Production Of Oxygen Free Radicals Research Articles

The effects of antioxidant supplementation on short-term mortality in sepsis patients

BackgroundThe occurrence and development of sepsis are related to the excessive production of oxygen free radicals and the weakened natural clearance mechanism. Further dependable evidence is required to clarify the effectiveness of antioxidant therapy, especially its impact on short-term mortality. ObjectivesThe purpose of this systematic review and meta-analysis was to evaluate the effect of common antioxidant therapy on short-term mortality in patients with sepsis. MethodsAccording to PRISMA guidelines, a systematic literature search on antioxidants in adults sepsis patients was performed on PubMed/Medline, Embase, and the Cochrane Library from the establishment of the database to November 2023. Antioxidant supplements can be a single-drug or multi-drug combination: HAT (hydrocortisone, ascorbic acid, and thiamine), ascorbic acid, thiamine, N-acetylcysteine and selenium. The primary outcome was the effect of antioxidant treatment on short-term mortality, which included 28-day mortality, in-hospital mortality, intensive care unit mortality, and 30-day mortality. Subgroup analyses of short-term mortality were used to reduce statistical heterogeneity and publication bias. ResultsSixty studies of 130,986 sepsis patients fulfilled the predefined criteria and were quantified and meta-analyzed. Antioxidant therapy reduces the risk of short-term death in sepsis patients by multivariate meta-analysis of current data, including a reduction of in-hospital mortality (OR = 0.81, 95% CI 0.67 to 0.99]; P = 0.040) and 28-day mortality (OR = 0.81, 95% CI 0.69 to 0.95]; P = 0.008). Particularly in subgroup analyses, ascorbic acid treatment can reduce in-hospital mortality (OR = 0.66, 95% CI 0.90 to 0.98; P = 0.006) and 28-day mortality (OR = 0.43, 95% CI 0.24 to 0.75]; P = 0.003). However, the meta-analysis of RCTs found that antioxidant therapy drugs, especially ascorbic acid, did substantially reduce short-term mortality(OR = 0.78, 95% CI 0.62 to 0.98; P = 0.030; OR = 0.57, 95% CI 0.36 to 0.91; P = 0.020). ConclusionsAccording to current data of RCTs, antioxidant therapy, especially ascorbic acid, has a trend of improving short-term mortality in patients with sepsis, but the evidence remains to be further demonstrated.

Application of Photodynamic Therapy in Cardiology.

The origins of photodynamic therapy (PDT) date back to 1904. Since then, the amount of research proving PDT and, consequently, its applicability to various disease states has steadily increased. Currently, PDT is mainly used in oncology to destroy cancer cells. It is being worked on for possible use in other medical fields as well, including cardiology. It can be used in the prevention of restenosis, often occurring after vascular surgical interventions, for destroying atherosclerotic plaques and as a new ablative method of ectopic centers in the treatment of atrial fibrillation. The purpose of this review is to summarize the knowledge to date regarding the therapeutic potential of using PDT for various pathological conditions in cardiology. The review also focuses on the current limitations associated with the use of PDT and identifies areas where more research is needed to develop better drug regimens. Materials and methods: The study analyzed 189 medical articles. The articles came from PubMed, Frontiers, Google Scholar, Science Direct and Web of Science databases. Through the excitation of light, a photosensitizer (PS) introduced into the body, the destruction of pathological cells occurs. PTD is widely used in oncology of the central nervous system (CNS). This process is made possible by the production of free oxygen radicals (ROS) and singlet oxygen, which generate oxidative stress that destroys sensitive cancer cells. In recent years, photosensitizers have also been discovered to have a strong affinity for macrophages that fill atherosclerotic plaques, making these compounds suitable for treating atherosclerosis. By inducing apoptosis of smooth muscle cells, inactivating basic fibroblast growth factor (FGF-β) and inhibiting endothelial cell hyperplasia, PDT can be used to prevent restenosis after surgical proceduresPDT appears to be a minimally invasive and highly effective therapeutic method, especially when combined with other therapeutic methods. Unfortunately, the small number of animal model studies and human clinical trials greatly limit the applicability of PDT on a wider scale. Current limitations, such as the depth of penetration, delivery of photosensitizer particles to the direct site of the lesion or the appropriate choice of photosensitizer in relation to the nature of the pathology, unfortunately make it impossible to replace current therapeutic approaches.

Aqueous Ozone Exposure Inhibits Sporulation in the Cyclospora cayetanensis Surrogate Eimeria acervulina

Ozone is a potent disinfecting agent used to treat potable water and wastewater, effectively clearing protozoa such as Giardia and Cryptosporidium spp. It is unclear whether ozone treatment of water or fresh produce can reduce the spread of the emerging parasite Cyclospora cayetanensis, which causes cyclosporiasis in humans. Obtaining viable C. cayetanensis oocysts to evaluate inactivation methods is challenging because we lack the means to propagate them in vitro, because of delays in case reporting, and because health departments typically add inactivating fixatives to clinical specimens. Research in various surrogate organisms has sought to bolster understanding of the biology of C. cayetanensis. Among these surrogates is the poultry parasite Eimeria acervulina, a closely related and easily cultured parasite of economic significance. We used this surrogate to evaluate the consequences of ozone treatment, using the sporulation state as an indicator of infectious potential. Treating with ozonated water acidified with citric acid reduced sporulation ability in a dose-dependent manner; treatment with up to 4.93 mg/L initial concentration of ozone resulted in a 93% inactivation of sporulation by 7 days posttreatment. This developmental arrest was accompanied by transcriptional changes in genes involved in regulating the response to reactive oxygen species (ROS) in a time course that is consistent with the production of oxygen free radicals. This study shows that ozone is highly effective in preventing sporulation of E. acervulina, a model coccidian used as a surrogate for Cyclospora. Furthermore, ozone exposure induced molecular responses to general oxidative stress, documented with several well-characterized antioxidant enzymes.

Graves hastalığında serum neopterin düzeylerinin değerlendirilmesi

Aim: Graves' disease is a disease with an autoimmune basis in which the synthesis and release of thyroid hormone from the thyroid gland increases. Interferon-gamma (IFN-γ) released from activated T lymphocytes causes macrophages to produce neopterin (NPT), increasing its concentration in serum and other body fluids. There is a relationship between NPT and the production of free oxygen radicals by these cells. In this study, it was aimed to measure serum NPT levels in individuals with Graves' disease.
 Material and Method: The study included 13 newly diagnosed Graves' patients (neopterin levels were measured at the time of first diagnosis and at the 3rd month of treatment) and 16 Graves' patients who were followed up in endocrinology outpatient clinics for at least one year. NPT levels of 23 healthy individuals without any disease were taken as the control group. Free triiodothyronine (T3), free thyroxine (T4), thyroglobulin, and thyroid stimulating hormone (TSH) levels were measured in the blood samples of the participants.
 Results: Serum NPT levels were found to be higher in Graves' patients compared to the control group (6.66 nmol/L in newly diagnosed patients, 9.24 nmol/L in patients at the 3rd month of treatment, 10.68 nmol/L in patients followed for one year or more, 1.44 nmol/L in the control group, respectively, p

The Importance of Metabolic and Environmental Factors in the Occurrence of Oxidative Stress during Pregnancy.

Metabolic changes in pregnant women begin in the first weeks after conception under the influence of placental hormones that affect the metabolism of all nutrients. An increased concentration of total lipids accompanies pregnancy and an increased accumulation of triglycerides in low-density lipoproteins (LDL) particles. Lipids in small dense LDL particles are more susceptible to oxidative modification than normal-density LDL particles. Unlike LDL high-density lipoproteins (HDL), lipoprotein particles have an atheroprotective role in lipid metabolism. The very growth of the fetus depends on the nutrition of both parents, so obesity is not only in the mother but also in the father. Nutritional programming of the offspring occurs through changes in lipid metabolism and leads to an increased risk for cardiometabolic diseases. Pregnancy is accompanied by an increased need for oxygen in the mitochondria of the placenta and a tendency to develop oxidative stress. Oxidative stress represents a disturbance in the balance of oxidation-reduction processes in the body that occurs due to the excessive production of free oxygen radicals that cellular homeostatic mechanisms are unable to neutralize. When the balance with the antioxidant system is disturbed, which happens when free oxygen radicals are in high concentrations, serious damage to biological molecules occurs, resulting in a series of pathophysiological and pathological changes, including cell death. Therefore, oxidative stress plays a significant role in the pathogenesis of many complications that can occur during pregnancy. The oxidative status of pregnant women is also influenced by socioeconomic living conditions, lifestyle habits, diet, smoking, and exposure to environmental air pollution. During a healthy pregnancy, the altered lipid profile and oxidative stress create an increased risk for premature birth and pregnancy-related diseases, and a predisposition to adult diseases.

Application of Chitosan Hydrogels in Traumatic Spinal Cord Injury; A Therapeutic Approach Based on the Anti-inflammatory and Antioxidant Properties of Selenium Nanoparticles

Purpose: The pathophysiological progression of traumatic Spinal Cord Injury (SCI) includes primary and secondary injury. Secondary injury destroys the spinal cord tissue and neurological disorders. After primary mechanical damage, inflammation is the most important factor inducing astrogliosis and scar formation. The activation of inflammatory cells in the area of damage produces free radicals, all of which damage cell membranes. A significant level of oxygen-free radical production is involved in the pathology of SCI. Therefore, limiting secondary damage is very important in the clinical treatment of acute traumatic spinal cord injury.
 Materials and Methods: In this review article, the articles indexed in various databases were used. The collection of articles was evaluated without time constraints using keywords inducing traumatic SCI, inflammation, oxidative stress, chitosan, and selenium nanoparticles.
 Results: Inflammation and oxygen-free radicals play a key role in secondary damage after SCI. Therefore, as a new therapeutic approach, the use of hydrogels based on chitosan has been considered in SCI. The biocompatibility and biological properties of chitosan have made it considered a suitable material for nerve regeneration.
 Conclusion: The use of reactive oxygen species scavengers, including metal nanoparticles, can control inflammation and oxidative stress in spinal cord injuries. Selenium nanoparticle treatment may reduce secondary damage in SCI by using its anti-inflammatory and antioxidant properties. Therefore, the use of selenium nanoparticles in the chitosan hydrogel bed can control the degeneration and functional improvement of the nerve tissue of the spinal cord.

Diabetes mellitus and anti-oxidative stress

The development of diabetes complications, both microvascular and cardiovascular, is significantly influenced by oxidative stress. Diabetes-related metabolic problems lead to an overproduction of mitochondrial superoxide in the heart, small and large vascular endothelial cells, and both. Five key pathways implicated in the pathophysiology of problems are activated as a result of the increased superoxide generation. The purpose of this review is to highlight new insights into the processes through which hyperglycemia produces oxygen free radicals.

P-566 Is the seminal oxidative stress the mirror of psychological stress perceived by infertile men?

Abstract Study question To assess the association between anxiety and depression scores and the levels of oxidative stress in seminal plasma of Tunisian infertile men. Summary answer Depression in hypofertile men is associated to higher levels of catalase in seminal plasma and thus to oxidative stress. What is known already Within the last decades, the knowledge concerning the link between psychological and oxidative stress in infertile men has been surging. In a limited number of studies aiming to elucidate the psychological aspect of male infertility, data related to increased incidence of depression and anxiety have been reported. It has also been reported that anxiety and depression may trigger the production of reactive free oxygen radicals leading to disruption of the balance between free radicals and antioxidants semen properties. Study design, size, duration This was a cross-sectional study performed in the Laboratory of Cytogenetics and Reproductive Biology of Fattouma Bourguiba University Teaching Hospital (Monastir Tunisia). A total of 282 patients were assessed for levels of anxiety and depression and evaluated for semen parameters. Among these, 105 patients were assessed for levels of superoxide dismutase (SOD) and 51 patients were evaluated for the levels of catalase in seminal plasma from September 2022 to January 2023. Participants/materials, setting, methods Were included patients addressed for semen quality assessment. All patients with a previously diagnosed psychological disorder, those who presented severe depression and/or anxiety symptoms or had a stressful life event were not included. Informed consent was obtained from all the participants. The subjects were evaluated for anxiety and depression symptoms using the valid Arab version of the HAD (Hospital Anxiety and Depression) scale. Semen analysis and results interpretation were performed according to 2021 WHO guidelines. Main results and the role of chance The mean HAD-D (depression) and HAD-A (anxiety) scores were of 6.56 ± 3.07 (IIQ [4-8]) and 7.94 ± 3.73 (IIQ [5-10]) respectively. The mean levels of SOD and catalase were of 42.32 ± 24.08 and 19599.82 ± 12745.36 respectively. The results showed that patients exhibiting elevated HAD-D scores have higher levels of catalase in seminal plasma compared to those with normally ranging HAD-D scores (29856.07±15904.51 VS 17968.14±11564.79 respectively; p= 0.02). However, SOD levels were similar between the two groups and no correlation was found between seminal oxidative stress as assessed by catalase and SOD levels and both HAD-D and HAD-A scores. Limitations, reasons for caution The main limitation reason could be related to the limited number of patients evaluated for levels of catalase in seminal plasma (N = 51). Furthermore, assessing hormone’s levels (LH, FSH and testosterone) would be of great interest in elucidating the implicated pathways leading to oxidative stress and impaired semen quality. Wider implications of the findings Our results shed the light on the elevated levels of the catalase in patients with high depression scores. The absence of correlation between antioxidant enzymes and psychological well-being of infertile patients is a reassuring finding. However, awareness and recognition of depressive symptoms in infertile men is crucial when managing infertility. Trial registration number not applicable

Mechanisms Suggesting a Relationship between Vitamin D and Erectile Dysfunction: An Overview

Vitamin D deficiency (VDD) and erectile dysfunction (ED) heavily burden the male population. The higher prevalence of both conditions in the elderly suggests a possible relationship between the two conditions. In addition, in vitro, animal, and human studies have revealed several mechanisms that may relate VDD to ED. The main mechanism by which vitamin D might exert its action on sexual function appears to be through the regulation of endothelial function. Indeed, VDD correlates with several markers of endothelial function. The action of vitamin D on the endothelium would be exercised both indirectly through its intervention in inflammatory processes and through the production of oxygen free radicals, and directly through the regulation of vascular stiffness, the production of nitric oxide, and the regulation of vessel permeability. Furthermore, the ubiquitous distribution of the vitamin D receptor in the human body means that this hormone can also exert a beneficial effect on erectile function by interfering with those comorbidities significantly associated with ED, such as hypertension, diabetes mellitus, hypercholesterolemia, chronic kidney disease, and hypogonadism. In this review, we thoroughly and carefully presented the evidence and mechanisms that would appear to relate vitamin D levels to erectile function. Furthermore, we have summarized the meta-analytic evidence for and against this association to provide a true representation of this topic. Data published to date suggest that low levels of vitamin D could contribute to worsening erectile function through several mechanisms. Therefore, vitamin D levels should be measured in patients with ED and maintained at adequate levels by specific supplementation in case of deficiency. However, the low quality and heterogeneity of clinical trials evaluating the effects of vitamin D administration on erectile function and ED-associated comorbidities do not allow for a univocal conclusion, and indicate the need for further studies to analyze these aspects.

Therapeutic potential of flavonoids in the management of obesity-induced Alzheimer's disease: an overview of preclinical and clinical studies.

Obesity is a global epidemic that affects people of all ages, genders, and backgrounds. It can lead to a plethora of disorders, including diabetes mellitus, renal dysfunction, musculoskeletal problems, metabolic syndrome, cardiovascular, and neurodegenerative abnormalities. Obesity has also been linked to neurological diseases such as cognitive decline, dementia, and Alzheimer's disease (AD), caused by oxidative stress, pro-inflammatory cytokines, and the production of reactive oxygen free radicals (ROS). Secretion of insulin hormone is impaired in obese people, leading to hyperglycaemia and increased accumulation of amyloid-β in the brain. Acetylcholine, a key neurotransmitter necessary for forming new neuronal connections in the brain, decreases in AD patients. To alleviate acetylcholine deficiency, researchers have proposed dietary interventions and adjuvant therapies that enhance the production of acetylcholine and assist in the management of AD patients. Such measures include dietary intervention with antioxidant and anti-inflammatory flavonoid-rich diets, which have been found to bind to tau receptors, reduce gliosis, and reduce neuroinflammatory markers in animal models. Furthermore, flavonoids like curcumin, resveratrol, epigallocatechin-3-gallate, morin, delphinidins, quercetin, luteolin, and oleocanthal have shown to cause significant reductions in interleukin-1β, increase BDNF levels, stimulate hippocampal neurogenesis and synapse formation, and ultimately prevent the loss of neurons in the brain. Thus, flavonoid-rich nutraceuticals can be a potential cost-effective therapeutic option for treating obesity-induced AD, but further well-designed, randomized, and placebo-controlled clinical studies are needed to assess their optimal dosages, efficacy, and long-term safety of flavonoids in humans. The main objectives of this review are to underscore the therapeutic potential of different nutraceuticals containing flavonoids that can be added in the daily diet of AD patients to enhance acetylcholine and reduce neuronal inflammation in the brain.

An insight into hypothesized biological mechanisms contributing to the Flash effect

In recent years, FLASH radiotherapy (FLASH RT) has gained attention in preclinical studies as a potential advancement in cancer treatment. The great advantage of FLASH RT is the ultra-fast, high doses delivery that have a similar or greater effect on cancer cells while sparing normal, healthy tissue surrounding the tumor site. This is known as the FLASH effect. However, currently, there are not enough in vitro and in vivo data to transpose FLASH RT to human trials. This mini review summarizes the available in vitro data on electron beam FLASH, focusing on possible mechanisms of the FLASH effect. Current studies have focused on various types of cancer, including lung cancer, glioblastoma, uterus adenocarcinoma, cervix carcinoma, prostate carcinoma, melanoma, breast cancer, head and neck squamous cell carcinoma, and colon adenocarcinoma. Several hypotheses have been proposed to explain the biological mechanisms contributing to the to the selective FLASH effect, including differences between healthy and cancer cells in production of reactive oxygen species and free radicals, limitation of Fenton reaction caused by high Fe2+/3+ levels in tumor cells, and impaired DNA damage repair mechanisms occurring in cancer.

Curcumin attenuates hydroxychloroquine-mediated apoptosis and oxidative stress via the inhibition of TRPM2 channel signalling pathways in a retinal pigment epithelium cell line.

Hydroxychloroquine (HCQ) is used in the treatment of several diseases, such as malaria, Sjögren's disease, Covid-19, and rheumatoid arthritis. However, HCQ induces retinal pigment epithelium death via the excessive increase of cytosolic (cROS) and mitochondrial (mROS) free oxygen radical production. The transient receptor potential melastatin 2 (TRPM2) cation channel is stimulated by ADP-ribose (ADPR), cROS, and mROS, although it is inhibited by curcumin (CRC). We aimed to investigate the modulating action of CRC on HCQ-induced TRPM2 stimulation, cROS, mROS, apoptosis, and death in an adult retinal pigment epithelial 19 (ARPE19) cell line model. ARPE19 cells were divided into four groups: control (CNT), CRC (5µM for 24h), HCQ (60µM for 48h), and CRC + HCQ groups. The levels of cell death (propidium iodide positive cell numbers), apoptosis markers (caspases -3, -8, and -9), oxidative stress (cROS and mROS), mitochondria membrane depolarization, TRPM2 current density, and intracellular free Ca2+ and Zn2+ fluorescence intensity were upregulated in the HCQ group after stimulation with hydrogen peroxide and ADPR, but their levels were downregulated by treatments with CRC and TRPM2 blockers (ACA and carvacrol). The HCQ-induced decrease in retinal live cell count and cell viability was counteracted by treatment with CRC. HCQ-mediated overload Ca2+ influx and retinal oxidative toxicity were induced in an ARPE19 cell line through the stimulation of TRPM2, although they were attenuated by treatment with CRC. Hence, CRC may be a potential therapeutic antioxidant for TRPM2 activation and HCQ treatment-induced retinal oxidative injury and apoptosis.

Effects of dietary supplementation with fermented papaya on oxidative stress, symptoms, and microbiome in Parkinson's disease

Background: Oxidative stress, understood as the alteration of the physiological equilibrium between the production of oxygen and nitrogen free radicals and their metabolic neutralization (redox imbalance), is a typical condition of several pathologies, including neurodegenerative ones.In Parkinson's disease (PD), oxidative phenomena typically interest the dopaminergic neurons of mesencephalic substantia nigra. Although it is unlikely that the redox imbalance represents the primary event of neurodegeneration, it is certain that it participates in cellular damage progression.Objectives: Interventions to prevent or reduce the extent of the oxidative stress in PD and the consequent oxidative damage are of crucial importance. With this study, we have evaluated the effects of prolonged treatment with fermented papaya preparation (FPP) on redox imbalance, clinical parameters, and intestinal microbiome of PD patients. Methods: For six months, one group of PD subjects were treated with FPP (n=19, verum) and another with placebo (n=20, control); then, in the following six months, the treatments were exchanged.Several blood biochemical and hematological parameters were measured at the start and at the end of treatments. Among them are some components of antioxidant barriers, free radicals (total peroxides) and biomarkers of oxidative damage on DNA and proteins. To check the effects of FPP treatment on intestinal bacterial flora, we also evaluated the modification of microbiome with regards to the relative amounts of different phyla, families, genera, and species. Furthermore, accurate evaluations were performed on motor symptoms and cognitive functions of patients with validated survey scales to check the effects of FPP treatment on clinical parameters and quality life. Results: Unlike the control group, the level of free radicals in the patients treated with FPP was not increased; the antioxidant barrier was strengthened and oxidative damages on proteins and especially on DNA were decreased. Even clinical features and quality life parameters of these patients have improved. Instead, the results of microbiome were inconclusive as changes resulted seemingly independent Ofelia the treatments.Conclusions: The study demonstrates that FPP may be a valuable aid in counteracting oxidative stress and improve the motor symptoms and cognitive functions in PD. This effect does not seem to depend on increased growth of a particular bacterial phylum because the microbioma composition does not change significantly following the treatment; it cannot be excluded, however, that FPP works otherwise by modifying not the quantity but rather the metabolism of some specific bacterial group or that it has effects on the integrity of the intestinal mucosa. Keywords: Papaya, oxidative stress, Parkinson’s disease, microbiome

Comment on "Determination of Orellanine in Human Biological Matrices Using Liquid Chromatography with High-Resolution Mass Spectrometry Detection: A Validated Method Applied to Suspected Poisoning Cases".

To the Editor, Following our recent published article presenting an analytical method to detect orellanine in human fluids (i.e., urine, plasma and whole blood) (1), we would like to provide additional information regarding the detection of orellanine in kidney biopsies. Indeed, renal biopsy analysis in order to demonstrate orellanine intoxication was proposed decades ago (2, 3), but the elements presented here make us consider this approach likely to be questionable. Some Cortinarius mushrooms contain a nephrotoxic mycotoxin called orellanine. Known since a massive poisoning in Poland in 1957, orellanus syndrome after a consumption of Cortinarius mushrooms is characterized by the long latency period (2–14 days) between intake and first symptoms (4). Renal damage observed from biopsies has shown acute tubular necrosis, interstitial nephritis and fibrosis (5). The mechanism of orellanine toxicity is not clearly understood. Proposed mechanisms include inhibition of different cellular enzymes, inhibition of RNA and DNA synthesis and production of oxygen free radicals generated via oxidated orellanine. It is also unclear whether it is orellanine that is toxic to kidney cells or a degradation product such as orellinine or an unidentified metabolite (1, 4, 5). Diagnosis of orellanine poisoning is based on a suspicion of ingestion of Cortinarius mushrooms and acute kidney injury. Therefore, the clinical diagnosis is difficult and deserves analytical confirmation. Some have proposed kidney biopsy to detect orellanine on the belief that orellanine or its metabolites persist in renal cells (2, 3). This was based on the postulate that the release of orellanine and its metabolites from renal cells was very slow, allowing for a greater detection window range.

Cellular mechanisms of the lufenuron growth regulator in adults of Anthonomus grandis (Coleoptera: Curculionidae)

Abstract Growth-regulating insecticides are used for several cotton pests when immature, and although not registered for Anthonomus grandis, their use causes a satisfactory population reduction in adults. However, it is not known which mechanisms are involved in this reduction. Thus, we studied which tissue and cellular changes may be involved in this process. Adults were fed with flower buds treated with lufenuron (4 ml commercial product /l) for 24 h. Then, the histology of the gonads, oxidative stress and apoptosis were evaluated after periods of 24 h and 48 h. Our study revealed that lufenuron activates the oxidative stress pathway in A. grandis, causing significant changes at the cellular level. These changes may have been caused by stimulation of the production of oxygen ions, free radicals and hydrogen peroxides, resulting in an increase in lipid peroxidation 48 h after treatment. These effects were confirmed by the presence of histopathologies in the gonads of this pest such as disorganization of the follicular cell epithelium, reduction of the yolk, disappearance of the germinal vesicle, reduction of sperm bundles and cysts. Such alterations injured the gonads and impaired tissue homeostasis. It is concluded that together these factors lead to a desirable population reduction when it comes to managing the pest in the field, because the aim is to keep it below the control level. In addition to this desired effect, it is worth noting that lufenuron is safer when compared to other commonly used products, another feature that makes its use quite interesting.

Treating Preeclampsia in the COVID-19 Era: Is Allopurinol Useful as an Adjuvant Therapy? A Case Report and Review of the Literature

Acute respiratory syndrome-related coronavirus 2, or SARS-CoV-2, mainly affects the vulnerable population, especially those with comorbidities, such as pregnant women. SARS-CoV-2 has been found to cause multiple manifestations, one of which is preeclampsia. In preeclampsia, uric acid is excessively produced in the ischemic placenta and is released into circulation by placental reperfusion. Another effect of uric acid is oxidative stress with the production of oxygen free radicals associated with severe preeclampsia and fetal hypoxia. In our case report, we present the situation of a 38-year-old pregnant woman who developed preeclampsia after infection with SARS-CoV-2 with rapid evolution and an increased level of uric acid. We discuss the option of Allopurinol treatment in the third trimester of pregnancy instead of premature birth, with excellent benefits for both the mother and newborn. Additional clinical correlations between antioxidant treatment with Allopurinol and placental findings are needed.

Manejo de endometrio refractario en las pacientes que recibieron técnicas de reproducción asistida: presentación de 2 casos clínicos

Background and objectiveThe endometrium is a dynamic tissue that undergoes changes throughout the menstrual cycle, including morphological, biochemical and molecular changes, necessary for a successful embryo implantation process. When insufficient endometrial thickness occurs embryo implantation takes place near the spiral arteries in the endometrial basal layer with high blood flow and high oxygen tension which leads to excess production of oxygen free radicals, a fact that can interfere with embryo implantation and development (Catt and Henman, 2000). Thus, an adequate assessment of this situation is essential to achieve an ongoing pregnancy. PatientsIn this article, we present the clinical cases of 2 patients with insufficient endometrium and how we have managed their situation through hysteroscopic and pharmacological treatment. ResultsPregnancies have been achieved in both clinical cases. One of the patients had an eutocic delivery at 32nd week of pregnancy and a healthy child of 2,100 grams was born. The other patient is still pregnant. ConclusionsThe prevalence of thin endometrium according to published studies is between 2.4% and 8.5% of women (Ribeiro et al., 2018; Kasius et al., 2014). Multiple studies have shown a correlation between thin endometrium, low implantation rates and lower percentages of ongoing pregnancy. A minimum endometrial thickness of 7 mm is suggested to increase these percentages.

Activity of Apo-Lactoferrin on Pathogenic Protozoa.

Parasites and other eventually pathogenic organisms require the ability to adapt to different environmental conditions inside the host to assure survival. Some host proteins have evolved as defense constituents, such as lactoferrin (Lf), which is part of the innate immune system. Lf in its iron-free form (apo-Lf) and its peptides obtained by cleavage with pepsin are microbicides. Parasites confront Lf in mucosae and blood. In this work, the activity of Lf against pathogenic and opportunistic parasites such as Cryptosporidium spp., Eimeria spp., Entamoeba histolytica, Giardia duodenalis, Leishmania spp., Trypanosoma spp., Plasmodium spp., Babesia spp., Toxoplasma gondii, Trichomonas spp., and the free-living but opportunistic pathogens Naegleria fowleri and Acanthamoeba castellani were reviewed. The major effects of Lf could be the inhibition produced by sequestering the iron needed for their survival and the production of oxygen-free radicals to more complicated mechanisms, such as the activation of macrophages to phagocytes with the posterior death of those parasites. Due to the great interest in Lf in the fight against pathogens, it is necessary to understand the exact mechanisms used by this protein to affect their virulence factors and to kill them.

In vitro evaluation of the intensifying photodynamic effect due to the presence of plasmonic hollow gold nanoshells loaded with methylene blue on breast and melanoma cancer cells

BackgroundHypoxia is one of the most important limiting factors in photodynamic therapy that can reduce the effectiveness of this treatment. By designing a nanocomplex of plasmonic nanoparticles and photosensitizers with similar optical properties, the rate of free oxygen radical production can be increased and the efficiency of photodynamic therapy can be improved. in this study, we tried to use the outstanding capacities of hollow gold nanoshells (HGNSs) as a plasmonic nanocarrier of methylene blue (MB) to improve the performance of photodynamic therapy. Methods and materialAfter synthesis and optimization of hollow gold nanoshells loaded with Methylene blue (HGNSs-PEG-MB), the characteristics of MB, HGNSs, HGNSs-PEG, HGNSs-PEG-MB, and their toxicity at different concentrations on the cell lines was determined. After determining of optimum concentration of nano agents, irradiation of cell was performed with non-coherent of light source with 670 nm wavelength and an intensity of 14.9 mW/cm2. Twenty-four hours after irradiation, an MTT assay was used to determine cell survival percentage. To compare the results, we defined different indexes such as treatment efficiency (TE), synergism ratio (SYN), and the amount of exposure required for 50% cell death (ED50). All the tests were repeated at least four times on the DFW and MCF-7 cancer cell lines. ResultsFor combination therapies with Lumacare irradiated HGNSs-PEG-MB, the UC index was less than one for all concentrations (P < 0.05). Also, the IC50 index for this nanostructure in non-irradiated conditions and less than 9 min irradiation time was lower than other treatment groups (P < 0.05). ED50 amounts for HGNSs-PEG-MB in all concentrations were greater than the other groups. TE Index was also reported to be greater than 1 in all irradiation conditions and concentrations. ConclusionIn this study, HGNSs-PEG in the role of nanocarriers for methylene Blue was used. The results showed that irradiated HGNSs-PEG-MB by 670 nm light severely induced cell death and greatly improved the efficiency of photodynamic therapy in melanoma and breast cancer cells.

Mitochondrial dysfunction in cell senescence and aging.

Mitochondrial dysfunction and cell senescence are hallmarks of aging and are closely interconnected. Mitochondrial dysfunction, operationally defined as a decreased respiratory capacity per mitochondrion together with a decreased mitochondrial membrane potential, typically accompanied by increased production of oxygen free radicals, is a cause and a consequence of cellular senescence and figures prominently in multiple feedback loops that induce and maintain the senescent phenotype. Here, we summarize pathways that cause mitochondrial dysfunction in senescence and aging and discuss the major consequences of mitochondrial dysfunction and how these consequences contribute to senescence and aging. We also highlight the potential of senescence-associated mitochondrial dysfunction as an antiaging and antisenescence intervention target, proposing the combination of multiple interventions converging onto mitochondrial dysfunction as novel, potent senolytics.