree. Les deux substances etaient administrees a visees preventive et curative (12 jours avant et 16 semaines apres l'exposition au carcinogene). L'administration du carcinogene engendrait un stress oxydatif : dans le foie, le taux de substances reagissant a l'acide thiobarbiturique (TBARS pour << thiobarbituric acid reactive substances >>) considerees comme etant un marqueur de la formation de derives reactifs de l'oxygene (ROS pour<>) augmentait tout comme le taux de proteines ayant subi des modifications oxydatives (OMP pour<< oxidatively modified proteins>>: derives aldehydes et cetones). L'administration de metformine permettait de retablir l'activite de la succinate deshydrogenase et de la lactate deshydrogenase, ainsi que la production de ROS associee et les taux d'OMP au niveau de chez des rates intactes, avec l'activation predominante de la superoxyde dismutase (SOD) et de la glutathion reductase (GR). Seule ou en association avec la metformine, la melatonine entramait aussi une diminution des taux de TBARS. Les taux d'OMP s'abaissaient dans tous les groupes recevant une prevention chimiotherapeutique. La hausse de la capacite antioxydante totale apres l'administration de melatonine, et tout particulierement de son association avec la metformine, pourrait provenir de l'entrainement du metabolisme anaerobie et de l'augmentation de l'activite de la SOD, de la GR et de la glutathion peroxydase. L'administration a long terme de metformine et de melatonine exerce des proprietes antioxydantes dans le foie, particulierement en association l'une avec l'autre. [Traduit par la Redaction] Mots-cles: metformine, melatonine, foie, regime alimentaire a teneur elevee en matieres grasses, stress oxydatif, carcinogenese mammaire., Introduction Breast cancer is the most common malignancy globally (Fitzmaurice et al. 2015) and in Europe accounts for 13.5% of all cancer cases (Ferlay et al. 2013). Among many factors, [...]