Oxidative Imbalance in Pediatric Anxiety Disorders: A Preliminary Comparative Study.

Background It is important to determine the possible related factors of anxiety disorder, one of the common psychiatric disorders of childhood. Our aims in this study were to compare oxidative stress markers between anxiety disorders in pediatric patients and healthy controls and to examine the relationship between anxiety symptom severity and oxidative stress indicators. Methods The study included 25 patients and 25 healthy controls. We measured the total oxidant capacity (TOS) and total antioxidant capacity (TAS) from the collected serum samples and calculated the oxidative stress index (OSI). We evaluated the clinical severity of the anxiety symptoms by the Revised Child Anxiety and Depression Scale-Child Version (RCADS-CV). Results The groups did not exhibit a noteworthy distinction in terms of TOS (p=0.128) and TAS (p=0.329). However, OSI was markedly elevated in the group with anxiety disorder (p=0.044). In the correlation analysis between anxiety symptom severity and oxidative stress indicators in the group with anxiety disorder, we found a positive correlation between TOS and RCADS total anxiety score (p=0.08). Conclusion These results may point to an oxidative dysfunction in anxiety disorders and the potential role of oxidative stress in their aetiology. Prospective, large-scale, randomized studies are needed to investigate if oxidative stress indicators can be used in the diagnosis of anxiety disorders and as new treatment targets.

C-terminal cross-linking telopeptide levels in COVID-19 patients: A prospective case-control study.

BACKGROUND: Coronavirus disease 19 (COVID-19) is a viral infection mediated by coronavirus-2 that causes severe acute respiratory syndrome (SARS-CoV-2). The disease may affect biochemical parameters and electrolytes. C-terminal cross-linking telopeptide (CTX-I) is released during mature bone resorption and is a biomarker for predicting bone resorption. OBJECTIVES: As the pandemic progressed, understanding the effects of COVID-19 disease remained critical. Inflammatory responses triggered by the virus can result in a bone metabolism regulation imbalance. As such, this study aimed to analyze serum levels of CTX-I, calcium (CA), phosphorus (P), magnesium (Mg), C-reactive protein (CRP), and alkaline phosphatase (ALP) in COVID-19 patients to investigate the relationship between bone resorption and the disease. MATERIAL AND METHODS: The study included 56 individuals with COVID-19 (divided into mild, moderate and severe subgroups depending on disease severity) and 25 healthy adults as a control group. Serum CTX-I concentrations were measured with enzyme-linked immunosorbent assay (ELISA). In addition, CRP, Ca, Mg, P, and ALP levels were measured using an automated clinical chemistry analyzer. RESULTS: Serum CTX-I levels were significantly higher in COVID-19 patients than in the control group (p < 0.05). Furthermore, a positive weak relationship was detected between CRP and CTX-I (r = 0.303, p < 0.05). CONCLUSIONS: Increased serum CTX-I levels in the patient group caused COVID-19-driven bone degradation, though serum CTX-I levels did not differ according to disease severity.

Modulatory role ulexit against thiamethoxam-induced hematotoxicity/hepatotoxicity oxidative stress and immunotoxicity in Oncorhynchusmykiss.

Contamination of the aquatic environment with different insecticides is a major concern in the aquatic ecosystem today. For this reason, in the designed study, Thiamethoxam (TMX) for which there is limited information on its negative effects on Oncorhynchus mykiss was investigated, its effects on hematotoxicity, oxidative status, cytotoxicity, DNA damage and apoptotic status indicators in blood/liver tissue. However, the antitoxic potential of ulexite (UX) supplementation in the elimination of TMX-mediated toxicity has been determined. LC50-96h value determined for TMX 0.73 mg/L has been determined. As a result of hematology profile, TMX application, RBC, Hgb and Hct values showed a temporal decrease compared to the control group, while increases were determined in MCV, MCH and MCHC values. It was determined that the inhibition/induction of hematological parameters was slowed down by adding UX to the medium. During the trial (48th and 96th hours), it was noted that TMX induced cortisol level, while UX supplementation slowed this induction at 48th hour. Antioxidant enzyme activities were significantly inhibited by TMX application, and MDA and MPO values increased as a result of the stimulation of ROS. It was determined that UX added to the medium showed activity in favor of antioxidants and tried to inhibit MDA and MPO levels. When Nrf-2, one of the inflammation parameters, was compared with the administration and control groups, it was determined that it inhibited depending on time, TNF-α, IL-6, DNA damage and apoptosis were induced, and UX suppressed this situation. The results obtained were evaluated as statistically meaningful. Briefly, it was determined that TMX induced oxidative damage in all tissues at 48th - 96th hours, whereas UX mitigated this situation. The results provide possible in vivo evidence that UX supplements can reduce TMX-mediated oxidative stress and tissues damage in O. mykiss blood and liver tissues.

Effect of climate change on hematotoxicity/hepatoxicity oxidative stress, Oncorhynchus mykiss, under controlled conditions.

Described as the 'main ecological factor', temperature, strongly affects the physiological stress responses of fish. In order to evaluate the effects of temperature variations on fish culture and food value chain, the present study was designed as a climate change model. Furthermore, the present study provides a theoretical basis for a better understanding of the mechanisms of the environmentally induced changes. In this direction, we examined the blood physiology and oxidative stress responses induced by temperature variation in the rainbow trout, a temperature-sensitive cold-water fish. The obtained results showed that climate changes promoted the inhibited activities' expressions and the development of potential tissue and hematological defense mechanisms against temperature-induced toxic damage. This study showed that climate change could be a subset of the studies on the stress physiology in aquaculture, which can be developed for new experimental designs and research collaborations. Furthermore, it highlights knowledge gaps to guide future research in this emerging field.

New sulfonamide derivatives based on 1,2,3-triazoles: synthesis, in vitro biological activities and in silico studies.

Eight new hybrid constructs containing a series of sulfonamide and 1,2,3-triazole units were designed and synthesized. Anticancer, antioxidant and cholinesterase activities of these hybrid structures were investigated. In our design, the Cu(I)-catalyzed click reaction between N,4-dimethyl-N-(prop-2-yn-1-yl)benzenesulfonamide (6) and aryl azides 8a-h was used. Antioxidant activity values of 9f (IC50: 229.46 ± 0.001 µg/mL) and 9h (IC50: 254.32 ± 0.002 µg/mL) hybrid structures were higher than BHT (IC50: 286.04 ± 0.003 µg/mL) and lower than Ascorbic acid (IC50: 63.53 ± 0.001 µg/mL) and α-Tocopherol (IC50: 203.21 ± 0.002 µg/mL). We determined that the cytotoxic effects of hybrid constructs 9d (IC50: 3.81 ± 0.1084 µM) and 9g (IC50: 4.317 ± 0.0367 µM) against A549 and healthy cell line (HDF) are much better than standard cisplatin (IC50: 6.202 ± 0.0705 µM). It was determined that the AChE inhibitory activities of all synthesized compounds were much better than Galantamine used as a standard. In particular, 9c (IC50: 13.81 ± 0.0026 mM) had ten times better activity than the standard Galantamine (IC50: 136 ± 0.008 mM). The ADMET properties of the molecules have been thoroughly examined and met the criteria for drug-like substances. They also have a high oral absorption rate, as they can effectively cross the blood-brain barrier and are easily absorbed in the gastrointestinal tract. In vitro experiments were confirmed by in silico molecular docking studies.Communicated by Ramaswamy H. Sarma.

A new treatment approach: Melatonin and ascorbic acid synergy shields against sepsis-induced heart and kidney damage in male rats.

AIM: To investigate the combined therapeutic potential of melatonin and ascorbic acid in mitigating sepsis-induced heart and kidney injury in male rats and assess the combination therapy's effects on inflammation, cellular damage, oxidative stress, and vascular function-related markers. MATERIALS AND METHODS: Cecal ligation and puncture (CLP) induced sepsis in male rats, which were divided into five groups: Sham, CLP, MEL (melatonin), ASA (ascorbic acid), and MEL+ASA (melatonin and ascorbic acid). Rats were treated, and heart and kidney tissues were collected for biochemical and histopathological analyses. Inflammatory markers (presepsin, procalcitonin, NF-κB, IL-1ß, IL-6, TNF-α), cellular damage marker (8-OHDG), oxidative status, nitric oxide (NO), vascular endothelial growth factor (VEGF), and sirtuin 1 (SIRT1) levels were assessed. KEY FINDINGS: Melatonin and ascorbic acid treatment reduced inflammatory and cellular damage markers compared to the CLP group. Combined treatment improved NO, VEGF levels, and increased SIRT1 expression, suggesting a synergistic effect in mitigating sepsis-induced inflammation, cellular damage, and oxidative stress. Histopathological analyses supported these findings, revealing reduced heart and kidney injury in the MEL+ASA group. SIGNIFICANCE: Our study highlights potential benefits of combining melatonin and ascorbic acid as a therapeutic strategy for alleviating sepsis-induced heart and kidney injury. The synergistic effects of these agents may provide stronger protection against inflammation, oxidative stress, and tissue damage, opening new avenues for future research and clinical applications in sepsis management.

Neutralization of iron oxide magnetic nanoparticle aquatoxicity on Oncorhynchus mykiss via supplementation with ulexite.

Nowadays, the unique features of nanoparticles (NPs) have encouraged new applications in different areas including biology, medicine, agriculture, and electronics. Their quick joining into daily life not only enhances the uses of NPs in a wide range of modern technologies but also their release into the aquatic environment causes inevitable environmental concerns. On the other hand boron exhibits key physiological effects on biological systems. This research was designed for evaluating the toxicity of magnetite nanoparticles (Fe3O4-MNPs) on aquatic organisms and obtaining data for the information gap in this area. In this study, Rainbow trout (Oncorhynchus mykiss) was considered as an aquatic indicator, and trials were designed as Ulexite (a boron mineral, UX) treatment against exposure to Fe3O4-MNPs. Synthesized and characterized Fe3O4-MNPs were exposed to rainbow trouts in wide spectrum concentrations (0.005-0.08 mL/L) to analyze its lethal dose (LC50) and cytoprotective properties by UX treatment were assessed against Fe3O4-MNPs applications for 96 h. For the initial toxicity analysis, hematological parameters (blood cell counts) were examined in experimental groups and micronucleus (MN) assay was performed to monitor nuclear abnormalities after exposure to NPs. Biochemical analyzes in both blood and liver samples were utilized to assess antioxidant/oxidative stress and inflammatory parameters. Also, 8-hydroxy-2'-deoxyguanosine (8-OHdG) assay was used to investigate oxidative DNA lesions and Caspase-3 analysis was performed on both blood and liver tissues to monitor apoptotic cell death occurrence. When antioxidant enzymes in blood and liver tissue were examined, time-dependent decreases in activity were determined in SOD, CAT, GPx, and GSH enzymes, while increased levels of MDA and MPO parameters were observed in respect to Fe3O4-MNPs exposure. It was found that TNF-α, Il-6 levels were enhanced against Fe3O4-MNPs treatment, but Nrf-2 levels were decreased at the 46th and 96th h. In the 96th application results, all parameters were statistically significant (p < 0.05) in blood and liver tissue, except for the IL-6 results. It was determined that the frequency of MN, the level of 8-OHdG and caspase-3 activity increased in respect to Fe3O4-MNPs exposure over time. Treatment with UX alleviated Fe3O4-MNPs-induced hematotoxic and hepatotoxic alterations as well as oxidative and genetic damages. Our findings offer strong evidence for the use of UX as promising, safe and natural protective agents against environmental toxicity of magnetite nanoparticles.

Microplastic-induced oxidative stress response in turbot and potential intake by humans.

Microplastic (MP) pollution has become a health concern subject in recent years. Althoughann increasing number of studies about the ingestion of microplastics by fish, research on the oxidative stress response to MPs in natural environments is quite limited. In this study, the identification and characterization of MPs in gill (G), muscle tissues (M), and gastrointestinal tract (GI) of turbot (Scophthalmus maximus) were evaluated. Oxidative damage of MPs on the brain (B), liver (L), gill (G), and muscle (M) tissues as well as their effect on superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), paraoxonase (PON), arylesterase (AR) myeloperoxidase (MPO), and malondialdehyde (MDA) biomarkers were evaluated. The potential transmission of MPs from muscle tissues to humans was examined. Results showed that gills contain the highest amounts of MPs, ethylene propylene is the most dominant polymer type, black and blue are the most common MP color, fiber is the most common shape, and 50-200 µm is the most common MP size. Results showed that MPs cause oxidative stress of tissues with inhibiting effect on enzyme activities and promoting impact on lipid peroxidation. The oxidative damage mostly affected the liver (detoxification organ) followed by gill tissue. The intake of MPS in the European Union was estimated by EFSA as 119 items/year, while in Turkey it is 47.88 items/year. This study shows that more research is needed in terms of ecosystem health and food chain safety. The risk assessment of MPs in living organisms and environmental matrices including food safety and human health should be considered a public health issue.

Neuroprotective properties of borax against aluminum hydroxide-induced neurotoxicity: Possible role of Nrf-2/BDNF/AChE pathways in fish brain.

The current study was designed to assess the possible neuroprotective effect of borax (BX) against the toxicity of aluminum hydroxide [AH, Al (OH)3] on brain of rainbow trout (Oncorhynchus mykiss) with multibiomarker approaches. For this purpose, the presence of the neuroprotective action by BX against the AH exposure was assessed by the activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), myeloperoxidase (MPO), acetylcholinesterase (AChE). In addition, we evaluated glutathione (GSH), malondialdehyde (MDA), DNA damage (8-OHdG), apoptosis (caspase 3), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), nuclear factor erythroid-2 (Nrf-2), and brain-derived neurotrophic factor (BDNF) levels in 96 h semi-static treatment. In the 48th and 96th hour samplings, apoptosis induced by AH in the Nrf-2/BDNF/AChE pathways in rainbow trout brain tissue was revealed by DNA damage, enzyme inhibitions and lipid peroxidations. On the contrary applications of BX supported antioxidant capacity without leading apoptosis, lipid peroxidation, inflammatory response and DNA damage. BX also increased the BDNF levels and AChE activity. Moreover, BX exerted a neuroprotective effect against AH-induced neurotoxicity via down-regulating cytokine-related pathways, minimising DNA damage, apoptosis as well as up-regulating GSH, AChE, BDNF and antioxidant enzyme levels. It can be concluded that the combination of borax with AH modulated the toxic effects of AH.

Triazole based novel molecules as potential therapeutic agents: Synthesis, characterization, biological evaluation, in-silico ADME profiling and molecular docking studies.

In this study, eight new compounds (7a-h) based on triazole compounds containing ester groups were synthesized with high yields. The structures of the synthesized compounds (7a-h) were elucidated by various spectroscopic methods (element analysis, FT-IR, 1H-(13C) NMR). Antioxidant, anticancer, and α-amylase enzyme inhibition activities of synthesized new triazole derivatives were carried out, and the effects of different groups on the activity were investigated. When the determined antioxidant properties of the compounds were examined, all synthesized compounds showed a moderate radical scavenging effect against radicals depending on the concentration (6.25-200 g/mL). All compounds except the three derivatives were found to have higher IC50 values than the standard drug acarbose (IC50: 891 µg/mL) according to the α-amylase enzyme inhibition results. Compound 7g (IC50: 50 g/mL) was discovered to have nearly eighteen (18) times the activity of the conventional medication acarbose (IC50: 891 µg/mL). Compounds synthesized for anticancer activity studies were screened against the Hela cell line, and the results were compared with standard cis-platinum (IC50: 16.30 µg/mL). Compound 7g (IC50: 19.78 µg/mL) was found to have almost the same activity as cis-platinum. Using Qikprop, the compounds were thoroughly tested for ADME qualities, and none violated any drug similarity standards. According to ADME data, whole physicochemical drug-likeness parameters of molecules remained within defined ranges as stipulated in the Lipinski rules (RO5) and revealed a high bioavailability profile. The molecular docking results with 2QV4 and 4GQR alpha-amylase enzymes demonstrated that all molecules have a high affinity, indicating polar and apolar interaction with critical amino acids in the α-amylase binding pocket.

Ulexite modulates the neurotoxicological outcomes of acetylferrocene-exposed rainbow trout.

In this study, the neuroprotective action potential by ulexite (UX) (18.75 mg/L) against acetylferrocene (AFC) (3.82 mg/L) induced neurotoxicity was aimed to investigate in brain tissues of Oncorhynchus mykiss. For this purpose, the effects on neurotoxicity markers, proinflammatory cytokines, antioxidant immune system, DNA, and apoptosis mechanisms were assessed on brain tissues in the 48-96  h of the 96- trial period. In this research, it was determined that brain-derived nerve cell growth factor (BDNF) level and acetylcholinesterase (AChE) activity were inhibited in the brain tissue compared to the control group by AFC. In addition, inhibition in glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), and glutathione (GSH) values (which are antioxidant system biomarkers), and inductions in malondialdehyde (MDA) and myeloperoxidase (MPO) amounts (which are indicators of lipid peroxidation) were determined (p < 0.05) after exposure to AFC. And, while tumor necrosis factor-α (TNF-α) and IL-6 levels were increased in the AFC-exposed group, Nrf-2 levels were found to be remarkably decreased. Upregulation was also detected in 8-hydroxydeoxyguanosine (8-OHdG) and caspase-3 levels, which are related to DNA damage and apoptosis mechanism. On the contrary, UX (single/with AFC) suppressed the AChE and BDNF inhibition by AFC. Moreover, UX mitigated AFC-induced oxidative, inflammatory, and DNA damage and attenuated AFC-mediated neurotoxicity via activating Nrf2 signaling in fish. Collectively, our findings revealed that UX supplementation might exert beneficial effects and may be considered as a natural and promising neuroprotective agent against AFC-induced toxicity.

High Fetuin-A Levels in Children with Celiac Disease.

OBJECTIVE: Fetuin-A is a multifunctional non-collagen protein that plays a role in bone mineralization. Celiac disease is a chronic inflammatory disorder of the small intestine due to exposure to gluten. In this research, it was aimed to investigate levels of Fetuin-A and its relationship with bone mineral density in children with celiac disease. MATERIALS AND METHODS: The study was conducted on 59 children with celiac and 29 healthy children. The celiac disease group was composed of three groups, newly diagnosed, gluten-free diet compliant and, non- gluten- free diet compliant patients. Serum Fetuin-A concentrations were measured by an enzyme-linked immuno- sorbent assay kit. Measurement of bone mineral density was performed a dual-energy x-ray absorptiometry. RESULTS: Serum Fetuin-A levels were 136.85 ± 38.09 µg/L and 112.95 ± 44.39 µg/L in the celiac disease and healthy control groups, respectively. There was a statistically significant difference between groups in levels of serum Fetuin-A (P < .05). A significant positive correlation was observed between serum Fetuin-A and bone mineral density Z-score in the celiac patients. CONCLUSION: Increased Fetuin-A levels and positive correlation between Fetuin-A and bone mineral density in children with celiac disease suggest that Fetuin-A may be a biomarker for celiac disease.

Borax relieved the acrylamide-induced hematotoxic, hepatotoxic, immunotoxic and genotoxic damages in rainbow trout by regulating apoptosis and Nrf2 signaling pathway.

Acrylamide(AA) is a compound with wide usage areas including paper, dyes, and plastics industries. Due to its broad spectrum and water solubility suggest that this vinyl compound may cause serious environmental problems. AA was shown to exhibit neurotoxic, immunotoxic, reproductive toxicant as well as carcinogenic potency on animals. Especially in recent years, the therapeutic effects of boron and boron containing compounds like borax(BX), ulexite(ULX) and colemanite(COL) had been reported. However, the ameliorative potential by boron compounds against AA-induced toxicities had not been investigated yet. Therefore, in this investigation rainbow trout were exposed acutely to AA in the presence and absence of BX. The hematological indices and genotoxic end-points were examined in the fish blood tissue. In addition to oxidative stress response, the levels of DNA damage, CASP3, TNF-α, Nrf-2 as well as IL-6 amounts were determined in both blood and liver tissues of fish. The obtained results executed that AA induced toxic conditions in both tissues. In fact, an increase in the amount of oxidative stress and ROS, and a decrease in GSH levels were observed. AA exposure led to an increase in CASP3levels and 8-OHdG formation. It was also found that Nrf-2 pathway contributed to the initiation of oxidative stress that associated with AA-induced toxicity. On the contrary, our findings indicated that co-exposure of BX with AA elicited oxidative stress and cell death. In a conclusion BX was suggested as a useful and effective natural agent for the prevention and early treatment of AA toxicity in fish.

Borax exerts protective effect against ferrocene-induced neurotoxicity in Oncorhynchus mykiss.

BACKGROUND: In recent years, therapeutic targets and the development of new drugs have shifted research towards inflammatory and oxidative stress pathways. Ferrocene (FcH) is a stable, small molecule that exhibits immunostimulatory and anti-tumor properties by a different mechanism and is effective at low doses in oral administration. However, it was surprising that there has been no performed investigation using FcH on aquaculture. On the other hand, recent papers reveal the key biological functions and health benefits due to daily boron intake in animals and humans. Therefore, we investigated the neurotoxic damage potential of FcH and its related neurotoxicity action mechanism in aquatic environments. In addition, the protective potential of borax (BX, or sodium borate) were evaluated againt in vivo neurotoxicity by FcH. METHODS: Neurotoxicity assessment was performed in rainbow trout brain tissue, acutely under semi-static conditions via determining a vide range of parameters including catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD) activities as well as glutathione (GSH), myeloperoxidase (MPO), glutathione (GSH), malondialdehyde (MDA levels), DNA damage (8-OHdG), apoptosis (caspase 3), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), nuclear factor erythroid-2 (Nrf-2), acetylcholinesterase (AChE) and brain-derived neurotrophic factor (BDNF) levels. In addition, the LC50 96 h level of FcH was determined for the first time in rainbow trout in this study. RESULTS: In the obtained results, while FcH caused inhibition in enzyme activities, it showed an inducing effect on MDA, MPO, BDNF, Nrf2, TNF-α and IL-6 levels. It was determined that this oxidative damage related alterations were significantly different (p < 0.05) in comparison between FcH treated and controls. Again, the LC50 96 h value in rainbow trout was determined as 11.73 mg/L, which is approximately 5% less than the value given for freshwater fish (12.3 mg/L). On the contrary, it was observed that BX has a mitigating effect on FcH-induced neurotoxicity. CONCLUSION: The present study suggests that borax may be useful for preventing or alleviating neurotoxicity induced by environmental contaminants or toxic chemicals.

Magnetic nanoparticles-induced neurotoxicity and oxidative stress in brain of rainbow trout: Mitigation by ulexite through modulation of antioxidant, anti-inflammatory, and antiapoptotic activities.

The prevalent exposition of metallic nanoparticles (MNPs) to the aquatic medium and their negative influence on human life is one of the major concerns global. Stress mechanization, as a non-specific and pervasive response, involves all physiological systems, particularly the closely interconnected neuroendocrine and immune systems. In this study, which was designed to obtain more data on the biological effects of ulexit, which prevents oxidative DNA damage by protecting against toxicity damage and offers new antioxidant roles. The concomitant use of ulexite (UX, as 18.75 mg/l) as a natural therapeutic agent against exposure to magnetic nanoparticles (Fe3O4-MNPs/0.013 ml/l) on Oncorhynchus mykiss was investigated for 96 h. The brain tissues were taken at the 48th and 96th hours of the trial period, the effects on neurotoxic, pro-inflammatory cytokine genes, antioxidant immune system, DNA and apoptosis mechanisms were analyzed. In the present study, it was determined that AChE activity and BDNF level in the brain tissue decreased over time in the Fe3O4-MNPs group compared to the control, and UX tried to depress this inhibition. While inhibition was determined in antioxidant system biomarkers (SOD, CAT, GPx, and GSH values), an induction was observed in lipid peroxidation indicators (MDA and MPO values) in Fe3O4-MNPs applied group. The same group data showed that TNF-α, IL-6, 8-OHdG and caspase-3 levels were increased, but Nrf-2 levels were decreased. The alterations in all biomarkers were found to be significant at the p < 0.05 level. In general, it was determined that Fe3O4-MNPs caused stress in O. mykiss and UX exhibited a positive effect on this stress management.

Trace elements released from dental implants with periimplantitis: a cohort study.

BACKGROUND: Pure titanium and Ti6Al4V alloy have been in use as dental implant contemporarily. Trace element release from implant bodies is a possible health problem. Well-healed and osseointegrated intrabony implants are only in contact with bone and blood, but in the case of periimplantitis, the possibility of corrosion and the release of trace elements from dental implant surfaces increases due to contact with external factors. AIMS: The aim of this study is to evaluate the trace element levels in the blood serum and saliva of patients who have dental implants with periimplantitis compared with the control group. METHODS: This study included 25 patients diagnosed with periimplantitis and 25 participants with healthy osseointegrated implants as the control group. The trace element levels in blood serum and saliva were measured by inductively coupled plasma-mass spectrometry (ICP-MS) and results were analyzed statistically. RESULTS: There is no statistically significant difference between groups for saliva samples except the aluminum (Al) levels of the study group are significantly lower than the control group (p < 0.05) and the mercury (Hg) levels of the study group are significantly higher than the control group (p < 0.05). On the other hand, there is a significant decrease in titanium (Ti), chromium (Cr), and iodine (I) in the blood serum samples of the study group (p < 0.05). There is no significant difference between the groups for other measured trace elements in the blood serum (p > 0.05). CONCLUSION: There is no statistically significant increase in titanium or aluminum levels in the study group compared with the control group.

Hematotoxic, oxidative and genotoxic damage in rainbow trout (Oncorhynchus mykiss) after exposure to 3-benzoylpyridine.

Pyridine is a basic heterocyclic organic compound. The pyridine ring is present in many important compounds, including agricultural chemicals, medicines and vitamins. Due to their widespread industrial use, bioaccumulation and non-target toxic effects are being considered as a great risk to human and environmental health. In this study, we aimed to evaluate the hematological, oxidative and genotoxic damage potentials by different concentrations (1, 1.5, and 2 g/L) of the ketone 3-Benzoylpyridine (3BP) on rainbow trout (Oncorhynchus mykiss). Alterations in the biomarker levels of oxidative DNA damage (8-hydroxy-2'-deoxyguanosine (8-OHdG)), apoptosis (Caspase-3), malondialdehyde (MDA) as well as antioxidant enzyme activities including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), myeloperoxidase (MPO), paraoxonase (PON), and arylesterase (AR) were assessed in brain, liver, gill and blood tissues. Acetylcholinesterase (AChE) activity was also determined in brain tissue. In addition, we analyzed micronucleus (MN) rates and hematological indices of total erythrocyte count (RBC), total leukocyte count (WBC), hemoglobin (Hb), hematocrit (Hct), total platelet count (PLT), mean cell hemoglobin concentration (MCHC), mean cell hemoglobin (MCH), and mean cell volume (MCV) in blood. LC50-96h value of 3BP was calculated as 5.2 g/L from the data obtained. A significant decrease in brain AChE activity was determined in clear time and dose dependent manners. While SOD, CAT, GPx, PON, and AR levels were decreased, MDA, MPO, 8-OHdG and Caspase-3 levels were increased in all tissues (p < 0.05). Again, the 3BP led to increases of MN formation at all applied concentrations in the rates of between 45.4 and 72.7%. Significant differences (p < 0.05) were found out in between all studied hematology parameters between 3BP-exposed and the control fish. In conclusion, ours study firstly indicated that the treatment doses of 3BP induced distinct hematological and oxidative alterations as well as genotoxic damage in rainbow trout.

Is Serum Progranulin Level a Biomarker in Autism and Cognitive Development Disorders?

OBJECTIVE: Cognitive developmental delay is a picture of the group of early-onset chronic diseases that affect 1.5-10% of children. Autism spectrum disorders are neurodevelopmental diseases with a genetic basis and abnormal brain development, characterized by disorders in areas that make up interpersonal relationships, such as communication, social cognition, and processing of emotional signals. Immune system dysfunction is thought to play a role in the pathogenesis of some neurological disorders, including autism. Progranulin is thought to be a regulator of the innate immune response. The purpose of this study was to look at plasma levels of progranulin, an anti-inflammatory neurotrophic factor, in children with autism spectrum disorder and cognitive developmental delay. MATERIALS AND METHODS: The study was conducted on 52 children who were patients and 35 healthy children. Of the 52 children of the patient group, 32 were diagnosed with CDD and 20 were diagnosed with cognitive developmental delay-autism spectrum disorder. Serum progranulin concentrations were measured using a human-specific sandwich enzyme-linked immunosorbent assay. RESULTS: Serum progranulin concentration was statistically lower in the patient group (110.746 ± 26.04) than in the healthy control group (137.346 ± 30.02). There was a statistically significant difference between the groups in levels of serum progranulin (P=.000). Receiver operating characteristic analysis was performed to evaluate the potential of progranulin as a biomarker to distinguish patients with cognitive developmental delay-autism spectrum disorder from healthy children. It detected a moderate area under the curve (0.743 ± 0.06) value and a more significant P value for progranulin (P=.000). CONCLUSION: Progranulin deficiency in patients with autism spectrum disorder-cognitive developmental delay may result in decreased neurotrophic support for many years, with cumulative damage associated with unregulated inflammation that may play a role in autism spectrum disorder-cognitive developmental delay. We believe that low progranulin levels could be a biomarker for autism spectrum disorder-cognitive developmental delay.

The effect of taxifolin on experimental testicular ischaemia reperfusion injury in rats. A biochemical and histopathological analysis / Efecto de la taxifolina en la lesión experimental testicular por reperfusión-isquemia en ratas. Análisis bioquímico e histopatológico

Objectives: The aim of the study is to investigate the protective effect of taxifolin (3,5,7,3,4-pentahydroxy flavanone), a strong antioxidant, against testicular I/R injury in rats biochemically and histopathologically.Materials and methods: 50mg/kg taxifolin was administered to taxifolin+testicular torsion–detorsion (TTTD, n-10) group of Albino Wistar male rats by oral gavage. Distilled water .5ml as a solvent was administered to testicular torsion–detorsion (TTD, n-10) and Healthy Control (SG, n-10) groups using the same method. An hour after the administration of taxifolin and distilled water, anaesthesia (ketamine 60mg/kg) was administered to all animal groups. TTD and TTTD group animals were subjected to testicular torsion at 720 degrees for four hours during anaesthesia. At the end of this period, testicular detorsion was applied and perfusion was allowed for four hours. Sham operation was applied to SG group.Results: Our biochemical experiment results showed that the amount of malondialdehyde (MDA) in testicular tissue of TTD group presented a significant increase compared to SG and TTTD groups whereas total glutathione (tGSH) and superoxide dismutase (SOD) levels decreased. In addition, while TTD group presented severe histopathological damage in germinal epithelium cell and seminiferous tubule, mild damage was observed in TTTD group.Conclusions: The results of our experiment indicate that taxifolin could be useful in the treatment of testicular I/R damage. (AU)

Objetivos: El objetivo del estudio fue analizar el efecto protector de la taxifolina (3,5,7,3,4-pentahidroxi flavanona), un fuerte antioxidante, en la lesión por reperfusión-isquemia (R/I) en ratas, a nivel bioquímico e histopatológico.Materiales y métodos: Se administraron 50 mg/kg de taxifolina a un grupo de ratas macho Albino Wistar con torsión-destorsión y taxifolina+testicular (TTTD, n-10) mediante una sonda oral, y una solución de 0,5 mL de agua destilada a un grupo con torsión-destorsión testicular (TTD, n-10) y a controles sanos (SG, n-10), utilizando el mismo método. Una hora después de la administración de taxifolina y agua destilada, se aplicó anestesia (ketamina 60 mg/kg) a todos los grupos de animales. Los grupos TTD y TTTD fueron sometidos a una torsión testicular a 720 grados por cuatro horas durante la anestesia. Al finalizar este período, se aplicó destorsión testicular, permitiéndose la perfusión durante cuatro horas. Se aplicó un placebo al grupo SG.Resultados: Los resultados de nuestro experimento bioquímico reflejaron que el incremento de malondialdehído (MDA) en el tejido testicular del grupo TTD presentó un aumento significativo en comparación con los grupos SG y TTTD, mientras que disminuyeron los niveles de glutatión (tGSH) y superóxido dismutasa (SOD). Además, mientras que el grupo TTD presentó daño histopatológico severo en las células del epitelio germinal y el tubo seminífero, se observó un daño leve en el grupo TTTD.Conclusiones: Los resultados de nuestro experimento indican que la taxifolina podría ser de utilidad para el tratamiento de la lesión testicular por R/I. (AU)

The effect of taxifolin on experimental testicular ischaemia reperfusion injury in rats. A biochemical and histopathological analysis.

OBJECTIVES: The aim of the study is to investigate the protective effect of taxifolin (3,5,7,3,4-pentahydroxy flavanone), a strong antioxidant, against testicular I/R injury in rats biochemically and histopathologically. MATERIALS AND METHODS: 50mg/kg taxifolin was administered to taxifolin+testicular torsion-detorsion (TTTD, n-10) group of Albino Wistar male rats by oral gavage. Distilled water .5ml as a solvent was administered to testicular torsion-detorsion (TTD, n-10) and Healthy Control (SG, n-10) groups using the same method. An hour after the administration of taxifolin and distilled water, anaesthesia (ketamine 60mg/kg) was administered to all animal groups. TTD and TTTD group animals were subjected to testicular torsion at 720 degrees for four hours during anaesthesia. At the end of this period, testicular detorsion was applied and perfusion was allowed for four hours. Sham operation was applied to SG group. RESULTS: Our biochemical experiment results showed that the amount of malondialdehyde (MDA) in testicular tissue of TTD group presented a significant increase compared to SG and TTTD groups whereas total glutathione (tGSH) and superoxide dismutase (SOD) levels decreased. In addition, while TTD group presented severe histopathological damage in germinal epithelium cell and seminiferous tubule, mild damage was observed in TTTD group. CONCLUSIONS: The results of our experiment indicate that taxifolin could be useful in the treatment of testicular I/R damage.