Reactive Oxygen Nitrogen Species Research Articles

The potential effect of melatonin on in vitro oocyte maturation and embryo development in animals.

Melatonin is a hormone mainly secreted by the pineal gland during the circadian cycle, with low levels during the daytime and prominent levels during the night. It is involved in numerous physiological functions including the immune system, circadian rhythm, reproduction, fertilization, and embryo development. In addition, melatonin exerts anti-inflammatory and antioxidant effects inside the body by scavenging reactive oxygen and reactive nitrogen species, increasing antioxidant defenses, and blocking the transcription factors of pro-inflammatory cytokines. Its protective activity has been reported to be effective in various reproductive biotechnological processes, including in vitro maturation, embryo development, and survival rates. In this comprehensive review, our objective is to summarize and debate the potential mechanism and impact of melatonin on oocyte maturation and embryo development through various developmental routes in different mammalian species.

Oxy-Inflammation in Humans during Underwater Activities.

Underwater activities are characterized by an imbalance between reactive oxygen/nitrogen species (RONS) and antioxidant mechanisms, which can be associated with an inflammatory response, depending on O2 availability. This review explores the oxidative stress mechanisms and related inflammation status (Oxy-Inflammation) in underwater activities such as breath-hold (BH) diving, Self-Contained Underwater Breathing Apparatus (SCUBA) and Closed-Circuit Rebreather (CCR) diving, and saturation diving. Divers are exposed to hypoxic and hyperoxic conditions, amplified by environmental conditions, hyperbaric pressure, cold water, different types of breathing gases, and air/non-air mixtures. The "diving response", including physiological adaptation, cardiovascular stress, increased arterial blood pressure, peripheral vasoconstriction, altered blood gas values, and risk of bubble formation during decompression, are reported.

Mesoscale size-promoted targeted therapy for acute kidney injury through combined RONS scavenging and inflammation alleviation strategy

Acute kidney injury (AKI) is a heterogeneous, high-mortality clinical syndrome with diverse pathogenesis and prognosis, but it lacks the effective therapy clinically. Its pathogenesis is associated with production of reactive oxygen/nitrogen species and infiltration of inflammatory cells. To overcome these pathogenic factors and improve the therapeutic efficiency, we synthesized triptolide-loaded mesoscale polydopamine melanin-mimetic nanoparticles (MeNP4TP) as the antioxidant plus anti-inflammatory therapeutic platform to synergistically scavenge reactive oxygen/nitrogen species (RONS), inhibit the activity of macrophages and dendritic cells, and generate Treg cells for AKI therapy. It was demonstrated that mesoscale size was beneficial for MeNP4TP to specifically accumulate at renal tubule cells, and MeNP4TP could significantly attenuate oxidative stress, reduce proinflammatory immune cells in renal, and repair renal function in cisplatin-induced AKI mouse model. MeNP4TP might be a potential candidate to inhibit oxidative damages and inflammatory events in AKI.

Hematopoiesis Revolves Around the Primordial Evolutional Rhythm of Purinergic Signaling and Innate Immunity – A Journey to the Developmental Roots

A cell's most significant existential task is to survive by ensuring proper metabolism, avoiding harmful stimuli, and adapting to changing environments. It explains why early evolutionary primordial signals and pathways remained active and regulate cell and tissue integrity. This requires energy supply and a balanced redox state. To meet these requirements, the universal intracellular energy transporter purine nucleotide-adenosine triphosphate (ATP) became an important signaling molecule and precursor of purinergic signaling after being released into extracellular space. Similarly, ancient proteins involved in intracellular metabolism gave rise to the third protein component (C3) of the complement cascade (ComC), a soluble arm of innate immunity. These pathways induce cytosol reactive oxygen (ROS) and reactive nitrogen species (RNS) that regulate the redox state of the cells. While low levels of ROS and RNS promote cell growth and differentiation, supra-physiological concentrations can lead to cell damage by pyroptosis. This balance explains the impact of purinergic signaling and innate immunity on cell metabolism, organogenesis, and tissue development. Subsequently, along with evolution, new regulatory cues emerge in the form of growth factors, cytokines, chemokines, and bioactive lipids. However, their expression is still modulated by both primordial signaling pathways. This review will focus on the data that purinergic signaling and innate immunity carry on their ancient developmental task in hematopoiesis and specification of hematopoietic stem/progenitor cells (HSPCs). Moreover, recent evidence shows both these regulatory pathways operate in a paracrine manner and inside HSPCs at the autocrine level.Graphical

Molecular mechanism of cleavage of SARS-CoV-2 spike protein by plasma generated RONS

Recently, it is been shown that cold atmospheric pressure plasmas Cold Atmospheric Plasma effectively inactivate the 2019-nCoV virus. Despite this promising finding, the precise mechanism of this inactivation remains unclear due to the limited number of studies conducted on the subject. Consequently, this paper focuses on the spike protein, a crucial part of the novel coronavirus, and the various reactive oxygen and nitrogen species (RONS) generated by the plasma. The study employs reactive molecular dynamics simulation and ReaxFF potential to explore the reactions between the spike protein molecules and different reactive oxygen nitrogen species (including H2O2, OH, O, O3, HOONO, and 1O2). The findings suggest that when a single RONS interacts with the spike protein, 1O2 and HOONO have the most potent ability to sever the spike protein. Additionally, the combined effect of long-lived and short-lived RONS presents a more potent decomposition impact.

Three-Step Depletion Strategy of Glutathione: Tunable Metal-Organic-Framework-Engineered Nanozymes for Driving Oxidative/Nitrative Stress to Maximize Ferroptosis Therapy.

Ferroptosis is a novel type of nonapoptotic programmed cell death involving the accumulation of lipid peroxidation (LPO) to a lethal threshold. Herein, we propose tunable zeolitic imidazolate framework (ZIFs)-engineered biodegradable nanozymes for ferroptosis mediated by both reactive oxygen species (ROS) and nitrogen species (RNS). l-Arginine is utilized as an exogenous nitric oxide donor and loaded into hollow ZIFs@MnO2 artificial nanozymes, which are formed by etching ZIFs with potassium permanganate and simultaneously generating a MnO2 shell in situ. The constructed nanozymes with multienzyme-like activities including peroxidase, oxidase, and catalase can release satisfactory ROS and RNS through a cascade reaction, consequently promoting the accumulation of LPO. Furthermore, it can improve the efficiency of ferroptosis through a three-step strategy of glutathione (GSH) depletion; that is, the outer MnO2 layer consumes GSH under slightly acidic conditions and RNS downregulates SLC7A11 and glutathione reductase, thus directly inhibiting GSH biosynthesis and indirectly preventing GSH regeneration.

Targeting Ferroptosis as a New Approach for Radiation Protection and Mitigation

Abstract: Radiation-induced normal cell toxicity (RINCT) is a major factor to consider while treating any ailment with radiotherapy. Clinical irradiation of tumors necessitates an understanding of the potential efficacy of radiation protective agents in reducing radiation damage to healthy tissues and their effects on tumor tissue radiosensitivity. Ferroptosis is a relatively new form of iron-dependent cell death that has been linked to a variety of disease pathologies. The key mediators of ferroptosis have been identified as lipid peroxidation and iron metabolism. Lipid peroxidation is the result of a reaction between reactive oxygen (ROS) and reactive nitrogen species (RNS) with phosphatidylethanolamine-containing polyunsaturated fatty acids (PUFAs). Ferroptosis inhibitors have been demonstrated to have anti-inflammatory effects in animal models of disease. It was recently shown that ionizing radiation (IR) generates severe ferroptosis, a critical component of RT-mediated normal cell toxicity. These findings support the use of ferroptosis inhibitor treatments for the treatment of radiation normal cell toxicity. Targeting lipid metabolic substrates and controlling ferroptosis by radiation could reduce toxicity and improve clinical outcomes. In this study, we address the relationships between radiotherapy and various types of radiation-induced cell death, and we discuss the interactions between ferroptosis and other kinds of controlled cell death generated by radiotherapy, and we investigate combination treatment options targeting ferroptosis in radiotherapy. This review will be a foundation for future research on ferroptosis in radiotherapy. Additionally, the relevant patents on ferroptosis inhibitors with various therapeutic potentials have been discussed.

The nuclear factor kappa B signaling pathway is a master regulator of renal fibrosis.

Renal fibrosis is increasingly recognized as a global public health problem. Acute kidney injury (AKI) and chronic kidney disease (CKD) both result in renal fibrosis. Oxidative stress and inflammation play central roles in progressive renal fibrosis. Oxidative stress and inflammation are closely linked and form a vicious cycle in which oxidative stress induces inflammation through various molecular mechanisms. Ample evidence has indicated that a hyperactive nuclear factor kappa B (NF-ƙB) signaling pathway plays a pivotal role in renal fibrosis. Hyperactive NF-ƙB causes the activation and recruitment of immune cells. Inflammation, in turn, triggers oxidative stress through the production of reactive oxygen species and nitrogen species by activating leukocytes and resident cells. These events mediate organ injury through apoptosis, necrosis, and fibrosis. Therefore, developing a strategy to target the NF-ƙB signaling pathway is important for the effective treatment of renal fibrosis. This Review summarizes the effect of the NF-ƙB signaling pathway on renal fibrosis in the context of AKI and CKD (immunoglobulin A nephropathy, membranous nephropathy, diabetic nephropathy, hypertensive nephropathy, and kidney transplantation). Therapies targeting the NF-ƙB signaling pathway, including natural products, are also discussed. In addition, NF-ƙB-dependent non-coding RNAs are involved in renal inflammation and fibrosis and are crucial targets in the development of effective treatments for kidney disease. This Review provides a clear pathophysiological rationale and specific concept-driven therapeutic strategy for the treatment of renal fibrosis by targeting the NF-ƙB signaling pathway.

Composition‐Reinforced Polydopamine Nanoenzyme for Improved Impairment of Prostatitis‐Damaged Sexual Behavior and Enhanced Anti‐Prostate Cancer

AbstractInflammation is pivotal in the pathogenesis and progression of the most challenging diseases and even cancer. Nanomedicine‐based strategy can be referred as a distinct solution to this complicated clinical obstacle by proposing an elaborated combination of effective therapeutic performances on inflammation and cancer. Herein, 2,2,6,6‐tetramethylpiperidine‐1‐oxyl doped polydopamine nanoparticles, termed as TPDA NPs, with the significantly improved reactive oxygen/nitrogen species (RO/NSs) scavenging performance and enhanced photothermal efficiency are designed and synthesized by constructing donor‐acceptor pairs, for prostate diseases treatment including anti‐inflammation and anti‐tumor. Benefiting from mimicking multi‐natural enzymes, including superoxide dismutase, catalase, peroxidase, and glutathione peroxidase, TPDA NPs can inhibit the NF‐κB signaling pathways by downregulating the CD36 expression for the treatment of oxidative stress‐induced prostatitis. Especially, TPDA NPs can improve the prostatitis‐associated impairment of sexual behavior. By virtue of the enhanced photothermal‐conversion efficiency, TPDA NPs ablate prostate cancer and simultaneously decrease inflammatory reaction. Therefore, this work provides a “three birds with one shot” paradigm to utilize rationally designed TPDA NPs for efficient management of prostate diseases.

Periodontal disease etiology and role of oxidative stress

The term "periodontal disease" is used to describe an array of inflammatory conditions that can affect the periodontium. In response to the challenge given by the bacteria, the gingival and periodontal tissues undergo a complicated chain of events involving communication It is between the membranes of a vital nature located under the gums and the person's immune inflammatory reaction. When there is an imbalance between the oxidants and the antioxidants in the body, this is known as oxidative stress. Antioxidants are compounds that may either seek out and destroy oxidants or prevent them from forming in the first place. Some of the oxidants produced by-products of normal cellular metabolism include reactive oxygen species and reactive nitrogen species. These byproducts are known as reactive oxygen and reactive nitrogen species, respectively. The presence of reactive oxygen species (ROS) has been shown to be associated with periodontal disease in research.

2D Nanozymes Modulate Gut Microbiota and T-Cell Differentiation for Inflammatory Bowel Disease Management.

Intestinal commensal microbiota dysbiosis and immune dysfunction are significant exacerbating factors in inflammatory bowel disease (IBD). To address these problems, Pluronic F-127-coated tungsten diselenide (WSe2 @F127) nanozymes are developed by simple liquid-phase exfoliation. The abundant valence transitions of elemental selenium (Se2- /Se4+ ) and tungsten (W4+ /W6+ ) enable the obtained WSe2 @F127 nanozymes to eliminate reactive oxygen/nitrogen species. In addition, the released tungsten ions are capable of inhibiting the proliferation of Escherichia coli. In a model of dextran sodium sulfate-induced colitis, WSe2 @F127 nanozymes modulate the gut microbiota by increasing the abundance of bacteria S24-7 and significantly reducing the abundance of Enterobacteriaceae. Moreover, WSe2 @F127 nanozymes inhibit T-cell differentiation and improve intestinal immune barrier function in a model of Crohn's disease. The WSe2 @F127 nanozymes effectively alleviate IBD by reducing oxidative stress damage, modulating intestinal microbial populations, and remodeling the immune barrier.

Molecular analysis of the human cytoglobin mRNA isoforms

Multiple functions have been proposed for the ubiquitously expressed vertebrate globin cytoglobin (Cygb), including nitric oxide (NO) metabolism, lipid peroxidation/signalling, superoxide dismutase activity, reactive oxygen/nitrogen species (RONS) scavenging, regulation of blood pressure, antifibrosis, and both tumour suppressor and oncogenic effects. Since alternative splicing can expand the biological roles of a gene, we investigated whether this mechanism contributes to the functional diversity of Cygb. By mining of cDNA data and molecular analysis, we identified five alternative mRNA isoforms for the human CYGB gene (V-1 to V-5). Comprehensive RNA-seq analyses of public datasets from human tissues and cells confirmed that the canonical CYGB V-1 isoform is the primary CYGB transcript in the majority of analysed datasets. Interestingly, we revealed that isoform V-3 represented the predominant CYGB variant in hepatoblastoma (HB) cell lines and in the majority of analysed normal and HB liver tissues. CYGB V-3 mRNA is transcribed from an alternate upstream promoter and hypothetically encodes a N-terminally truncated CYGB protein, which is not recognized by some antibodies used in published studies. Little to no transcriptional evidence was found for the other CYGB isoforms. Comparative transcriptomics and flow cytometry on CYGB+/+ and gene-edited CYGB−/− HepG2 HB cells did not unveil a knockout phenotype and, thus, a potential function for CYGB V-3. Our study reveals that the CYGB gene is transcriptionally more complex than previously described as it expresses alternative mRNA isoforms of unknown function. Additional experimental data are needed to clarify the biological meaning of those alternative CYGB transcripts.

Investigating the effect of atmospheric plasma on protein fibrinogen: Spectroscopic and biophysical analysis

AbstractCold atmospheric plasma (CAP) has gained significance in recent years and different prospects of it have been studied widely owing to its effectiveness and eco‐friendly nature. CAP has been used extensively in wound healing. However, a detailed understanding of the interaction of the CAP with different protein macromolecules present in our body is essential. In this study, we emphasize how CAP affects the protein fibrinogen. Fibrinogen is a major protein involved in blood clotting and the major protein in the blood. Numerous spectroscopic investigations have been done including UV spectroscopy, fluorescence spectroscopy, dynamic light scattering (DLS), and Zeta. This work shines a light on protein self‐assembly to bring the future possibilities of bio‐medicine with CAP treatment. Fibrinogen undergoes structural changes around tryptophan residue as evidenced by UV spectroscopy and quenching in fluorescence spectroscopy. The order of the fluorescence quenching is Oxygen > Helium > Argon gas plasma. 2,4‐dinitrophenylhydrazine (DNPH) assay supports fluorescence studies as more protein carbonyls are formed in the case of argon and oxygen gas plasma. DLS and Zeta potential measurements prove that the protein Fibrinogen undergoes a self‐assembly process to form organized assemblies in the presence of a plasma jet. Reactive oxygen and reactive nitrogen species produced in the plasma have been evaluated using various assays and correlated with the other studies. This study will help understand protein fibrinogen's self‐assembly process and pave the way for the CAP application in wound healing.

Size, Surface Properties, and Ion Release of Zinc Oxide Nanoparticles: Effects on Cytotoxicity, Dopaminergic Gene Expression, and Acetylcholinesterase Inhibition in Neuronal PC-12 Cells.

The extensive applications of zinc oxidenanoparticles (ZnO NPs) have resulted in a substantial risk of human exposure. However, the knowledge of the toxicity of these NPs in the nervous system is still limited. A comparative analysis of ZnO NPs of various sizes and NPs of the same size, with and without surface coating, and the potential role of released zinc ions is yet to be thoroughly explored. As a result, we have studied the cellular toxicity of two different-sized ZnO NPs, ZnO-22 (22nm) and ZnO-43 (43nm), and NPs with similar size but with polyvinylpyrrolidone coating (ZnO-P, 45nm). The findings from our study suggested a time-, size-, and surface coating-dependent cytotoxicity in PC-12 cells at a concentration ≥ 10μg/ml. ZnO NP treatment significantly elevated reactive oxygen and reactive nitrogen species, thereby increasing oxidative stress. The exposure of ZnO-22 and ZnO-43 significantly upregulated the expression of monoamine oxidase-A and downregulated the α-synuclein gene expression associated with the dopaminergic system. The interaction of NPs enzymes in the nervous system is also hazardous. Therefore, the inhibition activity of acetylcholinesterase enzyme was also studied for its interaction with these NPs, and the results indicated a dose-dependent inhibition of enzyme activity. Particle size, coating, and cellular interactions modulate ZnO NP's cytotoxicity; smaller sizes enhance cellular uptake and reactivity, while coating reduces cytotoxicity by limiting direct cell contact and potentially mitigating oxidative stress. Furthermore, the study of released zinc ions from the NPs suggested no significant contribution to the observed cytotoxicity compared to the NPs.

Harmfulness of prooxidants in bronchopulmonary dysplasia in preterm children

Introduction. Oxidative stress can be defined as the imbalance of the redox state of a certain system including living one (organelle, cell, organ/tissue), which excessively produces reactive oxygen and/or reactive nitrogen species (ROS/RNS) that exceed the capacity of the antioxidant defense system, which have the ability to slow down or even prevent the oxidative damage of macromolecules. Oxidative stress is a pathogenic mechanism of a large variety of diseases, including pulmonary one. Material and methods. 81 preterm born children included in the study were divided into the main group – preterm children with bronchopulmonary dysplasia (BPD), and the control group – preterm children without BPD. The comparison groups were prospectively evaluated clinical, instrumental and laboratory (TPA, prooxidant-antioxidant balance, nitric oxide metabolistes and MDA). Data were statistically analyzed using Microsoft Excel, MedCalc and SPSS and Contingency Table Analysis as a way to evaluate the performance of a diagnostic test. Results. In preterm children with BPD were found to be decreased by 29% (p < 0.001) the prooxidant-antioxidant balance (PAB) and the nitric oxide metabolistes (NO) level by 12% (p < 0.001) compared to children in the control group. The assessment of tissue oxidative damage markers revealed a significant 62% (p < 0.001) increase in malonic dialdehyde (MDA) content and a 4.86-fold (p < 0.001) increase in total prooxidant activity (TPA) in children with bronchopulmonary dysplasia compared to children in the control group. Our study confirms that TPA, PAB, MDA and NO values are reliable markers of hypoxic tissue damage at children with bronchopulmonary dysplasia and can be recommended for assessing the intensity of oxidative stress. Conclusions. Pulmonary bronchodysplasia is characterized by the imbalance of prooxidant-antioxidant processes with the exacerbation of prooxidant ones that trigger the oxidative/nitrosative stress and the deterioration of vital chemical compounds.

Enhancing the physicochemical properties and reactive species concentration of plasma activated water using an air bubble diffuser

Present study investigates the enhancement in plasma-activated water (PAW) properties (physicochemical properties and reactive oxygen-nitrogen species (RONS)) using bubble diffuser. In one setup, the diffuser attaches to the pencil plasma jet (PPJ) and producing discharge gas bubbles in water. In another setup, the bubbler agitates water during plasma-water interaction. Filamentary dielectric-barrier discharge (DBD) in the PPJ becomes diffusive DBD with bubbler agitation, resulting in higher discharge current and lower voltage. PAW (bubbler) exhibits enhanced physicochemical properties and reactive species (except H2O2). Bubbler-agitated PAW demonstrates substantial increases in properties and reactive species (75.4% NO3−, 702.4% NO2−, 1600% H2O2, 368.3% O3). Bubble diffuser enhances PAW technology for diverse applications.

Reactive oxygen/nitrogen species scavenging multi-enzyme mimetic ultrasmall calcium hexacyanoferrate (Ⅲ) nanozyme for hypertension remedy

Oxidative stress in the rostral ventrolateral medulla plays a pivotal role in the pathogenesis and progression of neurogenic hypertension, but limited strategy is currently available to maintain blood pressure and improve the life quality of patients with hypertension. The development of biocompatible nanomaterials with intrinsic antioxidative enzyme-mimicking activities is a promising approach to treat hypertension. Herein, we develop an ultrasmall calcium hexacyanoferrate (Ⅲ) nanoparticles (CaHF NPs) with the robust broad-spectrum reactive oxygen/nitrogen species (RONS) scavenging and anti-inflammation abilities for the treatment of hypertension. Specifically, CaHF NPs are simultaneously featured with superoxide dismutase-, peroxidase-, glutathione peroxidase- and catalase-like activities, protecting cell from oxidative stress-induced damage. Importantly, CaHF NPs alleviate hypertension through restoring endogenous redox homeostasis and reducing the secretion of proinflammatory cytokines. Our work not only provides a feasible therapeutic method for remedying hypertension, but also expands the biomedical applications of nanomaterials in treating oxidative stress-related central nervous system diseases.

Inhibition of Fungal Growth and Aflatoxin B1 Synthesis in Aspergillus flavus by Plasma-Activated Water.

The gaseous reactive oxygen/nitrogen species (RONS) generated by cold atmospheric plasma (CAP) can effectively inactivate Aspergillus flavus (A. flavus) and prolong the shelf-life of food. Plasma-activated water (PAW) is the extension of cold plasma sterilization technology. Without the limitation of a plasma device, PAW can be applied to more scenarios of food decontamination. However, the efficacy of PAW as a carrier of RONS for eradicating A. flavus or inhibiting its growth remains unclear. In this study, the immediate fungicidal effect and long-term inhibitory effect of PAW on A. flavus were investigated. The results demonstrated that 60-min instant-prepared PAW could achieve a 3.22 log reduction CFU/mL of A. flavus and the fungicidal efficacy of PAW gradually declined with the extension of storage time. Peroxynitrite (ONOO-/ONOOH) played a crucial role in this inactivation process, which could damage the cell wall and membrane structure, disrupt intracellular redox homeostasis, and impair mitochondrial function, ultimately leading to fungal inactivation. In addition to the fungicidal effect, PAW also exhibited fungistatic properties and inhibited the synthesis of aflatoxin B1 (AFB1) in A. flavus. By analyzing the cellular antioxidant capacity, energy metabolism, and key gene expression in the AFB1 synthesis pathway, it was discovered that PAW can significantly reduce ATP levels, while increasing SOD and CAT activity during 5-d cultivation. Meanwhile, PAW effectively suppressed the expression of genes related to AFB1 synthesis.

The effect of low-intensity cold atmospheric plasma jet on photoaging-induced hyperpigmentation in mouse model.

Cold atmospheric plasma (CAP) produces reactive oxygen/nitrogen species (RONS) in the target and can induce cytoprotective effects by activating hormesis-related pathways when its intensity is in the low range. The aim of this study is to evaluate the effect of low-intensified CAP (LICAP) on skin with photoaging-induced hyperpigmentation in an animal model. Changes in cell viability and RONS production following LICAP treatment were measured. For the in vivo study, 30 hairless mice underwent antecedent photoaging induction followed by the allocated therapy (i.e., LICAP, topical ascorbic acid (AA), or both). During the first 4 weeks of the treatment period (8 weeks), ultraviolet (UV)-B irradiation was concurrently administered. Visual inspection and measurement of the melanin index (MI) were performed to assess the change in skin pigmentation at Weeks 0, 2, 4, 6, and 8. RONS production increased linearly until the saturation point. Cell viability was not significantly affected by LICAP treatment. At Week 8, MI was significantly decreased in every treatment group compared with the values at Week 0 and Week 4. The treatment effect of the concurrent therapy group was superior to that of the LICAP and AA groups. LICAP appears to be a novel modality for photoprotection and pigment reduction in photodamaged skin. LICAP treatment and topical AA application seem to exert a synergistic effect.

Molecular investigation of Coxiella burnetii in the Middle and East Black Sea region in aborted bovine fetuses and investigation of the oxidant/antioxidant system

Coxiella burnetii (C. burnetii) is a causative microorganism that causes the zoonotic Q fever disease, which is generally asymptomatic in animals, but causes reproductive issues such as abortion, stillbirth, and infertility. C. burnetii infection poses a threat to farm economies as it affects productivity in farm animals. The purpose of this research was to look into the incidence of Q fever in eight provinces in the Middle and East Black Sea region and to measure reactive oxygen and reactive nitrogen species as well as antioxidant levels in bovine aborted fetal livers infected with C. burnetii. The study material consisted 670 bovine aborted fetal liver samples delivered to Samsun Veterinary Control Institute from eight provinces between 2018 and 2021. C. burnetii was analyzed by PCR in these samples and 47 (7,01%) were positive while 623 negative. Nitric oxide (NO), malondialdehyde (MDA) and reduced glutathione (GSH) activities were analyzed by spectrophotometric method in both 47 positive samples and 40 negative samples as control group. In the C. burnetii positive and control groups, MDA levels were determined to be 2.46 ± 0.18 and 0.87 ± 0.07 nmol/ml, NO levels were determined to be 1.77 ± 0.12 and 1.09 ± 0.07 nmol/ml, and reduced GSH activity was determined to be 5.14 ± 0.33 and 6.62 ± 0.46 µg/dl, respectively. In C. burnetii positive fetal liver tissue, MDA and NO levels were higher than the control group, while reduced GSH levels were lower than the control group. As a result, C. burnetii caused changes in free radical level and antioxidant activity in bovine aborted fetus liver.