Levels Of Lipid Peroxidation Products Research Articles

Pathogenetic role of a number of factors in the development and progression of preeclampsia with varying severity in pregnant women.

Context Preeclampsia is a common pregnancy complication, posing significant risks to both the mother and fetus. Predicting and determining the risks of this disease is crucial. Aims This research aims to understand the pathogenetic role of several factors in the development and progression of preeclampsia, particularly in relation to its severity in pregnant patients. Methods The study included 60 pregnant women diagnosed with either mild or severe preeclampsia and 40 healthy pregnant women for comparison. Blood plasma was analysed using biochemical methods, and blood microcirculation parameters were determined to identify homeostatic abnormalities in early preeclampsia. Key results A molecular genetic study revealed the frequency of the endothelial nitric oxide gene eNOSC774T . Homeostatic abnormalities were statistically correlated with polymorphic genotypes of the eNOSC774T gene. Conclusions The research found a correlation between the T774T eNOS genotype mutation and the severity of preeclampsia, alongside significant homeostasis abnormalities in patients. Implications The T774T mutant genotype of the eNOS gene and higher levels of lipid peroxidation products are strongly linked to the severity and progression of preeclampsia. This highlights a significant connection between genetic predisposition and biochemical abnormalities in the disease's development.

Oxidative processes in the immunocompetent organs of pink salmon Oncorhynchus gorbuscha and chum salmon Oncorhynchus keta (Salmonidae) during the marine period

The influence of various factors on the fish body is reflected in changes in metabolic processes, including an imbalance of redox processes. The study of the level of oxidative processes and antioxidant protection in the tissues of aquatic organisms is often used in ecological and ecologicaltoxicological studies to assess the environmental conditions. Obtaining such data when conducting comprehensive ichthyological studies makes it possible to assess the features of adaptation to various habitat conditions, as well as the health status of fish. Mature pink salmon Onchorhynchus gorbuscha and chum salmon O. keta were caught in the summer of 2018 in the open waters of the northwestern Pacific Ocean (east of the Kuril Ridge) using a mid-water trawl during a trawl survey. Immediately after catching, liver, kidney and spleen samples were taken from the fish. Test tubes with organ tissue samples were frozen at –20 °С. Homogenates were prepared from thawed organ samples under laboratory conditions. The level of lipid peroxidation products and antioxidant activity was evaluated. As a result, intertissue and interspecific similarities and differences in the studied parameters of pink salmon and chum salmon during the marine period of life were established. The detected differences in indicators are presumably related to the structural and functional organization of the tissues and organs studied, as well as species characteristics. The results can be used to monitor population health and compare with closely related species.

Green tea supplementation prevented oxidative stress, fibrosis, and myocardial damage in isoproterenol-induced Swiss albino mice

IntroductionOne of the main causes of death and morbidity in people with cardiovascular disorders is myocardial infarction. This study investigated the impact of green tea (GT) leaf powder on isoproterenol (ISO)-induced myocardial infarction in Swiss albino mice. Methods and materials4 to 5 weeks male Swiss albino mice were divided into four groups with 6 mice in every group: Control, ISO, Control + GT and ISO+ GT leaves powder. All of the mice were sacrificed at the end of the investigation. Heart organ and blood plasma samples were taken, and they were tested for oxidative stress indicators and several biochemical parameters. To investigate the formation of mononuclear cells and fibrosis in the heart histopathological staining of tissue sections was also carried out. ResultsIn this experiment, supplementation with green tea leaf powder in ISO-administered mice prevented the increased activity of the AST, ALT, and ALP enzymes. Additionally, three more tests were performed such as CK-MB, Creatinine, and Uric acid whose levels were increased by isoproterenol, and treatment of green tea reduced these elevated levels. Due to the supplementation of green tea leaf powder, ISO-administered mice had lower levels of lipid peroxidation product, nitric oxide, advanced protein oxidation product, and myeloperoxidase. Mice exposed to ISO had considerably higher levels of oxidative stress markers and lower levels of cellular antioxidants including catalase activity, SOD activity, and reduced glutathione concentration. Additionally, the heart of ISO-induced mice revealed substantial fibrosis and inflammatory cell infiltration. Furthermore, green tea leaf powder supplementation prevented inflammatory cell infiltration and fibrosis in ISO-administered mice. ConclusionIn conclusion, the findings imply that supplementing with green tea leaf powder might lower the risk of myocardial infarction in mice given ISO, potentially by reducing oxidative stress, inflammation, and fibrosis.

The influence of “Butaintersyl” on the antioxidant status of rats under conditions of toxic damage caused by tetrachloromethane

Tetrachloromethane (CCl4) is a toxic chemical substance known in scientific research as a model for studying the damage of parenchymal liver cells. The mechanisms of CCl4 toxicity include the activation of lipid peroxidation processes, the intensive formation of free radicals, and, as a result, the disruption of the pro-/antioxidant balance. This work aimed to study the effect of the liposomal drug “Butaintersyl” on the activity of the glutathione antioxidant protection system and the intensity of lipid peroxidation processes in the blood of rats under conditions of toxic damage caused by tetrachloromethane. The studies were conducted on white sexually mature young Wistar rats weighing 180–200 g, kept in the institute's vivarium of the State Scientific Research Control Institute of Veterinary Drugs and Feed Additives. In the blood of the rats, changes in the activity of glutathione peroxidase and the level of reduced glutathione were studied, as well as the levels of lipid peroxidation products: lipid hydroperoxides and TBA-active products. The development of oxidative stress in the first experimental group of rats was accompanied by the suppression of the glutathione antioxidant protection system, as evidenced by a decrease in blood glutathione peroxidase activity and the level of reduced glutathione. At the same time, the intoxicated animals showed an increase in lipid peroxidation processes, namely an increase in the blood levels of lipid hydroperoxides and TBA-active products throughout the study period. The studies showed that in cases of poisoning of various origins, it is advisable to use drugs that reduce the formation of reactive oxygen species and lipoperoxidation processes, exhibit antioxidant effects, and stabilize cell membranes. A special place among such drugs is occupied by the liposomal drug “Butaintersyl”. This drug ensures the stabilization of biological membranes. The liposomal drug “Butaintersyl” contributed to suppressing lipid peroxidation processes and activating the antioxidant protection system, as evidenced by the high content of reduced glutathione and glutathione peroxidase activity. Due to its antioxidant properties, the drug positively affected the activity of membrane-dependent enzymes. It reduced the level of endogenous intoxication, allowing it to be recommended for inclusion in prevention schemes for toxic liver damage caused by chemical compounds.

Knockdown of NADK promotes LUAD ferroptosis via NADPH/FSP1 axis

BackgroundLung cancer is a serious threat to human health and is the first leading cause of cancer death. Ferroptosis, a newly discovered form of programmed cell death associated with redox homeostasis, is of particular interest in the lung cancer, given the high oxygen environment of lung cancer. NADPH has reducing properties and therefore holds the potential to resist ferroptosis. Resistance to ferroptosis exists in lung cancer, but the role of NADK in regulating ferroptosis in lung cancer has not been reported yet.MethodsImmunohistochemistry (IHC) was used to analyse the expression of NADK in 86 cases of lung adenocarcinoma(LUAD) and adjacent tissues, and a IHC score was assigned to each sample. Chi-square and kaplan-meier curve was performed to analyse the differences in metastasis and five-year survival between the two groups with NADK high or low scores. Proliferation of NADK-knockdown LUAD cell lines was detected in vivo and vitro. Furthermore, leves of ROS, MDA and Fe2+ were measured to validate the effect and mechanism of NADK on ferroptosis in LUAD.ResultsThe expression of NADK was significantly evaluated in LUAD tissues as compared to adjacent non-cancerous tissues. The proliferation of NADK-knockdown cells was inhibited both in vivo and vitro, and increasing levels of intracellular ROS, Fe2+ and lipid peroxide products (MDA) were observed. Furthermore, NADK-knockdown promoted the ferroptosis of LUAD cells induced by Erastin/RSL3 by regulating the level of NADPH and the expression of FSP1. Knockdown of NADK enhanced the sensitivities of LUAD cells to Erastin/RSL3-induced ferroptosis by regulating NADPH level and FSP1 expression.ConclusionsNADK is over-expressed in LUAD patients. Knockdown of NADK inhibited the proliferation of LUAD cells both in vitro and in vivo and promotes the Erastin/RSL3-induced ferroptosis of LUAD cells by down-regulating the NADPH/FSP1 axis.

Saliva as a Diagnostic Tool for Early Detection of Exercise-Induced Oxidative Damage in Female Athletes.

Although blood still remains the most commonly utilized medium to detect increased levels of oxidative damage induced by exercise, saliva diagnostics have gained increasing popularity due to their non-invasive nature and athlete-friendly collection process. Given that the contribution of various phases of the menstrual cycle to the levels of oxidative damage may differ, the aim of this study was to evaluate an agreement between salivary and plasmatic levels of lipid peroxidation products in female swimmers in both the follicular (F) and luteal (L) phases of the menstrual cycle at rest and following exercise. Twelve well-trained female swimmers aged 19.6 ± 1.1 years old were examined. We measured diene conjugates (DCs), triene conjugates (TCs), and Schiff bases (SBs) in lipids immediately after their extraction from both saliva and blood plasma. All female swimmers were studied two times each, in the two different phases of one menstrual cycle, before and after high-intensity interval exercise (HIIE). Salivary and plasmatic levels of DCs, TCs, and SBs significantly increased post-exercise compared to pre-exercise, in both the F and L phases. A high positive correlation was observed between the concentrations of DCs, TCs, and SBs in the saliva and blood plasma of participants in the F and L phases, both at rest and following HIIE. Ordinary least products regression analysis indicates that there was no proportional and differential bias in the data. The Bland-Altman method also declares that there was no differential bias, since the line of equality was within the 95% confidence interval of the mean difference between salivary and plasmatic levels of DCs, TCs, and SBs in female swimmers, in both the F and L phases, before and after HIIE. There was also no proportional bias in the Bland-Altman plots. Thus, this is the first study to report a high agreement between the quantifications of DCs, TCs, and SBs in the saliva and blood plasma of female swimmers in both the F and L phases, at rest and following HIIE.

Lipid Peroxidation, Reduced Glutathione, and Glutathione Peroxidase Levels in Intervertebral Discs of Patients with Lumbar Degenerative Disc Disease.

BACKGROUND Either a reduction in antioxidant levels or an accumulation of reactive oxygen species can heighten susceptibility to oxidative damage in disc cells. To date, no research has investigated the levels of lipid peroxidation products (thiobarbituric acid reactive substances [TBARs]), reduced glutathione (GSH), and glutathione peroxidase (GPx) in excised human lumbar disc tissues affected by degenerative disease. Therefore, this study aimed to evaluate lipid peroxidation products in excised disc tissues from patients with degenerative disc disease. MATERIAL AND METHODS Forty-two patients were enrolled. Patients were divided into lumbar disc degeneration (LDD) and nonlumbar disc degeneration (nonLDD) groups according to Pfirrmann classification. Intervertebral discs were obtained from all patients during the operation and were homogenized for analysis. TBARs levels were measured using fluorometry. GSH levels and GPx activity were quantified spectrophotometrically using a kinetic method. RESULTS TBARs levels in excised discs from LDD patients (5.18±4.14) were significantly higher than those from nonLDD patients (2.56±1.23, P=0.008). The levels of TBARs tended to increase with the severity of degeneration according to the Pfirrmann classification. However, these 2 groups showed no significant differences in reduced glutathione levels or glutathione peroxidase activity (P>0.05). Patients with LDD exhibited a worse health-related quality of life, reflected in lower utility and EQ-VAS scores and higher Oswestry disability index scores. CONCLUSIONS There was a notable increase in lipid peroxidation products in the excised intervertebral discs of patients with LDD. This finding suggests that oxidative stress may contribute to the development of disc degeneration.

Improvement of high-density lipoprotein atheroprotective properties in patients with systemic lupus erythematosus after belimumab treatment.

Chronic inflammatory diseases, like Systemic Lupus Erythematosus (SLE), carry an increased risk for atherosclerosis and cardiovascular events, accompanied by impairment of atheroprotective properties of high-density lipoprotein (HDL). In SLE, serum BAFF (B cell-activating factor), a cytokine implicated in disease progression, has been correlated with subclinical atherosclerosis. We investigated the impact of treatment with belimumab -an anti-BAFF monoclonal antibody- on HDL atheroprotective properties and composition in SLE patients. Serum samples were collected from 35 SLE patients with active disease despite conventional therapy, before and after 6-month add-on treatment with belimumab, and 26 matched healthy individuals. We measured cholesterol efflux and antioxidant capacities, paraoxonase-1 activity, serum amyloid A1, myeloperoxidase and lipid peroxidation product levels of HDL. LC-MS/MS was performed to analyze the HDL lipidome. Following treatment with belimumab, cholesterol efflux and antioxidant capacities of HDL were significantly increased in SLE patients and restored to levels of controls. HDL-associated paraoxonase-1 activity was also increased, whereas lipid peroxidation products were decreased following treatment. HDL cholesterol efflux and antioxidant capacities correlated negatively with the disease activity. Changes were noted in the HDL lipidome of SLE patients following belimumab treatment, as well as between SLE patients and healthy individuals, and specific changes in lipid species correlated with functional parameters of HDL. HDL of SLE patients with active disease displays impaired atheroprotective properties accompanied by distinct lipidomic signature compared with controls. Belimumab treatment may improve the HDL atheroprotective properties and modify the HDL lipidomic signature in SLE patients, thus potentially mitigating atherosclerosis development.

Salivary lipid changes in young adult tobacco smokers and e-cigarette users: a hidden risk to oral health?

A cross-sectional, age- and gender-matched study was conducted to investigate the effects of different forms of nicotine delivery on salivary lipid profiles among young adult novice smokers compared to non-smokers. To assess the effect of smoking traditional cigarettes, e-cigarettes, and heated tobacco products (HTPs) on the levels of specific sphingolipids (sphingosine, sphinganine, and sphingosine-1-phosphate), various ceramides, and lipid peroxidation products [malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE)] in both unstimulated and stimulated saliva samples collected from healthy young adults who had been smoking for 1-3 years and used only 1 of the 3 nicotine delivering methods. Selection criteria included healthy young adults under 30 years old, with normal BMI and typical diet composition, and with no oral inflammatory lesions, orthodontic/dental appliances, or recent intake of medications or supplements. A total of 75 smokers and 25 non-smokers were enrolled in the study. Smokers were categorized into three groups, each comprising 25 individuals: traditional cigarette smokers, e-cigarette users, and HTPs smokers. Saliva samples were collected and analyzed for sphingolipid concentrations using ultra-high-performance liquid chromatography-tandem mass spectrometry. The concentrations of MDA and 4-HNE were measured using colorimetric and ELISA assays, respectively. The average smoking intensity inthe traditional cigarette group was 10 cigarettes per day. Salivary sphingolipid and ceramides concentrations were significantly lower in smokers compared to non-smokers across all nicotine delivery methods (p < 0.0001). Moreover, traditional cigarette smokers exhibited higher levels of 4-HNE and MDA in both stimulated and unstimulated saliva, compared to non-smokers (p < 0.01). In stimulated saliva, both MDA and 4-HNE in e-cigarette users, and MDA in HTPs users, showed significantly lower concentrations than their comparators in traditional cigarette smokers (p < 0.01). Different nicotine delivery methods impact salivary lipid profile during the initial period of smoking habit. Reduced sphingolipids and elevated lipid peroxidation products suggest a disturbed lipid balance in the oral cavity due to enhanced oxidative stress within the salivary glands of novice smokers.

Ameliorative Effect of Cinnamon and Rosemary Oils in Acrylamide–Induced Hepatic Injury in Rats

Liver diseases can result from various causes, such as viruses, bacteria, autoimmune disorders, or certain medications and toxic substances. While modern medicine offers treatments for these conditions, there needs to be more effective drugs that can protect and regenerate liver cells. Therefore, it is crucial to identify new treatment options and liver-protective agents that are both highly efficient and safe. This study is assigned to investigate the adverse effects of acrylamide on the liver in rats and explore whether these effects can be mitigated by co-administration of cinnamon oil (C.O.), rosemary oil (R.O.), or a combination of both oils during acrylamide exposure. A total of 70 male albino rats were divided randomly into 7 groups, each group of 10 rats, that received different treatments: control group, acrylamide-treated group (20 mg/kg b.wt), cinnamon oil-treated group (200 mg/kg b.wt), rosemary oil-treated group (250 mg/kg b.wt), acrylamide and cinnamon oil-treated group, acrylamide and rosemary oil-treated group, and acrylamide, cinnamon oil, and rosemary oil-treated group. These treatments were administered orally for 28 consecutive days. Blood and liver tissue samples were gathered at the end of the study to assess the outcomes. The results revealed that cinnamon oil and rosemary oils exhibited hepatoprotective effects, as evidenced by normalized liver function parameters (alanine transaminase, Aspartate transaminase, and Alkaline phosphatase), as well as improvements in nonenzymatic parameters (total protein, albumin, cholesterol, triglyceride, low-density lipoprotein, and high-density lipoprotein). The observed hepatoprotection of cinnamon oil and rosemary oils was attributed to their ability to reduce oxidative stress caused by acrylamide, as demonstrated by lower levels of liver cell lipid peroxidation product (malondialdehyde) and enhanced activity of antioxidative enzymes (glutathione and catalase) in liver tissue. Keywords: Cinnamon, Rosemary, Acrylamide, Liver, Rats, Antioxidants.

Ameliorative Effect of Cinnamon and Rosemary Oils in Acrylamide–Induced Hepatic Injury in Rats

Liver diseases can result from various causes, such as viruses, bacteria, autoimmune disorders, or certain medications and toxic substances. While modern medicine offers treatments for these conditions, there needs to be more effective drugs that can protect and regenerate liver cells. Therefore, it is crucial to identify new treatment options and liver-protective agents that are both highly efficient and safe. This study is assigned to investigate the adverse effects of acrylamide on the liver in rats and explore whether these effects can be mitigated by co-administration of cinnamon oil (C.O.), rosemary oil (R.O.), or a combination of both oils during acrylamide exposure. A total of 70 male albino rats were divided randomly into 7 groups, each group of 10 rats, that received different treatments: control group, acrylamide-treated group (20 mg/kg b.wt), cinnamon oil-treated group (200 mg/kg b.wt), rosemary oil-treated group (250 mg/kg b.wt), acrylamide and cinnamon oil-treated group, acrylamide and rosemary oil-treated group, and acrylamide, cinnamon oil, and Rosemary oil-treated group. These treatments were administered orally for 28 consecutive days. Blood and liver tissue samples were gathered at the end of the study to assess the outcomes. The results revealed that cinnamon oil and rosemary oils exhibited hepatoprotective effects, as evidenced by normalized liver function parameters (alanine transaminase, Aspartate transaminase, and Alkaline phosphatase), as well as improvements in nonenzymatic parameters (total protein, albumin, cholesterol, triglyceride, low-density lipoprotein, and high-density lipoprotein). The observed hepatoprotection of cinnamon oil and rosemary oils was attributed to their ability to reduce oxidative stress caused by acrylamide, as demonstrated by lower levels of liver cell lipid peroxidation product (malondialdehyde) and enhanced activity of antioxidative enzymes (glutathione and catalase) in liver tissue. Keywords: Cinnamon, Rosemary, Acrylamide, Liver, Rats, Antioxidants

Tick-borne encephalitis virus transmitted singly and in duo with Borrelia burgdorferi sensu lato and Anaplasma phagocytophilum bacteria by ticks as pathogens modifying lipid metabolism in human blood

BackgroundTicks are vectors of various pathogens, including tick-borne encephalitis virus causing TBE and bacteria such as Borrelia burgdorferi sensu lato and Anaplasma phagocytophilum causing e.g. viral-bacterial co-infections (TBE + LB/HGA), which pose diagnostic and therapeutic problems. Since these infections are usually accompanied by inflammation and oxidative stress causing metabolic modifications, including phospholipids, the aim of the study was to assess the level of polyunsaturated fatty acids and their metabolism (ROS- and enzyme-dependent) products in the blood plasma of patients with TBE and TBE + LB/HGA before and after pharmacotherapy.MethodsThe total antioxidant status was determined using 2,20-azino-bis-3-ethylbenzothiazolin-6-sulfonic acid. The phospholipid and free fatty acids were analysed by gas chromatography. Lipid peroxidation was estimated by measuring small molecular weight reactive aldehyde, malondialdehyde and neuroprostanes. The reactive aldehyde was determined using gas chromatography coupled with mass spectrometry. The activity of enzymes was examined spectrophotometrically. An analysis of endocannabinoids and eicosanoids was performed using a Shimadzu UPLC system coupled with an electrospray ionization source to a Shimadzu 8060 Triple Quadrupole system. Receptor expression was measured using an enzyme-linked immunosorbent assay (ELISA).ResultsThe reduced antioxidant status as a result of infection was accompanied by a decrease in the level of phospholipid arachidonic acid (AA) and docosahexaenoic acid (DHA) in TBE, an increase in DHA in co-infection and in free DHA in TBE with an increase in the level of lipid peroxidation products. The enhanced activity of enzymes metabolizing phospholipids and free PUFAs increased the level of endocannabinoids and eicosanoids, while decreased 15-PGJ2 and PGE2 was accompanied by activation of granulocyte receptors before pharmacotherapy and only tending to normalize after treatment.ConclusionSince classical pharmacotherapy does not prevent disorders of phospholipid metabolism, the need to support treatment with antioxidants may be suggested.

MicroRNA expression and oxidative stress markers in pectoral muscle of broiler chickens fed diets supplemented with phytobiotics composition

Phytobiotic compositions are commercially used in broiler production, mostly to improve general health and the production parameters. Moreover, some of their active substances may change the expression of miRNA in different tissues. Therefore, the purpose of this study was to evaluate the effect of the phytobiotic composition (PBC) containing white mustard, calamus, turmeric, and common ivy on production parameters, oxidative stress markers and expression of selected miRNAs in pectoral muscle of broiler chickens. The experiment was performed on broiler chickens fed the control diet (without PBC), and a diet supplemented with 60 or 100 mg/kg of PBC for 35 days. After the experiment, samples (blood and muscle) were collected for analyses. The analyzed production parameters included: feed conversion ratio, feed intake and body weight. There was no effect on growth performance of broiler chickens but feeding diet supplemented with 60 mg/kg phytobiotics significantly increased the expression of miR-30a-5p, miR-181a-5p, and miR-206, and decreased that of miR-99a-5p, miR-133a-5p, miR-142-5p, and miR-222 in pectoral muscle of chickens. The addition of 100 mg/kg phytobiotics significantly increased miR-99a-5p and miR-181a-5p expression, and caused down-regulation of the expression of miR-26a-5p and miR-30a-5p. Chickens fed diet supplemented with 100 mg/kg PBC had lower level of lipid peroxidation products in blood, while in the muscle tissue it was higher in birds fed a diet with the addition of 60 mg/kg as compared to the control group. The results suggest that this unique composition of phytobiotics does not affect productive traits but can change expression of miRNAs that are crucial for muscle physiology and pathology in broiler chickens. This additive may also protect against the oxidative stress but the effect is dose dependent.

Parvalbumin Interneuron Disorders Triggered by Oxidative Stress as a Common Mechanism Causing Schizophrenia in the Elderly: a Literature Review Study

Schizophrenia is a functional psychotic disorder with the main disturbance of the thought process and the disintegration of the thought process, affect or emotion, volition and psychomotor accompanied by a distortion of reality, especially due to delusions and hallucinations, fragmented associations resulting in incoherence, inadequate affect and emotion, and psychomotor which shows withdrawal, ambivalence and bizzare behavior. The research design used is the literature review method. Literature study is research carried out by researchers by collecting a number of articles or journals related to research problems and objectives. The study results show that various literature shows evidence that schizophrenia in the elderly occurs due to changes in antioxidant enzymes in schizophrenia. Increased levels of lipid peroxidation products and nitric oxide (NO) occurred in schizophrenia, while superoxide dismutase activity was found to decrease significantly in this disorder, but glutathione peroxidase and catalase activity had no effect in schizophrenia patients. In schizophrenic patients, it was found that there was an increase in the production of free radicals, therefore the administration of anti-oxidants is necessary to increase antioxidants which can reduce symptoms in schizophrenic patients.

Modifications of DAMPs levels in extracellular environment induced by aminolevulinic acid-based photodynamic therapy of esophageal cancer cells

Purpose Immunogenic cell death plays an important role in anticancer treatment because it combines cell death with appearance of damage associated molecular patterns that have the potential to activate anticancer immunity. Effects of damage associated molecular patterns induced by aminolevulinic acid-based photodynamic therapy were studied mainly on dendritic cells. They have not been deeply studied on macrophages that constitute the essential component of the tumor microenvironment. The aim of this study was to analyze features of esophageal cancer cell death in relation to release capacity of damage associated molecular pattern species, and to test the effect of related extracellular environmental alterations on macrophages. Material and methods Esophageal Kyse 450 carcinoma cells were subjected to aminolevulinic acid-based photodynamic therapy at different concentrations of aminolevulinic acid. Resting, IFN/LPS and IL-4 macrophage subtypes were prepared from monocytic THP-1 cell line. Cell death features and macrophage modifications were analyzed by fluorescence-based live cell imaging. ATP and HMGB1 levels in cell culture media were determined by ELISA assays. The presence of lipid peroxidation products in culture media was assessed by spectrophotometric detection of thiobarbituric acid reactive substances. Results Aminolevulinic acid-based photodynamic therapy induced various death pathways in Kyse 450 cells that included features of apoptosis, necrosis and ferroptosis. ATP amounts in extracellular environment of treated Kyse 450 cells increased with increasing aminolevulinic acid concentration. Levels of HMGB1, detectable by ELISA assay in culture media, were decreased after the treatment. Aminolevulinic acid-based photodynamic therapy induced lipid peroxidation of cellular structures and increased levels of extracellular lipid peroxidation products. Incubation of resting and IL-4 macrophages in conditioned medium from Kyse 450 cells treated by aminolevulinic acid-based photodynamic therapy induced morphological changes in macrophages, however, comparable alterations were induced also by conditioned medium from untreated cancer cells. Conclusion Aminolevulinic acid-based photodynamic therapy leads to alterations in local extracellular levels of damage associated molecular patterns, however, comprehensive studies are needed to find whether they can be responsible for macrophage phenotype modifications.

DYNAMICS OF INDICATORS OF THE BLOOD ANTIOXIDANT SYSTEM OF RATS UNDER CONDITIONS OF OXIDATIVE STRESS AND THE ACTION OF THE LIPOSOMAL PREPARATION

The aim of the study – to study the effect of the liposomal drug «Butaintersil» on theantioxidant status of rats under conditions of oxidative stressMaterials and methods. Modeling of oxidative stress was performed on sexually maturemale Wistar rats with a body weight of 180-200 g. In the blood of rats, changes inglutathione peroxidase activity and the level of reduced glutathione, as well as the levels oflipid peroxidation products, lipid hydroperoxide, and TBC-active products, were studied.Results. Intramuscular injection of a 50 % oily solution of tetrachloromethane at a doseof 0.25 ml/100 g of the animal’s body weight led to a change in the activity of the glutathionesystem of antioxidant protection: a decrease in the activity of glutathione peroxidaseand the level of reduced glutathione. At the same time, an increase in lipid peroxidationprocesses, namely an increase in the level of lipid hydroperoxides and TBC-activeproducts during the entire research period was observed in the intoxicated animals. In itsturn, with the additional administration of the liposomal drug «Butaintersil» to animalsunder conditions of tetrachloromethane intoxication, strengthening of the antioxidantstatus of the body of experimental animals was established. Thus, on the 14th day of the experiment, the activity of glutathione peroxidase and the level of reduced glutathionewere the highest in the blood of rats of the second experimental group, where comparedto intoxicated animals, they were 2.1 and 2.37 times higher, respectively. Also, underthe influence of the studied liposomal drug, changes in the levels of lipid peroxidationproducts in the blood of rats of the second experimental group were detected, namely,a decrease in the level of lipid hydroperoxides and TBC-active products in their blood.Conclusions. The obtained results indicate the corrective effect of Butaintersil on theparameters of the antioxidant protection of the body of rats after their intoxication withtetrachloromethane.

Piceatannol protects against myocardial ischemia/reperfusion injury by inhibiting ferroptosis via Nrf-2 signaling-mediated iron metabolism

Myocardial tissue ischemia damages myocardial cells. Although reperfusion is an effective technique to rescue myocardial cell damage, it may also exacerbate myocardial cell damage. Ferroptosis, an iron-dependent cell death, occurs following myocardial ischemia-reperfusion (I/R). Piceatannol (PCT) is a natural stilbene compound with excellent antioxidant properties that protect against I/R injury and exerts protective effects against ferroptosis-induced cardiomyocytes following I/R injury; however, the exact mechanism remains to be elucidated. PurposeThis study aims to investigate the protective effect and mechanism of PCT on myocardial ischemia-reperfusion injury. MethodsAn ischemia-reperfusion model was established via ligation of the left anterior descending branch of mice's hearts and hypoxia-reoxygenation (H/R) of cardiomyocytes. ResultsDuring ischemia-reperfusion, Nuclear factor E2-related factor 2 (Nrf-2) expression was downregulated, the left ventricular function was impaired, intracellular iron and lipid peroxidation product levels were elevated, and cardiomyocytes underwent ferroptosis. Furthermore, ferroptosis was enhanced following treatment with an Nrf-2 inhibitor. After PCT treatment, Nrf-2 expression significantly increased, intracellular ferrous ions and lipid peroxidation products significantly reduced, Ferroportin1 (FPN1) expression increased, and transferrin receptor-1 (TfR-1) expression was inhibited. ConclusionsPCT regulates iron metabolism through Nrf-2 to protect against myocardial cell ferroptosis induced by myocardial I/R injury.

Oral administration of resveratrol reduces oxidative stress generated in the hippocampus of Wistar rats in response to consumption of ethanol.

Chronic ethanol intake has been found to favor hippocampal deterioration and alter neuronal morphological maturation; resveratrol has been suggested as an antioxidant that may counteract these effects. The objective of this study was to analyze the effect of resveratrol on oxidative stress markers, endogenous antioxidant system in the hippocampus, and the behavior of male Wistar rats administered different concentrations of ethanol. The animals, at 3 months old, were randomly distributed into 11 study groups (n = 6/group), orally administered (5 days on, 2 days off) with water (control), ethanol (10, 20, 30, 40 or 50%), or ethanol (10, 20, 30, 40 or 50%) plus resveratrol (10 mg/Kg/day) for 2 months. Subsequently, the production of nitrites, malondialdehyde, and 4-hydroxy-alkenal (HNE) and the enzymatic activity of catalase and superoxide dismutase (SOD) were quantified. The levels of nitric oxide and lipid peroxidation products were significantly increased in each ethanol concentration and were statistically different compared to the control group; however, resveratrol significantly reduced oxidative stress caused by high ethanol concentration. The SOD and CAT did not present significant changes with respect to the controls in any of the study groups. In the different concentrations of ethanol used, GR increases significantly in the groups administered with resveratrol but not GPx. Resveratrol was shown to maintain the results similar to the control at most ethanol concentrations. Our results suggest that resveratrol prevents oxidative stress induced by ethanol in the hippocampus by decreasing cellular lipid peroxidation, but does not prevent the activation of catalase or SOD enzymes; however, allows glutathione to be kept active and in adequate concentrations in its reduced form and avoids alterations in the locomotor system.

Enhancing date seed phenolic bioaccessibility in soft cheese through a dehydrated liposome delivery system and its effect on testosterone-induced benign prostatic hyperplasia in rats.

The consumption of dairy products, including soft cheese, has been associated with numerous health benefits due to their high nutritional value. However, the phenolic compounds bioaccessibility present in soft cheese is limited due to their poor solubility and stability during digestion. So, this study aimed to develop an innovative soft cheese enriched with date seed phenolic compounds (DSP) extracted ultrasonically and incorporated into homogeneous liposomes and study its attenuation effect on testosterone-induced benign prostatic hyperplasia (BPH) in rats. Date seed phenolic compounds were extracted using 98 and 50% ethanol along with water as solvents, employing ultrasonication at 10, 20, and 30-min intervals. The primary and secondary DSP-liposomes were prepared and dehydrated. The particle size, zeta potential, encapsulation efficiency, and morphology were measured. Incorporating dehydrated liposomes (1-3% w/w) into soft cheese and their impact on BPH using male Sprague-Dawley rats was assessed. After inducing BPH, rats were fed a cheese diet with dehydrated DSP-liposomes. Over 8 weeks, parameters including nutrition parameters, prostate enlargement analysis, biochemical parameters, hormones level, oxidative stress, and cytokines were analyzed. The results showed that ultrasound-assisted extraction effectively reduced the extraction time and 30 min extraction EtOH 50% was enough to extract high yield of phenolic compounds (558 mg GA/g) and flavonoids (55 mg qu/g) with high antioxidant activity (74%). The biological results indicate that prostate weight and prostate index% were diminished in the treatment groups (1 and 2) compared to the BPH control group. The high antioxidant content present in the DSP-liposomes acted as the catalyst for suppressing the responses of the inflammatory cytokines, inhibiting the anti-inflammatory IL-10 production, and suppressing the elevated levels of lipid peroxidation products compared to the BPH group. The treatment group (2) supplemented with dehydrated secondary DSP-liposomes exhibited the most significant variance (p < 0.05) as opposed to the BPH group. Liposomal encapsulation was proved to be a feasible approach for administering DSP in soft cheese, thereby establishing new functional food category possessing prophylactic properties against the advancement of BPH in rats.

Indicators of free radical oxidation in neutrophils of patients with primary and recurrent soft tissue sarcomas

Purpose of the study. To carry out a comparative analysis of lipid peroxidation intensity and antioxidant system indices in blood neutrophils of patients with primary and relapsed soft tissue sarcomas (STS) depending on sex and age.Patients and methods. Of the 81 patients included in the study, 48 had primary STS, 5 patients with continued growth, and 28 patients with recurrent STS. The patients were divided by sex and age; the level of lipid peroxidation products, superoxide dismutase (SOD) activity, total peroxidase activity (TPA), glutathione peroxidase (GPx) activity and reduced glutathione (RG) content in blood neutrophils were investigated by conventional spectrophotometric methods. The comparison groups (donors) consisted of 12 men and 17 women divided into the same age subgroups: ≤ 45 years and &gt; 45 years.Results. In donors, there was a multiple decrease in the SOD/TPA ratio with age, especially in women, and in men this was accompanied by an age-related decrease in GPx activity. In primary sarcomas in older women and in men with continued growth and recurrence, there was an increase in diene conjugates (DC). In men over 45 years of age, there was an increase in SOD, TPA, and GPx. Women of the older age group were characterized by activation of SOD and GPx, expressed in the relapsed process to a significantly greater extent than in men, and an increase in RG was observed in women. The increase in both components of the glutathione system and SOD activity was especially significant in the development of relapses in women for periods exceeding three years, which was accompanied by a decrease in DC content. Conclusions. Neutrophils are characterized by an increase in DC content in patients of both sexes in the older age group with primary and recurrent STS, with its highest content in men with continued growth and relapses. GPx activity, increased in both men and women in the older age group in all variants of STS development, may play an important role in the antioxidant protection of blood cells in STS. Thus, the most pronounced activation of GPx, accompanied by a maximum increase in reduced glutathione and activation of SOD, contributes to a decrease in the level of DC and the absence of MDA increase in women with slow development of recurrences.