Antioxidant Reserve Research Articles

Effects of carvacrol on hormonal, inflammatory, antioxidant changes, and ovarian reserve in polycystic ovary syndrome in Wistar rats.

The study, which explored the effects of carvacrol on female reproductive health, particularly in terms of hormonal, inflammatory, antioxidant, and ovarian reserves in polycystic ovary syndrome, could significantly influence future treatments and clinical practice. The study, conducted on thirty-five female Wistar albino rats, was designed to mimic the conditions of polycystic ovary syndrome in humans. The rats were randomly assigned into five groups: control (C), vehicle (V), polycystic ovary syndrome (PCOS), carvacrol (CAR), and polycystic ovary syndrome+ carvacrol (PCOS + CAR). The following practices were applied to the groups during the study. Normal saline was administered to the C group, DMSO to the V group, letrozole (1mg/kg/day) to the PCOS group, carvacrol (20mg/kg) to the CAR group, and letrozole and carvacrol together to the PCOS + CAR group for twenty-one days. At the end of the administration, blood, and ovarian samples were taken for hormone analysis (E2, and AMH), inflammatory (TNF-α, IL-6), oxidant-antioxidant analysis (malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase (GSH-Px), and catalase), and histopathological examinations. Ovary, and body weights were measured, and the ovary index was calculated. As a result, it was observed that carvacrol caused beneficial effects through inflammatory, and antioxidant mechanisms in PCOS.

Protective Effects of Lemna minor Linn. On Hepatic and Cognitive Impairments in Acetaminophen Induced Hepatic Encephalopathy in Rats

Aim: Lemna minor Linn., an aquatic plant, is a promising novel therapeutic agent that has been traditionally used in ethnobotanical practices as an ecofriendly supplement for the management of various ailments. This study involves the evaluation of ethanolic extract of Lemna minor Linn. against Paracetamol-induced Hepatic Encephalopathy using in vitro and in vivo Models. Methods: The acute oral toxicity study of the ethanolic extract of Lemna minor (EELM) was conducted following the OECD-425 guidelines over a 14-day period. A total of nine animals were used for this toxicity assessment. The EELM was tested in Paracetamol(PCM)-induced bioactivation animal model at two different dosages 200 and in comparison with silymarin as a standard compound. The In vivo experimental study was conducted using Sprague Dawley rats which was divided into 5 groups each group containing 6 animals so the total no of animals used in the study was 30 animals. The treatment groups included: normal control ( ), 100mg/kg silymarin (standard) and the EELM of two different doses of 200 and , p.o were administered to rats 10 hr before paracetamol ( ) treatment. Rats were orally administered their respective doses every day for total 30days. Paracetamol-induced oxidative liver damage disrupted normal levels of liver enzymes, total protein, and bilirubin, while also depleting antioxidant reserves. This oxidative stress was strongly associated with paracetamol toxicity, leading to a marked depletion of glutathione (GSH) and impairing both memory and cognitive function in the animals. Behavioral parameters are performed to evaluate the effect of drugs on cognitive behaviour of animals. Morris water maze test was performed to study how animals learn and remembers the spatial information relying on distal cues to locate the hidden platform in an opaque water. Additionally, elevated plus maze was performed to measures the anxious behaviour of rats, the criterion was tested based on the conflict between rats innate instincts to explore new environment and avoid open, well-lit areas. The potential protective effects of EELM was evaluated by measuring serum enzyme levels and antioxidants status in the liver and brain, further histopathological analysis was performed respectively. Results: The acute toxicity study did not report any mortality or toxicity signs in animals. PCM toxicity led to a statistically increase in the liver and body weight, along with brain water content. The PCM-intoxicated group exhibited a marked reduction in the level of superoxide dismutase (SOD) and glutathione (GSH) in the brain and liver, as well as an increase in lipid peroxidation and serum biomarkers (AST, ALT, ALP, and total bilirubin). EELM significantly ( ) reduced liver injury by inhibiting ALT, AST and ALP levels in serum. SOD, GSH and MDA liver content were significantly ( ) elevated by EELM, compared to PCM treated rats. Comparing the treatment and induced group, the treated group successfully recovered the activity of antioxidant levels and also been acknowledged for restored liver functioning by alleviating oxidative stress and also GSH level in brain was significantly increased by EELM and preserved the histology of brain, which was chronically produced over a period of 30 days. Conclusion: The findings of this investigation indicate the traditional use of Lemna minor in hepatoprotection and neuroprotection by regulating oxidative stress and mitigating reactive oxygen species (ROS). The insights gained from this research contribute to the development of novel therapeutic agents and paves the way for further studies on Lemna minor to enhance health outcomes, particularly in the management of neurodegenerative diseases.

Effect of ultrahigh frequency ozone therapy on oxidative metabolism in the blood of rats with ischemic skin flaps: A preclinical experimental randomized study

Background. Maintaining and restoring skin microcirculation in surgical flaps, as well as accelerating rehabilitation after skin flap transplantation, in order to mitigate the consequences of burns and injuries, remain a pressing issue. In addition to various timings and techniques for plastic surgery, physiotherapeutic approaches prove to be efficient and include low-intensity electromagnetic radiation in millimeter waves as their prominent techniques. In recent years, experts have paid an increasing attention to the application of low-intensity electromagnetic radiation across different frequency ranges for the enhancement of microcirculation in patients after surgical correction of burn consequences. However, this approach is yet to be further validated. Objective. To investigate the effect of different combinations of ultrahigh frequency electromagnetic radiation with ozone therapy on the oxidative metabolism of blood in rats using a model of ischemic skin flaps. Methods. A preclinical experimental randomized study was conducted on 100 adult male Wistar rats weighing between 200 and 250 grams. Five equal-sized groups of animals were formed in the study: Group 1: intact (no interventions), and Groups 2, 3, 4, and 5: after surgical intervention (modeling of ischemic skin flaps). Animals in Group 2 (control group) received no therapeutic procedures. Rats in Groups 3 and 5 underwent a 10-minute course of electromagnetic radiation exposure with a dose of 0.06 mJ for seven days. Animals in Group 3 were exposed to electromagnetic radiation of ultrahigh frequency with a range of 53–78 GHz. Animals in Group 4 received injections of ozonized saline solution (with a saturating ozone concentration in the ozonized oxygen mixture of 3000 µg/L) daily for 7 days, administered intraperitoneally at a volume of 1 mL. Group 5 underwent a combined treatment: daily exposure to ultrahigh frequency electromagnetic radiation along with intraperitoneal ozone therapy (the application modalities of these treatments were similar to those used in Groups 3 and 4, respectively). The intensity of lipid peroxidation, peroxide resistance in erythrocytes, and overall antioxidant system activity were assessed in order to investigate the balance of pro- and antioxidant systems in plasma and erythrocytes. Additionally, the study involved determination of the level of malondialdehyde content and evaluation of the activity of superoxide dismutase and catalase in erythrocytes. The obtained date were analyzed, using MS Office 2013 (Microsoft Corporation, USA) and Statistica 10 (StatSoft, USA). Results. The conducted analysis revealed an antioxidant effect from ultrahigh frequency electromagnetic radiation, with this effect being enhanced by ozone therapy. In addition, the study detected the inhibition of free radical oxidation under the ultrahigh frequency electromagnetic radiation and ozone therapy. Conclusion. Thus, the positive effects of the studied therapeutic factors manifest at the systemic level, as evidenced by the optimization of biochemical parameters and indicators of oxidative metabolism in the plasma of animal blood. It has been established that ultrahigh frequency electromagnetic radiation, administered in a noise mode, exerts a regulatory effect on pro- and antioxidant systems in the body, as demonstrated in a model of transplanted skin flap. This intervention leads to a reduction in the severity of oxidative stress and an enhancement of antioxidant reserves in the blood. The observed effect is further amplified with the additional application of ozone therapy.

Blocking Metallothionein-2 Expression by Copper-Doped Carbon Dots Induces Cellular Antioxidant System Collapse for Antitumor Therapy.

The insufficient antioxidant reserves in tumor cells play a critical role in reactive oxygen species (ROS)-mediated therapeutics. Metallothionein-2 (MT-2), an intracellular cysteine-rich protein renowned for its potent antioxidant properties, is intricately involved in tumor development and correlates with a poor prognosis. Consequently, MT-2 emerges as a promising target for tumor therapy. Herein, we present the development of copper-doped carbon dots (Cu-CDs) to target MT-2 to compromise the delicate antioxidant reserves in tumor cells. These Cu-CDs with high tumor accumulation and prolonged body retention can effectively suppress tumor growth by inducing oxidative stress. Transcriptome sequencing unveils a significant decrease in MT-2 expression within the in vivo tumor samples. Further mechanical investigations demonstrate that the antitumor effect of Cu-CDs is intricately linked to apolipoprotein E (ApoE)-mediated downregulation of MT-2 expression and the collapse of the antioxidant system. The robust antitumor efficacy of Cu-CDs provides invaluable insights into developing MT-2-targeted nanomedicine for cancer therapies.

Anxiety-depressive disorders after COVID-19

The 2019 coronavirus (COVID-19) pandemic has reached more than 194 million people as of July 26, 2021, and continues to spread worldwide. During the course of the long pandemic, evidence of damage to various organs and systems, such as the nervous system and parts of it, began to emerge. Oxidative stress is one of the main causes of neuronal dysfunction and death, mainly due to excessive formation of reactive oxygen species and depletion of antioxidant reserves. Oxidative stress is characterized by an imbalance between the production of reactive oxygen species (ROS) and antioxidant defense mechanisms of the body. This process is involved in the onset and development of many neurological diseases. In this review, we analyzed and summarized the results of studies showing the association of neurological diseases, such as stroke, Parkinson's disease, and other neurological diseases, with excessive formation of oxidative stress products. This article aims to provide an overview of the relationship between oxidative stress and a range of neurological conditions, shedding light on the underlying mechanisms and potential therapeutic implications. Objective of the study was to determine the level of anxiety-depressive disorders among patients who underwent COVID-19. 90 people were examined and selected according to inclusion and exclusion criteria. To assess higher nervous functions, we used the hospital scales HADS I, HADS II, Beck depression scale. To date, our study has not found a clear link between the virus in the body and anxiety-depressive manifestations in patients, which may suggest that the main cause of the disorders lies in the social aspects of the pandemic.

The Effect of Red Dragon Fruit Juice (Hylocereus Polyrhizus) on Liver Histopathological Images in Wistar Rats Exposed to Cigarette Smoke

Cigarette smoke contains toxic components, carbon monoxide, hydrogen cyanide, carbon dioxide, and tar, which can trigger the formation of ROS (Reactive Oxygen Species) and reduce antioxidant reserves, which impact oxidative stress and are known to cause damage to liver cell membranes. Red dragon fruit (Hylocereus polyrhizus) is a fruit that is rich in antioxidants that inhibit ROS and prevent damage to liver cells by cigarette smoke. This study aims to assess the effect of administering red dragon fruit juice on liver microscopic images in Wistar rats exposed to cigarette smoke. It was an experimental study with a post-test-only control group design. Thirty-five male Wistar rats (Rattus novergicus) were randomized into five groups. Four groups were exposed to cigarette smoke (K-, P1, P2, and P3), and the fifth group was used as a control (K). All the P-groups were given red dragon fruit juice 2 g/2.5 ml, 4 g/2.5 ml, and 8 g/2.5 ml, respectively, for twenty-eight days. On the 29th day, the livers of Wistar rats were taken for preparation and microscopic observation. The research data were analyzed using the Kruskall-Wallis and Mann-Whitney post hoc tests to determine group differences. The average liver cell damage in K, K-, P1, P2, and P3 were 1.23, 2.51, 1.57, 1.51, and 1.43, respectively. There was a significant difference in damage between the K- group and the P1 (p = 0.002), P2 (p = 0.004), and P3 (p = 0.002) groups. The administration of red dragon fruit juice can protect the liver cells of rats exposed to cigarette smoke.

The Role of Ergothioneine in Red Blood Cell Biology: A Review and Perspective.

Oxidative stress can damage tissues and cells, and their resilience or susceptibility depends on the robustness of their antioxidant mechanisms. The latter include small molecules, proteins, and enzymes, which are linked together in metabolic pathways. Red blood cells are particularly susceptible to oxidative stress due to their large number of hemoglobin molecules, which can undergo auto-oxidation. This yields reactive oxygen species that participate in Fenton chemistry, ultimately damaging their membranes and cytosolic constituents. Fortunately, red blood cells contain robust antioxidant systems to enable them to circulate and perform their physiological functions, particularly delivering oxygen and removing carbon dioxide. Nonetheless, if red blood cells have insufficient antioxidant reserves (e.g., due to genetics, diet, disease, or toxin exposure), this can induce hemolysis in vivo or enhance susceptibility to a "storage lesion" in vitro, when blood donations are refrigerator-stored for transfusion purposes. Ergothioneine, a small molecule not synthesized by mammals, is obtained only through the diet. It is absorbed from the gut and enters cells using a highly specific transporter (i.e., SLC22A4). Certain cells and tissues, particularly red blood cells, contain high ergothioneine levels. Although no deficiency-related disease has been identified, evidence suggests ergothioneine may be a beneficial "nutraceutical." Given the requirements of red blood cells to resist oxidative stress and their high ergothioneine content, this review discusses ergothioneine's potential importance in protecting these cells and identifies knowledge gaps regarding its relevance in enhancing red blood cell circulatory, storage, and transfusion quality.

Heavy Metal Exposure-Induced Cardiovascular Diseases: Molecular Mechanisms and Therapeutic Role of Antioxidants.

Globally, cardiovascular diseases (CVDs) are the main cause of mortality every year worldwide. CVD health is influenced by various health factors, such as blood pressure, cholesterol levels, and glucose control. The main risk factors include smoking, physical activity, food intake, and body mass index. Around 90% of CVDs could be prevented by controlling these risk factors. Heavy metals are indigenous to the environment of the earth. However, modern lifestyles have led to the exploitation of our environment by unconstrained use of heavy metals. Though heavy metals are essential components, they are hazardous to humans and living systems due to their persistent and non-degradable nature. The mainpurpose of this study is to provide a literature review on the mechanisms of heavy metals, particularly arsenic, lead, and cadmium, that cause cardiovascular diseases. The major mechanism by which heavy metals result in various modalities of cardiovascular disease is the generation of reactive species and the depletionof the antioxidant reserves inside the biological system. The generation of reactive species gradually leads to the activation of various signaling pathways, resulting in either apoptosis or unrestricted cell growth. These unfavorable conditions result in a state when there is an imbalance between reactive species generation and antioxidant activity. Both endogenously present antioxidants and dietary antioxidants are very much essential in regulating the redox potential of the body. They help in the detoxification and excretion of heavy metals and their metabolites in the biological system. Therefore, recognizing the role of heavy metals in cardiovascular health is crucial for developing preventive strategies and interventions aimed at mitigating their adverse effects on human health.

THE RELATIONSHIP BETWEEN OXIDATIVE STRESS AND NEUROLOGICAL DISORDERS: MINI REVIEW

Oxidative stress is one of the main causes of neuronal dysfunction and death, mainly due to excessive formation of reactive oxygen species and depletion of antioxidant reserves. Oxidative stress is characterized by an imbalance between the production of reactive oxygen species (ROS) and antioxidant defense mechanisms of the body. This process is involved in the onset and development of many neurological diseases. In this review, we analyzed and summarized the results of studies showing the association of neurological diseases, such as stroke, Parkinson’s disease, and other neurological diseases, with excessive formation of oxidative stress products. This article aims to provide an overview of the relationship between oxidative stress and a range of neurological conditions, shedding light on the underlying mechanisms and potential therapeutic implications.

Nanomedicine-mediated recovery of antioxidant glutathione peroxidase activity after oxidative-stress cellular damage: Insights for neurological long COVID.

Nanomedicine for treating post-viral infectious disease syndrome is at an emerging stage. Despite promising results from preclinical studies on conventional antioxidants, their clinical translation as a therapy for treating post-COVID conditions remains challenging. The limitations are due to their low bioavailability, instability, limited transport to the target tissues, and short half-life, requiring frequent and high doses. Activating the immune system during coronavirus (SARS-CoV-2) infection can lead to increased production of reactive oxygen species (ROS), depleted antioxidant reserve, and finally, oxidative stress and neuroinflammation. To tackle this problem, we developed an antioxidant nanotherapy based on lipid (vesicular and cubosomal types) nanoparticles (LNPs) co-encapsulating ginkgolide B and quercetin. The antioxidant-loaded nanocarriers were prepared by a self-assembly method via hydration of a lyophilized mixed thin lipid film. We evaluated the LNPs in a new in vitro model for studying neuronal dysfunction caused by oxidative stress in coronavirus infection. We examined the key downstream signaling pathways that are triggered in response to potassium persulfate (KPS) causing oxidative stress-mediated neurotoxicity. Treatment of neuronally-derived cells (SH-SY5Y) with KPS (50 mM) for 30 min markedly increased mitochondrial dysfunction while depleting the levels of both glutathione peroxidase (GSH-Px) and tyrosine hydroxylase (TH). This led to the sequential activation of apoptotic and necrotic cell death processes, which corroborates with the crucial implication of the two proteins (GSH-Px and TH) in the long-COVID syndrome. Nanomedicine-mediated treatment with ginkgolide B-loaded cubosomes and vesicular LNPs showed minimal cytotoxicity and completely attenuated the KPS-induced cell death process, decreasing apoptosis from 32.6% (KPS) to 19.0% (MO-GB), 12.8% (MO-GB-Quer), 14.8% (DMPC-PEG-GB), and 23.6% (DMPC-PEG-GB-Quer) via free radical scavenging and replenished GSH-Px levels. These findings indicated that GB-LNPs-based nanomedicines may protect against KPS-induced apoptosis by regulating intracellular redox homeostasis.

FEATURES FUNCTIONING OF THE DETOXIFICATION SYSTEM AT THE THREAT TERMINATION OF PREGNANCY AS A CONSEQUENCE OF ACCUMULATION OF 137CS

To date, there is no consensus on the pathogenesis of miscarriage. In modern life, human health is signifi cantly infl uenced by environmental factors. In this regard, 37 years after the accident at the Chornobyl nuclear power plant, the question of remote cytogenetic and hereditary eff ects in the off spring of parents aff ected by radiation remains relevant. Ecosystems contaminated with radioactive substances are a source of exposure for humans. Internal irradiation is the cause of reproductive losses. Radiation stress aff ects the course of redox processes in the body. Biochemical indicators are markers of the infl uence of environmental factors on a person. The study is dedicated to determining the state of peroxide hemostasis in the case of miscarriage. Aim: to determine the peculiarities of the functioning of the detoxification system in case of miscarriage due to the accumulation of 137Cs.Material and methods. The fi rst (research) group included women with reproductive losses in anamnesis and signs oftermination of the current pregnancy; the second (control) group included women with an uncomplicated history and course of pregnancy. Additionally, the fi rst group was divided into subgroups according to pregnancy outcomes: А – 38 women who gave birth at 37-40 weeks, despite the complicated course of the current pregnancy, В – 13 women who gave birth at 28-36 weeks + 6 days, С – 9 women who birth at 22-27 weeks + 6 days. The state of peroxide hemostasis in women was studied using biochemical studies. Accumulation of 137Cs with diff erent activity was detected in the placentas of the examined women of both groups using β-spectrometry. Morphological examination of placentas was performed according to the protocol. The severity of placental damage was studied by Olympus BX51 and Axioskop 40 microscopes. Analyzing the results revealed a relationship between biochemical indicators, the activity of 137Cs, and pregnancy scenarios. Statistical data analysis was performed using Microsoft Excel (2016) and Fisher angular transformation. The diff erence between comparative values was considered signifi cant at p < 0.05 (probability index greater than 95 %). Permission to conduct research was obtained from the Medical Ethics Committee of the SI «Institute of Pediatrics, Obstetrics, and Gynecology named academic Elena M. Lukyanova of the National Аcademy of Мedical Sciences of Ukraine» (protocol No 3 of 07.06.2017).Scientifi c research work is to «Develop the latest and improve existing technologies for diagnosis, prevention, and treatmentof premature termination of pregnancy in women with miscarriage taking into account the passport of the placenta» (2018-2020). Code VN.20.00.02.18, state registration number 0118U000039, KPKV 6561040.Results. It has been confi rmed that the state of the environment plays a decisive role in the pathogenesis of miscarriage. Ithas been proven that placental dysfunction caused by abnormal oxidative stress due to the action of incorporated 137Cs leads to pregnancy termination. As a result of the depletion of the antioxidant reserve, the compensatory capabilities of the placenta decrease. It was established that activity in the placenta up to 1.0 Bq/kg of 137Cs does not aff ect the course of gestation. The compensatory capacity of the placenta remains preserved even with the accumulation of 1.1 to 4.4 Bq/kg of 137Cs. At the same time, it is possible to prolong the pregnancy until the term of timely delivery. Internal irradiation with an activity of 4.5-10.4 Bq/kg of 137Cs causes damage to the stroma of the maternal surface of the placenta and premature birth at 28-36 weeks + 6 days. At the same time, newborns are viable due to the preservation of compensatory reactions in the placenta. Accumulation of more than 10.4 Bq/kg of 137Cs causes antenatal death of the fetus and early premature birth due to damage to maternal and fetal structures of the placenta. An increase in the content of malondialdehyde and a decrease in the activity of superoxide dismutase in the blood indicate the severity of radiation damage.Conclusions. Internal exposure to 137Cs disrupts the architecture and functional capacity of the placenta. Extreme eff ectsdepend on the activity of 137Cs, the compensatory capabilities of the placenta, and the pregnant woman’s body. Activation of lipid peroxidation acts as a biochemical amplifi er of radiation exposure. An increase in the blood of malondialdehyde, diene conjugates, and free SH groups is associated with the severity of radiation damage. An early marker of primary placental dysfunction, premature birth, and antenatal fetal loss is an increase in MDA content in the blood by 12.0 % and a decrease in SOD by 6.5 % relative to permissible values. An early marker of exhaustion of the compensatory reserve is an increase in the content of MDA in the blood by 23.3 % and a decrease in SOD by more than 18.2 % relative to the permissible values. Decompensation of adaptation mechanisms in the system «mother- placenta-fetus» leads to antenatal losses.

Evaluation of uterine antioxidants in bitches suffering from cystic endometrial hyperplasia-pyometra complex.

Cystic endometrial hyperplasia-pyometra complex (CEH-P) is a common disease in sexually mature bitches. Disease progression leads to oxidative stress, resulting in the depletion of uterine antioxidants and lipid peroxidation of associated cells, which further aggravates the condition. The concentration of antioxidant enzymes, the level of lipid peroxidation within the uterine tissue, and its reflection in the serum and urine need to be elucidated. The aim of this study was to analyze the concentration of antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), glutathione peroxidase (GPx), and the lipid peroxidation marker malonaldehyde (MDA) in three types of samples, i.e., serum, urine, and uterine tissue. For this purpose, 58 pyometra-affected and 44 healthy bitches were included in the present study. All animals underwent ovariohysterectomy (OVH). Our data indicated highly significant difference (p<0.01) in the antioxidant concentrations of uterine, serum and urine samples. Furthermore, there was a highly significant (p<0.01) difference in the serum levels of ferric reducing antioxidant power (FRAP) and free radical scavenging activity (FRSA) indicated poor capacity to overcome oxidative stress in the CEH-Pyometra condition. We showed that CEH-P induces oxidative stress, which further depletes the antioxidant enzyme reserves in the uterus. Thus, the weak antioxidant defence predisposes to uterine damage and disease progression. The simultaneous depletion of antioxidants and an increase in lipid peroxidation in the serum and urine may also act as early indicators of uterine pathology.

Environmental relevant concentrations of polystyrene nanoplastics and lead co-exposure triggered cellular cytotoxicity responses and underlying mechanisms in Eisenia fetida

Heavy metal pollution of soils and the widespread use of plastics have caused environmental problems worldwide. Nanoplastics (NPs) contaminants in water and soil environments can adsorb heavy metals, thereby affecting the bioavailability and toxicity of heavy metals. In this paper, the effect of co-exposure of polystyrene microspheres with 100 nm particle size and lead acetate (Pb) on the Eisenia fetida coelomocytes was investigated. The environmental concentration of NPs used was 0.01 mg/L and the concentration of Pb ranged from 0.01 to 1 mg/L, and the exposed cells were incubated at 298 k for 24 h. Our study demonstrated that exposure of cells to environmental relevant concentrations of NPs did not significantly affect the cytotoxicity of Pb exposure. It was shown that co-exposure induced cellular production of reactive oxygen species (ROS, increased to 134.4 %) disrupted the antioxidant system of earthworm body cavity cells, activated superoxide dismutase and catalase (CAT), produced reduced glutathione, and inhibited glutathione-dependent enzyme (GST) activity (Reduced to 64 %). Total antioxidant capacity (T-AOC) is first enhanced against ROS due to the stress of NPs and Pb. When the antioxidant reserves of cells are exhausted, the antioxidant capacity will decrease. The level of malondialdehyde, a biomarker of eventual lipid peroxidation, increased to 231.7 %. At the molecular level, due to co-exposure to NPs and Pb, CAT was loosely structured and the secondary structure is misfolded, which was responsible for exacerbating oxidative damage in E. fetida coelomocytes. The findings of this study have significant implications for the toxicological interaction and future risk assessment of co-contamination of NPs and Pb in the environment.

Клинико-лабораторные исследования в комплексной диагностике и лечении увеитов у детей

This work is devoted to the analysis of the effectiveness of new clinical and laboratory studies and their possible application in treatment of uveitis in children. The paper assesses the study of the glutathione-reducing system as a factor in the vulnerability of eye tissues to the effects of free radicals and peroxidation products during inflammation. The dependence of the clinical picture of uveitis and the frequency of detection of eye tissue antigens in the blood was analyzed to assess the localization and stage of the pathological process, which will undoubtedly determine the tactics of the therapy. Evaluation of the main indicators of the activity of peroxidation processes in uveitis is proposed to be carried out according to the original method for determining the functional activity of polymorphonuclear leukocytes (PNLs). It was proved that there is a close relationship between the level of PNLs activity, the level of intensity of peroxide processes and the ophthalmic picture of uveitis. Based on the results obtained in the following work, the use of pharmaceutical antioxidants, both traditional and those known drugs in which antioxidant properties were discovered for the first time, was proposed. This paper offers a concept of the development of toxic-allergic uveitis, including successive stages of the formation of immune complexes, inflammation, an increase in the functional activity of PMNs, their chemotaxis into the inflammation zone, infiltration through the capillary walls in the eye tissue, which leads to an avalanche-like increase in the level of oxidants, depletion of endogenous reserves of antioxidants, damage to cell membranes. Understanding these processes serves as an explication for developing optimal treatment regimens for uveitis and other inflammatory ophthalmpathology. Keywords: uveitis, retinal antigens, glutathione system, antioxidants, polymorphonuclear leukocytes, peroxidation, reactive oxygen species

Measurement of Antioxidant Activity Combination of Robusta Coffee (Coffea canephora), Matoa Leaves (Pometia pinnata) and Stevia Leaves (Stevia rebaudiana) with Various Solvent Extractions

Antioxidants are chemical compounds that can donate one or more electrons to free radicals, so that these free radicals can be be suppressed. The human body does not have excess antioxidant reserves, so if there is excessive exposure to radicals, the body needs antioxidants. There is concern about the possibility of unknown side effects from synthetic antioxidants, causing natural antioxidants to become a much-needed alternative. The development of coffee drinks, growing rapidly and increasingly diverse. Some of them like the taste of pure coffee without any additives and many of them choose to add herbal plants, which have antioxidant properties to enhance their coffee drinks and also add natural sweeteners instead of sugar. This study aims to study the antioxidant activity of a combination of robusta coffee extract (Coffea canephora), matoa leaf (Pometia pinnata) and stevia leaf (Stevia rebaudiana), with various solvents, using the DPPH (1,1-Diphenyl-2-pikrihidrazil) method. The results showed that the ethanol extract of robusta coffee had antioxidant activity with an IC50 value of 18.96 ppm, the ethanol extract of matoa leaf had an IC50 value of 5.46 ppm, and the stevia leaf extract of ethyl acetate had an IC50 value of 17.54 ppm. The value of antioxidant activity in the combination of the three in comparison (4:4:2), has an IC50 value of 9.94 ppm. Robusta coffee, matoa leaves and stevia leaves are beverage that have very strong antioxidant activity. The results of the ANOVA test on the extraction various solvents and samples showed a value (p &lt;0.01) indicating that there was a significant difference.

Glutathione-related antioxidant defence, DNA damage, and DNA repair in patients suffering from post-COVID conditions.

Post-COVID conditions are defined as the continuation of the symptoms of Coronavirus Disease 2019 (COVID-19) 3 months after the initial Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection, with no other explanation. Post-COVID conditions are seen among 30%-60% of patients with asymptomatic or mild forms of COVID-19. The underlying pathophysiological mechanisms of post-COVID conditions are not known. In SARS-CoV-2 infection, activation of the immune system leads to increased production of reactive oxygen molecules, depleted antioxidant reserve, and finally occurrence of oxidative stress. In oxidative stress conditions, DNA damage increases and DNA repair systems impair. In this study, glutathione (GSH) level, glutathione peroxidase (GPx) activity, 8-hydroxydeoxyguanosine (8-OHdG) level, basal, induced, and post-repair DNA damage were investigated in individuals suffering from post-COVID conditions. In the red blood cells, GSH levels and GPx activities were measured with a spectrophotometric assay and a commercial kit. Basal, in vitro H2O2 (hydrogen peroxide)-induced, and post-repair DNA damage (DNA damage after a repair incubation following H2O2-treatment, in vitro) were determined in lymphocytes by the comet assay. The urinary 8-OHdG levels were measured by using a commercial ELISA kit. No significant difference was found between the patient and control groups for GSH level, GPx activity, and basal and H2O2-induced DNA damage. Post-repair DNA damage was found to be higher in the patient group than those in the control group. Urinary 8-OHdG level was lower in the patient group compared to the control group. In the control group, GSH level and post-repair DNA damage were higher in the vaccinated individuals. In conclusion, oxidative stress formed due to the immune response against SARS-COV-2 may impair DNA repair mechanisms. Defective DNA repair may be an underlying pathological mechanism of post-COVID conditions.

Oxidation‑reduction potential parameters worsen following intraarterial therapy in patients with reduced collateral circulation and middle cerebral artery occlusions.

Collateral circulation is important for cerebral perfusion in acute ischemic strokes. Monitoring the oxidation-reduction potential (ORP) may be useful to assess collateral status or treatment efficacy. The objectives of the present study were to determine if the ORP was associated with collateral circulation status in middle cerebral artery (MCA) occlusions and to identify patterns in the ORP and the collateral circulation status among patients treated with intraarterial therapy (IAT) over time. The present pilot study was nested within a prospective cohort study measuring the ORP of the peripheral venous plasma of stroke patients. The population included in the present study were patients with MCA (M1/M2) occlusions. Two ORP parameters were examined: Static ORP (sORP; mV), indicating oxidative stress, and capacity ORP (cORP; µC), indicating antioxidant reserves. Collateral status was retrospectively graded using Miteff's system as good (grade 1) or reduced (grade 2/3). Comparisons were made between collateral status groups (reduced vs. good collaterals) in all patients, within a subset including only patients who received IAT, and between thrombolysis in cerebral infraction scale score (TICI) groups (0-2a vs. 2b/3). The Fisher's exact test, Student's t-test and Wilcoxon tests were used (α<0.20). The 19 patients were categorized based on their collaterals: Good collaterals (53%) and reduced collaterals (47%). The baseline characteristics were similar with the exception that the patients with good collaterals had a lower international normalized ratio (P=0.12) and were more likely to have a stroke on the left side (P=0.18) or to have a mismatch (P=0.05). The admission sORP values were comparable (169.5 vs. 164.2 mV; P=0.65), as was admission cORP (P=0.73). When considering only the patients who received IAT (n=12), admission sORP (P=0.69) and cORP (P=0.90) were also statistically similar. On day 2, after IAT, both groups experienced a worsening in ORP measures; however, the patients with good collaterals had a significantly lower sORP (169.4 vs. 203.5 mV; P=0.02) and a higher cORP (0.2 vs. 0.1 µC; P=0.002) compared with the patients with reduced collaterals. Neither sORP nor cORP were significantly different between TICI score groups on admission or on day 2. Upon discharge, patients with a TICI of 2b-3 had a significantly better sORP (P=0.03) and cORP (P=0.12) compared with those with a TICI of 0-2a. In conclusion, upon patient admission, the ORP parameters were not significantly different between the collateral circulation status groups for MCA occlusions. The ORP parameters worsened after IAT regardless of the collateral circulation status; however, after IAT, on day 2, patients with good collaterals experienced less oxidative stress (sORP) and had higher antioxidant reserves (cORP) than patients with reduced collaterals.

Beneficial Effects of Ginkgoselect™ Phytosome™ on Cognitive Impairment and Oxidative Stress in Mild-Moderate Dementia

In this study, we investigated for the first time the effects of a standardized extract from Ginkgo biloba leaves formulated with phospholipids Ginkgoselect™ Phytosome™, GBP) in combination with Standard Management (SM) in mild-moderate Alzheimer’s Disease (AD), focusing on the modulation of subject’s cognitive ability and oxidative status. Participants with cognitive impairment freely decided to continue their SM protocol (donepezil 10 mg/day, rivastigmine 4.6 mg/day in patch and memantine 20 mg/day; n=37), or to receive GBP tablets 120 or 240 mg/day in combination with SM (n=43). Subjects were assessed at baseline and after 6 months for cognitive functions and exclusive mental abilities through specific neuropsychological tests, namely the Mini Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA). We also evaluated the oxidative status through the determination of plasmatic derived reactive oxygen metabolites and anti-oxidant reserve through Plasma Antioxidant Test. After 6 months of supplementation with GBP to SM, subjects reported a significantly higher improvement in cognitive and neuropsychological functions, compared to those receiving only SM. Moreover, participants in the GBP with SM group reported a more remarkable decrease in oxidative load and an increase in the concentration of antioxidant molecules compared to the control group. Supplementation with GBP to SM demonstrates a positive effect in subjects with AD, helping them maintain or even increase their cognitive abilities, and improving their oxidative status both by reducing oxidative damage and by increasing the antioxidant reserve.

The effect of antioxidants on lipid peroxidation in modern pentathlon athletes

Analysis of the data of modern literature on this problem, as well as the results of previous studies Stankevych L.G, Zemtsova I.I. (2014), showed that a significant acceleration of free radical oxidation processes, under various nonspecific effects on the body, which occurs in tissues and organs during physical activity, can lead to the oxidation of unsaturated fatty acids (SFA) of membrane lipids, which causes a change in the physicochemical properties of the membranes and leads to changes in the concentration of a number of organic and inorganic components in the cell, the release of enzymes, amino acids, and trace elements from the cell and subcellular formations, which can reduce sports performance and slow down recovery processes. One of the ways to solve this problem is to use antioxidants in muscle activity; data on their use as nonspecific means of stimulating the effectiveness of training activity are often scattered and contradictory and therefore require further clarification. Objective: To substantiate the possibility of regulating the adaptive reactions of modern pentathlon athletes in the pre-competition period by targeted correction of the state of the AO system with the help of antioxidants. Results: Under the influence of the AO-complex, a decrease in the content of MDA was found both at rest and after exercise, which indicates an increased reserve of the body's AO system. The study of the state of individual links of the AO system under the influence of the AO complex revealed a significant activity of SOD and CAT after exercise (10 km) in the experimental group compared to the control group. Conclusions. The conducted studies of the antioxidant status of the body of athletes are of great practical importance, since they allow us to recommend the use of agents with antioxidant properties for the implementation of anti-stress measures during competitions, to increase the antioxidant reserve of the body and to preserve the health of athletes.

Endogenous intoxication in development of experimental periodontitis of bacterial-immune genesis

Excessive lipoperoxidation is accompanied by accumulation of peroxidation products and depletion of antioxidant re-serves, which cause hyperenzymemia and the accumulation of toxic substances. The level of endotoxicosis is determined by the content of hydrophilic and hydrophobic products in the blood. To define the pathogenetic role of endogenous intoxication in the dynamics of development of experimental periodontitis of bacterial-immune genesis. The experiment was conducted on rats. The animals were divided into three groups: group 1 - control group/intact; group 2 - model periodontitis at 7 days; group 3 - model periodontitis at 30 days. The experimental bacterial-immune periodon-titis was induced by injection into the tissue of the periodontal complex of the microorganisms' mixture diluted with egg's albumin. For the study, we selected the blood serum in which the content of middle molecular weight molecules and erythrocyte intoxication index were determined. The results were statistically analyzed by means of non-parametric indices methods. The development of generalized periodontitis is characterized by the occurrence of oxidative stress, which leads to violation of the metabolism in the mucous membrane of the oral cavity resulting in the accumulation of toxic products and the development of endogenous intoxication. The results show that the content of middle molecular weight molecules (aromatic amino and chain amino acids) determined on day 7 of the experiment was 1.11 times higher than that of the control group (p<0.01) and by 1.16 times (p<0.01), respectively. Comparing the levels of the above hydrophilic components of endogenous intoxication at 30 days of experimental peri-odontitis, we found a probable increase in these indicators compared with those at 7 days of the experiment. Studying the level of eryth-rocyte intoxication index, we found that at 7 days of experimental periodontitis this index was 1.28 times higher (p<0.01) than that of the intact group and continued to increase at 30 days. The dynamics of experimental periodontitis of bacterial-immune genesis show that the highest rates of endogenous intoxication are found in the late stages of the dynamics of the inflammatory process in the periodontium, namely at 30 days of the experiment, which may indicate chronic inflammation.