Quantification of Heavy Metals in the Nasal Turbines of Smokers and Nonsmokers.

OBJECTIVES: Cigarette smoke is known to contain toxic heavy metals. In this study, heavy metal levels in the nasal turbinate tissues of smokers and nonsmokers were measured and compared with Inductively Coupled Plasma-Mass Spectrometry (ICP-MS). METHODS: Forty patients who come to the Otorhinolaryngology outpatient clinic due to nasal obstruction and are given an appointment for partial turbinate reduction operation due to inferior turbinate hypertrophy, according to their smoking status, were divided into two groups: those who had smoked one pack/day for at least 10 years and those who had never smoked. The levels of heavy metals (Al, As, Ba, Cd, Cr, Co, Cu, Pb, Mn, Hg, Ni, Se, and Ag) were compared by ICP-MS in nasal turbinate tissues. RESULTS: Al (p = 0.002), Cr (p < 0.001), Co (p < 0.001), Ni (p = 0.001), Cu (p < 0.001), As (p < 0.001), Se (p < 0.001), Ag (p < 0.001), Cd (p = 0.001), Ba (p = 0.008), Hg (p < 0.001), and Pb (p < 0.001) values in the smoker group were found to be significantly higher than the values of nonsmokers. Although the Mn level was high in smokers, no significant difference was observed (p = 0.299). CONCLUSIONS: Smoking can cause nasal and sinus problems. In this study, we observed that the smoking group had significantly higher levels of almost all the heavy metals investigated in the nasal turbinate tissues. As smoking damages, the mucociliary system and the mucosa, heavy metals from cigarettes may accumulate further and cause harm to the nasal tissues. LEVEL OF EVIDENCE: Level 3 Laryngoscope, 2024.

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.

Molecular mechanisms of resveratrol and its silver nanoparticle conjugate in addressing sepsis-induced lung injury.

Sepsis is a life-threatening condition characterized by a systemic inflammatory response to infection. Despite extensive research on its pathophysiology, effective therapeutic approaches remain a challenge. This study investigated the potential of resveratrol (RV) and silver nanoparticle-enhanced resveratrol (AgNP-RV) as treatments for sepsis-induced lung injury using a rat model of polymicrobial sepsis induced by cecal ligation and puncture (CLP). The study focused on evaluating changes in oxidative status (TAS, TOS, and OSI) and the expression of inflammatory and apoptotic markers (IL-1ß, TNF-α, P2X7R, TLR4, Caspase-3, and Bcl-2) in lung tissue. Both RV and AgNP-RV demonstrated potential in mitigating oxidative stress, inflammation, and apoptosis, with AgNP-RV exhibiting greater efficacy than RV alone (p < 0.05). These findings were corroborated by histopathological analyses, which revealed reduced tissue damage in the RV- and AgNP-RV-treated groups. Our study highlights the therapeutic potential of RV and, particularly, AgNP-RV in combating sepsis-induced oxidative stress, inflammation, and apoptosis. It also underscores the promise of nanoparticle technology in enhancing therapeutic outcomes. However, further investigations are warranted to fully understand the mechanisms of action, especially concerning the role of the P2X7 receptor in the observed effects. Nonetheless, our research suggests that RV and AgNP-RV hold promise as novel strategies for sepsis management.

ENHANCED EFFICACY OF RESVERATROL-LOADED SILVER NANOPARTICLE IN ATTENUATING SEPSIS-INDUCED ACUTE LIVER INJURY: MODULATION OF INFLAMMATION, OXIDATIVE STRESS, AND SIRT1 ACTIVATION.

ABSTRACT: Sepsis-induced acute liver injury is a life-threatening condition involving inflammation, oxidative stress, and endothelial dysfunction. In the present study, the preventive effects of resveratrol (RV) alone and RV-loaded silver nanoparticles (AgNPs + RV) against sepsis-induced damage were investigated and compared in a rat model of polymicrobial sepsis induced by cecal ligation and puncture (CLP). Rats were divided into four groups: Sham, CLP, RV, and AgNPs + RV. Pro-inflammatory cytokines (TNF-α, IL-1ß, IL-6), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, presepsin, procalcitonin (PCT), 8-hydroxy-2'-deoxyguanosine (8-OHDG), vascular endothelial growth factor (VEGF), and sirtuin-1 (SIRT1) levels were assessed to determine the treatments' effects. AgNPs + RV treatment significantly reduced pro-inflammatory cytokines, NF-κB activation, presepsin, PCT, 8-OHDG, and VEGF levels compared with the CLP group, indicating attenuation of sepsis-induced liver injury. Both RV and AgNPs + RV treatments increased SIRT1 levels, suggesting a potential role of SIRT1 activation in mediating the protective effects. In conclusion, AgNPs + RV treatment demonstrated extremely enhanced efficacy in alleviating sepsis-induced liver injury by modulating inflammation, oxidative stress, and endothelial dysfunction, potentially mediated through SIRT1 activation. In this study, the effect of AgNPs + RV on sepsis was evaluated for the first time, and these findings highlight AgNPs + RV as a promising therapeutic strategy for managing sepsis-induced liver injury, warranting further investigation.

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.

The effects of metyrosine on ischemia-reperfusion-induced oxidative ovarian injury in rats: Biochemical and histopathological assessment.

The aim of this study is to investigate the effect of metyrosine on ischemia-reperfusion (I/R) induced ovarian injury in rats in terms of biochemistry and histopathology. Rats were divided into: ovarian I/R (OIR), ovarian I/R+50 mg/kg metyrosine (OIRM) and sham (SG) operations. OIRM group received 50 mg/kg metyrosine one hour before the application of the anesthetic agent, OIR and SG group rats received equal amount of distilled water to be used as a solvent orally through cannula. Following the application of the anesthetic agent, ovaries of OIRM and OIR group rats were subjected to ischemia and reperfusion, each of which took two hours. This biochemical experiment findings revealed high levels of malondialdehyde (MDA) and cyclo-oxygenase-2 (COX-2) and low levels of total glutathione (tGSH), superoxide dismutase (SOD) and cyclo-oxygenase-1 (COX-1) in the ovarian tissue of OIR group, with significant histopathological injury. In metyrosine group, MDA and COX-2 levels were lower than the OIR group whereas tGSH, SOD and COX-1 levels were higher, with slighter histopathological injury. Our experimental findings indicate that metyrosine inhibits oxidative and pro-inflammatory damage associated with ovarian I/R in rats. These findings suggest that metyrosine could be useful in the treatment of ovarian injury associated with I/R.

Could Fetuin-A Be a Biomarker for Autism Spectrum Disorder and Cognitive Developmental Delay?

Early detection of cognitive developmental delay (CDD) and autism spectrum disorder (ASD) is challenging, despite the numerous scientific studies conducted and different therapeutic strategies. Lack of a biomarker for autism is a limiting factor for early diagnosis, which could provide better outcome with early start of therapy. Because of the high serum fetuin-A concentration during intrauterine life, it has been suggested that fetuin-A may have a role in brain development. The current study sought to determine if fetuin-A, a multifunctional glycoprotein thought to have a role in brain development, may be used as a biomarker for the diagnosis of ASD and developmental delay. The study involved 55 children with cognitive developmental delays and 40 healthy children. Two categories of children with cognitive developmental delays were identified. The participants were subjected to a psychiatric assessment as well as developmental testing. Only 54.5% of the 55 individuals had CDD, whereas 45.5% had ASD. Using an ELISA kit, the levels of serum fetuin-A were determined spectrophotometrically. The serum fetuin-A levels in the patients from the test group were found to be significantly lower than in the healthy individuals (p < 0.001). The cutoff value for the serum fetuin-A levels for cognitive developmental delay and autism spectrum disorder was 518 µg/liter, according to the results of ROC analysis (84.6% sensitivity and 91.4% specificity, AUC: 0.95, p < 0.001). The findings suggest that the serum fetuin-A level may be used to diagnose autism spectrum disorder and cognitive developmental delays.

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.

High Serum Progranulin Levels in COVID-19 Patients: A Pilot Study.

In this study, we aimed to determine whether the progranulin level in serum predicts the course and severity of the disease in COVID-19 (+) patients and whether it can be used as a biomarker in these patients. Therefore, we sampled 61 people infected with COVID-19, and the cases were divided into the following groups: asymptomatic, noncomplicated, moderate, and severe. Concentrations of progranulin, TNF-α, IL-6 from in serum obtained from all participants were measured using commercially available ELISA kits, as well as WBC, PLT, NE, LY, ALT, AST, Hb, PCT, and CRP were examined with clinical analyzer. All measurements obtained for the patient samples were compared with those of 20 healthy individuals. The serum progranulin concentration was statistically higher in the COVID-19 (+) patient group than in the control group of healthy individuals [112.6 ± 54.8, 0.0 (0.0-54.2 pg/ml, respectively p = 0.000)]. ROC analysis was performed to evaluate the progranulin potential as a biomarker for COVID-19 (+) patients. A larger AUC (0.931 ± 0.08) value and a more significant p-value for progranulin than for CRP (p = 0.000) was detected. As a result, we believe that progranulin reaches high levels in the COVID-19 disease and may be a determinant in diagnosis and prognosis, and may be a better biomarker than CRP.

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 role of adropin, HIF-1α and apelin biomarkers in the diagnosis of acute mesentaric ischemia.

OBJECTIVE: The absence of a specific biomarker for acute mesenteric ischemia diagnosis results in a delay in diagnosis and treatment, as well as a high mortality rate. The current research examined whether the proteins adropin, HIF-1α, and apelin may be used to help in the early detection of acute mesenteric ischemia. MATERIALS AND METHODS: A total of 20 patients with acute mesenteric ischemia, 20 patients with abdominal pain, and 20 healthy controls were included in the study. The levels of adropin, HIF-1, and apelin in the serum were determined using the ELISA method. RESULTS: Adropin concentrations were significantly higher in the acute mesenteric ischemia group than in the abdominal pain and healthy control groups (p < 0.05). HIF-1α levels were considerably greater in patients with acute mesenteric ischemia compared to both the abdominal pain group and the healthy control group (p < 0.05). There was no difference in apelin levels between the acute mesenteric ischemia and abdominal pain groups (p > 0.05). HIF-1α was found to be moderate (AUC: 0.705) and adropin was found to be a weak biomarker (AUC: 0.692) in the ROC analysis for acute mesenteric ischemia. CONCLUSION: In this study of 20 patients with acute mesenteric ischemia, we found adropin and HIF-1α levels to be increased compared to patients with abdominal pain who did not have acute mesenteric ischemia.

Effects of ketamine, thiopental and their combination on the rat liver: A biochemical evaluation.

BACKGROUND: In the literature, it has been suggested that ketamine-related oxidative organ damage results from increased blood adrenaline level, and thiopental-related oxidative damage is caused by decreased adrenaline level, suggesting that ketamine-thiopental combination (KT) may be beneficial in reducing the hepatotoxic effect of ketamine. OBJECTIVES: To biochemically investigate the effects of ketamine, thiopental and KT on the liver in rats. MATERIAL AND METHODS: Male albino Wistar type rats received intraperitoneally (ip.) 30 mg/kg ketamine in the ketamine alone (KG) group (n = 6), 15 mg/kg thiopental in the thiopental alone (TG) group (n = 6), and 30 mg/kg ketamine + 15 mg/kg thiopental in the ketamine+thiopental (KTG) group (n = 6). The same volume of distilled water as solvent was given to the healthy (HG) animal group. This procedure was repeated once daily for 30 days. At the end of this period, the animals were killed by decapitation and their livers were removed. In liver tissue, malondialdehyde (MDA), total glutathione (tGSH), total oxidant status (TOS), total antioxidant status (TAS), tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1ß), and interleukin-6 (IL-6) levels were measured. The IL-1ß, IL-6, TNF-α, adrenalin (ADR), noradrenalin (NDR), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels were determined in blood samples taken from the tail veins. RESULTS: In the group treated with ketamine and thiopental alone, MDA, TOS, IL-1ß, IL-6, TNF-α, ADR, NDR, ALT, and AST levels were found to be high, and those of tGSH and TAS to be low. However, there was no significant change in the levels of these parameters in the KTG. CONCLUSIONS: These results indicate that oxidative stress and inflammation developed in the liver tissue of the group that used ketamine and thiopental alone, suggesting that the KT form may be safer in terms of toxicity in the clinical usage.

The effect of taxifolin on high-dose-cisplatin-induced oxidative liver injury in rats.

BACKGROUND: Cisplatin is a non-specific platinum-based (derivative) chemotherapeutic agent that causes an increase in free radicals activity in the liver. Antioxidant activity of taxifolin has been demonstrated previously, and it has been reported that taxifolin inhibits the hydroxyl, radical in experimental studies. OBJECTIVES: No studies were found in the current literature examining the protective effect of taxifolin on cisplatin-induced oxidative liver damage. We aimed to determine the protective effect of taxifolin on cisplatin-induced hepatotoxicity in an experimental study. MATERIAL AND METHODS: In total, 18 albino Wistar male rats were assigned into 3 groups: healthy controls (HC group), 5 mg/kg of cisplatin administered for 8 days (CIS group) and 50 mg/kg of taxifolin + 5 mg/kg of cisplatin administered for 8 days (TCG group). Malondialdehyde (MDA), total glutathione (tGSH), total oxidant (TOS), and total antioxidant (TAS) capacity levels were measured in the extracted liver tissue. RESULTS: Liver tissue MDA and TOS levels were significantly higher in the CIS group. In contrast, tGSH and TAS levels were significantly lower in the CIS group, administered cisplatin alone (p < 0.001), compared to other groups. In the TCG group, administered cisplatin + taxifolin, MDA and TOS levels were significantly lower, whereas tGSH and TAS levels were significantly higher than in the CIS group (p < 0.001). CONCLUSIONS: These results suggest that taxifolin may be useful in preventing cisplatin-related liver injury.

Coenzyme Q10 effect on cisplatin-induced oxidative retinal injury in rats.

AIM: In this study, it was aimed to investigate the effect of coenzyme Q10 (CoQ10) on cisplatin-induced oxidative retinal damage in rats biochemically and histopathologically. MATERIALS AND METHODS: Thirty male Wistar albino rats were divided into 3 groups randomly: untreated control (C group), only 2.5 mg/kg cisplatin daily administrated group for 2 weeks (CP group), 2.5 mg/kg cisplatin + 20 mg/kg orally CoQ10 daily administrated group for 2 weeks (CoQC group). At the end of experimental period, blood samples obtained before sacrification for the biochemical examination of serum malondialdehyde (MDA), total glutathione (tGSH), total oxidant system (TOS), total antioxidant systemic (TAS) levels and after eyes were removed for examined histopathology. RESULTS: As a result of our study, severe histopathological damage was detected in the retinal tissue of the cisplatin group with serum malondialdehyde (MDA) and total oxidant system (TOS) levels were high and total glutathione (tGSH) and total antioxidant systemic (TAS) levels were low. However, it was observed that the histopathological damage associated with cisplatin was decreased in the retinal tissue of the CoQ10 group, which inhibited the increase in blood serum MDA/TOS levels and decrease in tGSH/TAS levels. CONCLUSION: The biochemical and histopathological results of our study were compatible with each other, so we concluded that the damage to the rat retinal tissue caused by cisplatin may be reversible with coenzyme.

Effect of diazepam, sertraline and melatonin on the stress-induced reproductive disorders and intrauterine growth restriction in female rats.

OBJECTIVE: Psychological stress is an important factor triggering depression and anxiety. Infertility is known to cause stress; however, it is not clearly known whether stress causes infertility as well. In addition, there are different opinions accounting for the relation of stress-induced oxidative stress to infertility and intrauterine growth restriction. The aim of the study is to examine the effect of sertraline, diazepam and melatonin on the infertility, intrauterine growth restriction and oxidative stress that can be caused by forced immobilization stress management (FISM) in female rats. MATERIALS AND METHODS: Wistar rats were grouped as healthy rats (HG) applied distilled water, stress treated control group (SC), and 20 mg/kg sertraline + stress (SS), 2 mg/kg diazepam + stress (DS) and 10 mg/kg melatonin + stress (MS) treated rats. The medicines were administered orally once a day for 30 days. At the end of this period, oxidant/antioxidant parameters were measured through the blood samples collected from the tail veins of all rats. Then the rats were kept in a suitable environment for 2 months for breeding. RESULTS: FISM caused oxidative stress in blood serum of animals, infertility and intrauterine growth restriction (decrease in birth weight of the baby). Best medicines to suppress FISM-related oxidative stress are melatonin > diazepam > sertraline respectively, while sertraline > diazepam > melatonin were most successful in terms of preventing infertility. The best medicines preventing the FISM-caused intrauterine growth restriction were found to be melatonin > diazepam > sertraline, respectively. CONCLUSION: FISM causes oxidative stress in animals. Oxidative stress is understood to affect the intrauterine growth negatively although it is not a major component in the pathogenesis of infertility. While melatonin is only effective in preventing the oxidative stress-related intrauterine growth restriction, antidepressants and anxiolytic treatment were found to be helpful in preventing both infertility and intrauterine growth restriction.

Effect of taxifolin on cisplatin-associated oxidative optic nerve damage in rats.

AIM: To investigate the effect of taxifolin on cisplatin-induced oxidative and proinflammatory optic nerve damage in rats. METHODS: A total of 18 albino Wistar male rats were assigned into 3 groups, as follows; Group 1: Control group, Group 2: Only cisplatin administered group for 14 days (Cisplatin group), and Group 3: Taxifolin + cisplatin administered group for 14 days (CIS + TAX group). Serum malondialdehyde (MDA), total Glutathione (tGSH), Nuclear Factor-Kappa B (NF-ƘB), Total Oxidative Status (TOS) and Total Antioxidant Status (TAS) levels were collected from the left eyes of rats. Rats' right eyes were enucleated for histopathological evaluations of optic nerves. RESULTS: NF-ƘB, MDA and TOS levels were statistically significantly higher (p < 0.001) in cisplatin group when compared to other 2 groups, the tGSH and TAS levels of which were statistically significantly lower (p < 0.001). Regarding these parameters, in cisplatin group NF-ƘB, MDA and TOS levels were statistically significantly increased with cisplatin administration and giving taxifolin concomitantly with cisplatin prevented this elevation. On the other hand, tGSH and TAS levels were statistically significantly decreased with cisplatin administration and routine simultaneous application of taxifolin with cisplatin prevented this decrease. In histopathological findings, haemorrhage was observed in the perineum of the injured optic nerves in the cisplatin treated group. And also edoema and degeneration in nerve fascicles in damaged optic nerves were seen in the cisplatin group. In the taxifolin treated group histopathological examinations were close to normal appearance, except mild edoema in nerve fascicles. CONCLUSION: Cisplatin causes oxidative stress on the rat optic nerves, and these changes lead to significant histopathological damage. Taxifolin, which we used to prevent oxidative damage to the optic nerves caused by cisplatin, has been emphasized as a powerful antioxidant agent in many previous scientific investigations. Concomitant administration of taxifolin may prevent these adverse effects of cisplatin, as well as histopathological damage. Further studies are needed to fully determine the effects of cisplatin and taxifolin on the eye.

Effect of Rutin on Cytarabine-Associated Pulmonary Oedema and Oxidative Stress in Rats.

Cytarabine is effectively used in the treatment of adult acute leukemia, but it has a dose-limiting side effect of fatal pulmonary oedema because it increases the vascular permeability of the alveolar capillaries. The aim of the present study was to conduct a radiological, biochemical and histopathological investigation of the effect of rutin on cytarabine-associated pulmonary oedema in rats. Rats were treated with a combination of rutin+cytarabine by administering oral rutin at a dose of 50 mg/kg; other rat groups were orally administered the same volume of physiological saline. One hour after administration of rutin or saline, the rutin+cytarabine and cytarabine groups received an intraperitoneal injection of cytarabine (200 mg/kg). This administration procedure was repeated once a day for 14 days. Radiologically, 50% of the animals given cytarabine alone showed lung oedema, but the rutin+cytarabine group showed no oedema. The inclusion of rutin decreased the amounts of cytarabine-associated malondialdehyde, tumour necrosis factor-α, and nuclear factor-κB in the lung tissue. Rutin also inhibited the reduction of total glutathione by nitric oxide. These findings suggest that rutin may be a beneficial adjunct that can minimise the development of cytarabine-associated pulmonary oedema.

Agomelatine prevents indomethacin-induced gastric ulcer in rats.

BACKGROUND: Gastric ulcer is a very common gastrointestinal disease that may be dangerous and even may lead to death. The current study was conducted to detect the prophylactic effects of agomelatine on indomethacin-induced gastric ulcer. METHODS: In this study, a total of 5 groups were created as the sham, ulcer, omeprazole, agomelatine 1 mg/kg and agomelatine 5 mg/kg groups. The effects of agomelatine on indomethacin-induced gastric injury were investigated. Total antioxidant and oxidant levels; the oxidant parameters like oxidative stress index and the inflammation markers such as tumor necrosis factor-α, interleukin-1ß, interleukin-6 and interleukin-10 levels in stomach tissue were determined by ELISA. In addition, the gastric mucosal injury occurred in stomach wall was examined with histopathological methods. RESULTS: While the levels of the inflammatory markers, total oxidant status and oxidative stress index increased at an obvious level especially in the indomethacin group, the total antioxidant status levels decreased. It was observed that these parameters were improved at a significant level in agomelatine 1 mg/kg and agomelatine 5 mg/kg groups when compared to ulcer group; and the results were similar to omeprazole group. It was also observed that our histopathological findings were consistent with all our other results. CONCLUSIONS: The results of this study showed that agomelatine usage in indomethacin-induced gastric ulcer model provides beneficial results.

The effect of Liv-52 on liver ischemia reperfusion damage in rats.

BACKGROUND: Liver ischemia reperfusion (I/R) damage which is frequently seen in clinical hepatobiliary surgeries has no effective treatment for it. Liv-52, known to have hepatoprotective effects, is a natural antioxidant drug licensed by the Ministry of Health of India. The aim of our study is to investigate the effect of Liv-52 on liver damage induced by I/R in rats. METHODS: Albino Wistar male rats were divided into three groups; liver I/R (IR), 20 mg/kg Liv-52 + liver ischemia reperfusion (LIR) and sham operation applied to control group (HG). Liv-52 was administered to the LIR group (n = 6) 1 h prior to I/R application and distilled water was given orally to IR (n = 6) and HG (n = 6) groups as a solvent. Ischemia was determined as 1 h, and reperfusion was identified as 6 h in animals. RESULTS: Increased levels of alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase, malondialdehyde, myeloperoxidase, and decreased levels of superoxide dismutase, and glutathione related enzymes caused by I/R application have been converged to healthy group level with Liv-52 treatment and the damage in liver tissue has been improved histopathologically. CONCLUSIONS: Liv-52 may be beneficial for preventing liver I/R damage in pre-surgery application.

Effects of anakinra on the small intestine mucositis induced by methotrexate in rats.

Intestinal mucositis is an important problem in the patients receiving cancer treatment. We aimed to investigate the effect of anakinra, which is a well known anti-oxidant and anti-inflammatory agent, on methotrexate-induced small intestine mucositis in rats. Forty rats were divided into 4 groups with 10 in each group. The healthy group (HG) and the methotrexate group (MTXG) were given distilled water, while the methotrexate + anakinra 50 (MTX+ANA50) and the methotrexate + anakinra 100 (MTX+ANA100) groups were intraperitoneally administered 50 and 100 mg/kg of anakinra. After one hour, the MTXG, MTX+ANA50 and MTX+ANA100 groups were given oral methotrexate at a dose of 5 mg/kg. This procedure was repeated once a day for 7 days. After the rats had been sacrificed, the small intestine tissue of rats were removed for the assesment of biochemical markers, histopathological evaluation and gene expression analyze. Statistical analyses of the data were performed using one-way ANOVA. Malondialdehyde (MDA), myeloperoxidase (MPO) and interleukin-6 (IL-6) levels were significantly higher, whereas total glutathione (tGSH) levels were significantly lower in MTXG (P<0.001) compared to other groups. MTX also increased IL-1ß and TNF-α gene expression levels in MTXG (P<0.001). Inflammatory cell infiltration and damage to the villus were observed histopathologically in the MTXG group, whereas only mild inflammation was seen in the MTX+ANA100 group. A dose of 100 mg/kg of anakinra prevented the increase of the biochemical markers and gene expression levels better than a dose of 50 mg/kg. Intestinal mucositis caused by MTX may be preventible by co-administered anakinra.