Investigation of oxidant/antioxidant and anti-inflammatory effects of apigenin on apoptosis in sepsis-induced rat lung.

We suppose that apigenin may inhibit the cellular process of sepsis-induced lung injury, which is considered to be a major cause of morbidity and mortality, and may improve inflammation and oxidative stress. The aim of this study was to investigate the potential protective effect of apigenin in a rat model of polymicrobial sepsis. Eight groups consisting of a total of 64 female Wistar albino rats were used for this study. Pro-inflammatory (TNF-α, IL-1-ß, IL-6) and anti-inflammatory (TGF-ß, IL-10) cytokine levels were measured with the enzyme-linked immunosorbent assay technique, oxidant/antioxidants parameters were measured using the spectrophotometric method and Bax and Caspase-3 immunohistochemical methods. TNF-α, TGF-ß, IL-1ß, and IL-6 levels significantly increased in the sepsis-induced group than in the control groups, while IL-10 levels decreased. Lipid peroxidase (LPO), an oxidative stress marker, increased, while the antioxidant defense parameters of superoxide dismutase (SOD), catalase (CAT) activities, glutathione (GSH) levels decreased. Although Bax and Caspase-3 immunoreactivity and H score levels significantly increased in the sepsis group, significant decreases were found in the groups treated with apigenin. In conclusion, we are of the opinion that apigenin treatment improves lung injury by inhibiting oxidative stress and inflammatory cell damage.

Sinapic acid reduces ischemia/reperfusion injury due to testicular torsion/detorsion in rats.

This study aimed to investigate the protective effect of sinapic acid (SA) on biochemical and histopathological changes in an experimental testicular torsion-detorsion rat model. Twenty-four rats were randomised into four groups: sham group, ischemia/reperfusion (IR) group subjected to testicular torsion for 2 hr and then detorsion for 4 hr, and two groups treated with SA1 and SA2 (10 mg/kg and 20 mg/kg, by single intraperitoneal injection, 30 min before reperfusion). Serum testosterone, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) were measured by an autoanalyzer, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), protein carbonyl (PC), and nitric oxide (NO) oxidative stress parameters by spectrophotometric methods, and tumour necrosis factor (TNF-α), interleukin-1 beta (IL-1ß), and interleukin 6 (IL-6) parameters by the Elisa method. In addition, immunohistochemical and histopathological examinations were performed on testicular tissues. There was no significant difference between the groups in terms of serum testosterone, FSH and LH levels (p > .05). SA significantly reduced increased testicular damage, oxidative stress, inflammation, cell death and also restored decreased antioxidant enzyme activities (p < .05). Pre-treatment of rats with SA reduced testicular dysfunction and morphological changes IRI. SA's antioxidant, anti-inflammatory, and antiapoptotic properties were found to be protective against testicular IR.

Milrinone ameliorates ischaemia-reperfusion injury in experimental testicular torsion/detorsion rat model.

This experimental study aims to evaluate the efficacy of milrinone against ischaemia-reperfusion injury due to testicular torsion/detorsion. Group 1 was defined as the control group. Testicular torsion/detorsion model was performed in Group 2. Group 3 had similar procedures to the rats in Group 2. In addition, 0.5 mg/kg of milrinone was administered intraperitoneally immediately after testicular torsion in Group 3. Histopathological examinations indicated a dramatic improvement in terms of inflammation, haemorrhage, oedema, congestion, Cosentino and Johnson scores in Group 3 compared to Group 2 (p = .037, p = .045, p = .018, p = .040, p = .033 and p = .03 respectively). Blood biochemical analyses, superoxide dismutase (SOD), glutathione peroxidase (GSH-px) activity and total antioxidant status (TAS) levels increased significantly in Group 3 compared to Group 2 (p = .001, p = .024 and p < .001). Malondialdehyde (MDA), protein carbonyl (PC), interleukin 1beta (IL-1beta), tumour necrosis factor-alpha (TNF-alpha) and total oxidant status (TOS) levels decreased in Group 3 compared to Group 2 (p = .001, p = .018, p < .001, p = .036 and p = .002 respectively). Tissue biochemical analyses determined an increase in SOD and GSH-px activity in Group 3 compared to Group 2, while PC and MDA levels were reduced (p = .001, p < .001, p = .038 and p < .001 respectively). Milrinone attenuates ischaemia-reperfusion injury that causes highly harmful effects due to testicular torsion/detorsion.

Protective effects of dexmedetomidine on ischaemia-reperfusion injury in an experimental rat model of priapism.

The study aimed to investigate the effects of dexmedetomidine against ischaemia-reperfusion injury occurring after priapism in a model of induced-priapism in rats. A total of 18 male rats were randomised into three groups. Group 1 was the control group. A priapism model was performed rats in Group 2 and then ischaemia-reperfusion injury was evaluated. Group 3 had similar procedures to the rats in Group 2. Rats in Group 3 additionally had 100 µg/kg dexmedetomidine administered intraperitoneally immediately after reperfusion. Blood and tissue samples were analysed. Biochemical analysis of blood samples revealed a decrease in the levels of the pro-inflammatory cytokines including interleukin-1 beta (IL-1 Beta), interleukin-6 (IL-6), and tumour necrosis factor-alpha (TNF-alpha) in Group 3 compared to Group 2 (p:.04, p:.009 and p:.009, respectively). Similarly, the highest malondialdehyde (MDA) level was in Group 2 (p:.002). The levels of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were significantly higher in Group 3 than that of Group 2 (p:.037 and p:.045, respectively). Direct microscopic examinations revealed positive changes in desquamation, oedema, inflammation and vasocongestion scores in Group 3 compared to Group 2 (p:.007, p:.008, p:.007 and p:.006, respectively). Dexmedetomidine has a protective effect against ischaemia-reperfusion injury in penile tissue.

The effect of 2100 MHz radiofrequency radiation of a 3G mobile phone on the parotid gland of rats.

PURPOSE: We aimed to evaluate the effect of 2100 MHz radiofrequency radiation on the parotid gland of rats in short and relatively long terms. MATERIAL AND METHODS: Thirty Wistar albino rats were divided into four groups. Groups A and B served as the control groups (for 10 days and 40 days, respectively), and each group included six rats. Groups C and D were composed of nine rats each, and they were the exposure groups. The rats were exposed to 2100 MHz radiofrequency radiation emitted by a generator, simulating a third generation mobile phone for 6 hours/day, 5 days/week, for 10 or 40 days. Following exposure, the rats were sacrificed and parotid glands were removed. Histopathological and biochemical examinations were performed. RESULTS: Although there were no histopathological changes in the control groups except for two animals in group A and three animals in group B, the exposure groups C (10 days) and D (40 days) showed numerous histopathological changes regarding salivary gland damage including acinar epithelial cells, interstitial space, ductal system, vascular system, nucleus, amount of cytoplasm and variations in cell size. The histopathological changes were more prominent in group D compared to group C. There was statistically significant different parameter regarding variation in cell size between the groups B and D (p=0.036). CONCLUSION: The parotid gland of rats showed numerous histopathological changes after exposure to 2100 MHz radiofrequency radiation, both in the short and relatively long terms. Increased exposure duration led to an increase in the histopathological changes.

Morin attenuates arsenic-induced toxicity in 3T3 embryonic fibroblast cells by suppressing oxidative stress, inflammation, and apoptosis: In vitro and silico evaluations.

This study aims to investigate the curative effects of Morin, a flavonoid, against arsenic toxicity in 3T3 embryonic fibroblast cells and its effect on the molecular mechanisms of cells. The cytotoxicity and viability of the cells were measured by MTT and LDH tests. Arsenic (0.74 µM) was used to trigger toxicity and Morin (50 µM) was used for treatment. The levels of oxidative stress biomarkers and the activities of antioxidant enzymes were measured by spectrophotometric method, and inflammatory markers were measured by ELISA method. While mRNA expression levels of Bax, Bcl-2 levels, and Caspase-3 activity were measured by qRT-PCR technique, TUNEL staining was performed to detect DNA breaks and DAPI staining to visualize nuclear changes. Protein structures were retrieved from the protein data bank. OpenBabel and Autodock programs were used for the molecular docking study. Morin rescued the 3T3 embryonic fibroblast cells exposed to arsenic. However, Arsenic decreased the activities of antioxidant enzymes in cells and significantly increased oxidative stress, inflammation, and apoptosis. Morin treatment reduced oxidative damage and TNF-α and IL-1ß levels. Arsenic-induced Caspase-3 mRNA expression level and Bax protein mRNA expression level were significantly increased, while Bcl-2 mRNA expression level was significantly decreased. While Caspase-3 mRNA expression level and Bax protein mRNA expression level decreased with morin treatment, Bcl-2 mRNA expression level increased significantly. Molecular docking study results showed good binding affinity of morin in SOD, GSH-Px, Bax, Bcl-2, Caspase-3, TNF-α, and IL-1ß structures. Morin showed antioxidant, anti-inflammatory, and anti-apoptotic effects against Arsenic-induced cellular toxicity.

Etomidate alleviates ovarian ischemia-reperfusion injury in rats.

BACKGROUND: This study investigates the protective effects of etomidate against oxidative damage in an experimental model of ovarian ischemia-reperfusion injury. METHODS: A total of 24 female rats were randomized into three groups. Group 1 served as the control. Group 2 underwent an ovarian torsion/detorsion procedure. Group 3 underwent similar procedures as Group 2; additionally, 4 mg/kg of etomidate was administered intraperitoneally 30 minutes before ovarian detorsion. Blood samples were analyzed for lipid peroxidation, pro-inflammatory cytokine levels, and antioxidant enzyme activity RESULTS: Biochemical analysis of blood samples revealed reductions in pro-inflammatory cytokines, including interleukin-1 Beta (IL-1ß), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), in Group 3 compared to Group 2 (p=0.005, p=0.016, and p<0.001, respectively). Additionally, a decrease in malondialdehyde (MDA) levels was observed in Group 3 compared to Group 2 (p<0.001). In contrast, activities of antioxidant enzymes, including superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), were significantly increased in Group 3 compared to Group 2 (p=0.031 and p=0.001, respectively). Furthermore, Group 3 demonstrated notable reductions in histopathological scores for follicular degeneration, vascular occlusion, bleeding, and inflammation compared to Group 2 (p<0.001, p<0.001, p<0.001, and p=0.001, respectively). CONCLUSION: Etomidate alleviates ischemia-reperfusion injury in a rat ovarian torsion-detorsion model by improving both histopathological and biochemical outcomes.

Effects of ketamine on penile tissues in an experimental priapism model in rats.

BACKGROUND: This study aimed to evaluate the histopathological and biochemical effects of ketamine on penile tissues following ischemia-reperfusion injury induced by priapism. METHODS: Twenty-four male rats were randomized into three groups. Group 1 served as the control group. Group 2 underwent the priapism model to induce ischemia-reperfusion injury. Group 3, the treatment group, experienced a similar ischemia-reperfusion model as Group 2; additionally, 50 mg/kg of ketamine was administered intraperitoneally just before reperfusion. Blood biochemical analyses and penile histopathological evaluations were performed. RESULTS: In Group 3, significant improvements were observed in all histopathological scores, including desquamation, edema, inflammation, and vasocongestion compared to Group 2 (p<0.001). Blood biochemical analyses showed that the malondialdehyde (MDA) levels were recorded as 10 in Group 2, with a significant decrease in Group 3 (p=0.013). Similarly, proinflammatory cytokine levels, including interleukin-1 beta (IL-1ß), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), were found to be suppressed in Group 3 compared to Group 2 (p=0.003, p=0.022, and p=0.028, respectively). Antioxidant enzyme activities, such as glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD), were higher in Group 3 compared to Group 2 (p=0.016 and p=0.024, respec-tively). CONCLUSION: Ketamine is an effective anesthetic agent in alleviating the effects of penile ischemia-reperfusion injury.

Protective Effects of Syringic Acid on Ischemia-Reperfusion Injury in Testicular Torsion: An Experimental Study in a Rat Model.

AIM: The purpose of this study was to assess the effectiveness of syringic acid in preventing ischemia-reperfusion injury following detorsion in a rat model of induced testicular torsion. MATERIAL AND METHODS: In our study, a total of 24 rats, eight in each group, were used. Group 1 served as the control group. Group 2 underwent testicular torsion and detorsion. Group 3 underwent the same procedures as Group 2, but also received 100 mg/kg syringic acid immediately following ischemia. Spectrophotometric analysis was performed on blood samples, and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), as well as the values of malondialdehyde (MDA), were evaluated under direct microscopic examination of the testis to determine tissue injury. The architecture of the seminiferous tubules and spermatogenesis processes were graded using the Johnsen and Cosentino scoring systems. RESULTS: The mean value of MDA was higher in Group 2 compared to the other groups (p < 0.001). Group 3 demonstrated a decline in the concentrations of proinflammatory cytokines, such as tumor necrosis factor-alpha, interleukin-6, and interleukin-1 beta, as indicated by biochemical analysis of blood samples, when compared to Group 2 (p-values: 0.045, 0.001, and <0.001, respectively). In addition, the improvement in Johnsen and Cosentino scores was significantly higher in Group 3 compared to Group 2 (p = 0.028 and p = 0.001, respectively). CONCLUSION: These findings suggest that syringic acid has a protective effect against testicular oxidative damage.

Investigation of the Effects of Apigenin, a Possible Therapeutic Agent, on Cytotoxic and SWH Pathway in Colorectal Cancer (HT29) Cells.

Purpose: Colorectal cancer (CRC) is one of the most common and fatal malignancies in humans, still leading to serious morbidity and mortality. We here aimed to investigate the effects of flavonoid apigenin, which is considered to have anti-tumoral activity on CRC with high epidemiological prevalence, on cell proliferation and cell survivals, and the positive and negative dose-dependent effects of genetic or mutational alterations in SWH pathway components on HT29 CRC cell lines. Methods: Human colon cancer cell lines HT-29 were commercially available. In each flask, 5 groups were formed, each of which consists of 5,000 cells for different dose groups and the cells were plated. After a 24 and 48 h incubation period, cytotoxicity values were measured by MTT assay and gene expression was assessed by real-time polymerase chain reaction (PCR) analysis method. Results: Application of 12.5 and 25 nM of apigenin significantly increased cell death in HT29 cell lines. LATS1, STK3 and TP53 gene expression decreased in the same dose groups compared to control and other groups. Conclusion: It has been concluded that TP53 gene is strongly correlated with LATS1 and STK3 genes among the SWH pathway factors in the progression of CRC and could be used as an important marker for early detection of malignant transmission. In addition, it may be effective in CRC cases especially when 25 nM of apigenin applies for therapeutic purpose.

An Experimental Rat Model Study: Is There Any Effect of Syringic Acid on Ischemia-Reperfusion Injury in Priapism?

Purpose The purpose of this research is to examine the impact of syringic acid on ischemia-reperfusion injury in cavernosal tissue, utilizing a rat model of induced priapism. Materials and methods A total of 24 rats were allocated into three groups. Group 1 was designated as the control group, while Group 2 underwent ischemia-reperfusion injury assessment using the priapism model. Group 3 underwent the same procedures as Group 2, with the addition of intraperitoneal administration of syringic acid (100 mg/kg) 60 min after priapism initiation. All rats underwent penectomy, and sufficient blood samples were collected. Histopathological assessment of penile cavernosal tissue involved grading tissue damage, inflammation, vasocongestion, desquamation, and edema on a scale of 0-3 (0: normal, 1: mild, 2: moderate, 3: severe). Result Significant differences were observed among the three groups in terms of IL-1 beta and TNF-alpha levels (p=0.001 and p<0.001, respectively). IL-1 beta and TNF-alpha levels in Group 2 were found to be significantly higher than Group 3 (p=0.003 and p=0.004). There was also a significant difference among the three groups in terms of median MDA levels (p<0.001). Furthermore, the median MDA level in Group 2 was found to be significantly higher than that in Group 3 (p<0.001). While significant differences were observed among the three groups in terms of median SOD and GSH-px levels, no significant difference was found among the groups in terms of median PC levels (p=0.004, p= 0.048, and p=0.159, respectively). In direct microscopic examination, a significant improvement in pathological scores was noted in Group 3 compared to Group 2 (p<0.001). Conclusion Syringic acid demonstrated protective properties against ischemia-reperfusion injury caused by priapism in cavernosal tissue.

Does oxidative status affect serum sclerostin levels in patients with type 2 diabetes mellitus?

INTRODUCTION: Sclerostin is a glycoprotein known as a negative regulator of bone formation, predominantly expressed by mature  osteocytes. There is no causative evidence information on the role of sclerostin in the pathogenesis of type 2 diabetes mellitus (T2DM) in humans. AIM: This study aimed to investigate the relationship between serum sclerostin levels and oxidative status and biochemical parameters in T2DM patients and healthy people. MATERIALS AND METHODS: This cross-sectional study, conducted in a clinical trial center, included 45 subjects with T2DM and 45 subjects as controls. RESULTS: Serum sclerostin, total oxidative status (TOS), albumin, and ferritin levels were significantly higher in T2DM patients than in the control group (p<0.05). Total antioxidant status (TAS) was significantly higher in the control group (p<0.05). There was a weak positive correlation between sclerostin and TOS (r=0.23, p=0.03) and a weak negative correlation between sclerostin and TAS (r=-0.28, p=0.03). CONCLUSIONS: We have demonstrated that serum sclerostin levels increase in patients with T2DM and that the increased sclerostin levels are associated with oxidative stress.

Clinical and Cytokine Profile of Children With COVID-19: A Report From Turkey.

Background We aimed to analyze the expression of infection-related biomarkers and inflammatory cytokines in laboratory-confirmed cases and compare the differences between clinically severe and non-severe ones. Method We randomly selected 35 patients who were hospitalized with the diagnosis of coronavirus disease 2019 (COVID-19). Blood serum was obtained at the time of admission to the hospital, on the third to the fifth day, and at the time of discharge. Result The median age of our patients was 56.5±69.7 months (range: 1-205 months). The mean pro-B-type natriuretic peptide (pro-BNP) was significantly higher at the time of admission than on the third to the fifth day of illness. The mean pro-B-type natriuretic peptide levels at three time points were significantly higher in patients with severe cases than in mild-moderate cases. However, there was no significant difference between the clinical severity with regard to the cytokine levels at disease onset and recovery. Conclusion In the study, it was shown that cytokines play an important role in the pathogenesis of COVID-19. Therefore, it may be beneficial to use agents such as tocilizumab in the treatment.

Toxicity of carbon tetrachloride, free radicals and role of antioxidants.

Several chemicals, including environmental toxicants and clinically useful drugs, cause severe cellular damage to different organs of our body through metabolic activation to highly reactive substances such as free radicals. Carbon tetrachloride is an organic compound of which chemical formula is CCl4. CCl4 is strong toxic in the kidney, testicle, brain, heart, lung, other tissues, and particularly in the liver. CCl4 is a powerful hepatoxic, nephrotoxic and prooxidant agent which is widely used to induce hepatotoxicity in experimental animals and to create hepatocellular carcinoma, hepatic fibrosis/cirrhosis and liver injury, chemical hepatitis model, renal failure model, and nephrotoxicity model in recent years. The damage-causing mechanism of CCl4 in tissues can be explained as oxidative damage caused by lipid peroxidation which starts after the conversion of CCl4 to free radicals of highly toxic trichloromethyl radicals (•CCl3) and trichloromethyl peroxyl radical (•CCl3O2) via cytochrome P450 enzyme. Complete disruption of lipids (i.e., peroxidation) is the hallmark of oxidative damage. Free radicals are structures that contain one or more unpaired electrons in atomic or molecular orbitals. These toxic free radicals induce a chain reaction and lipid peroxidation in membrane-like structures rich in phospholipids, such as mitochondria and endoplasmic reticulum. CCl4-induced lipid peroxidation is the cause of oxidative stress, mitochondrial stress, endoplasmic reticulum stress. Free radicals trigger many biological processes, such as apoptosis, necrosis, ferroptosis and autophagy. Recent researches state that the way to reduce or eliminate these CCl4-induced negative effects is the antioxidants originated from natural sources. For normal physiological function, there must be a balance between free radicals and antioxidants. If this balance is in favor of free radicals, various pathological conditions occur. Free radicals play a role in various pathological conditions including Pulmonary disease, ischemia / reperfusion rheumatological diseases, autoimmune disorders, cardiovascular diseases, cancer, kidney diseases, hypertension, eye diseases, neurological disorders, diabetes and aging. Free radicals are antagonized by antioxidants and quenched. Antioxidants do not only remove free radicals, but they also have anti-inflammatory, anti-allergic, antithrombotic, antiviral, and anti-carcinogenic activities. Antioxidants contain high phenol compounds and antioxidants have relatively low side effects compared to synthetic drugs. The antioxidants investigated in CCI4 toxicity are usually antioxidants from plants and are promising because of their rich resources and low side effects. Data were investigated using PubMed, EBSCO, Embase, Web of Science, DOAJ, Scopus and Google Scholar, Carbon tetrachloride, carbon tetrachloride-induced toxicity, oxidative stress, and free radical keywords. This study aims to enlighten the damage-causing mechanism created by free radicals which are produced by CCl4 on tissues/cells and to discuss the role of antioxidants in the prevention of tissue/cell damage. In the future, Antioxidants can be used as a therapeutic strategy to strengthen effective treatment against substances with high toxicity such as CCl4 and increase the antioxidant capacity of cells.

Evaluation of oxidative stress biomarkers in acute mercury intoxication.

INTRODUCTION: Very few studies have evaluated the association between mercury exposure and oxidative stress in humans, particularly in children. AIM: This is the first report where we aimed to determine the oxidative stress status of children who were accidentally exposed to elemental mercury. MATERIALS AND METHODS: In the present study, the study group was composed of 86 randomly selected children poisoned by mercury; the control group was composed of 78 children who had no history of mercury exposure. At admission, blood samples were collected. Blood superoxide dismutase activity, catalase enzyme activity, and glutathione peroxidase activity were measured by Fridovich, Beutler, and Lawrence Burk methods respectively, and the results were given as U/g Hb. Malondialdehyde level was measured by Ohkawa methods, and the results were given as mmol/ml. RESULTS: Catalase activity was significantly lower in the patient group compared to the control group (1.28±0.62 vs. 3.90±0.86 U/g Hb, p=0.010). In exposed children, SOD activity was significantly higher than the controls (5936±810 vs. 2226±464 U/g Hb, p=0.03), while the GSH-Px activity was significantly lower (13.01±3.21 vs. 34.97±7.32 U/g Hb, p=0.013). The MDA levels of the mercury group were significantly higher than the MDA levels of the control group (2.85±0.84 vs. 2.05±0.79 mmol/ml, p=0.04). CONCLUSIONS: The results of the present study showed that acute mercury poisoning causes an alteration of oxidative stress status in children exposed to elemental mercury.

Evaluation of Oxidative Stress Biomarkers in Patients with Henoch-Schönlein Purpura.

INTRODUCTION: Henoch-Schönlein Purpura (HSP) is a systemic vasculitic syndrome characterized by non-thrombocytopenic purpura, arthritis/arthralgia, abdominal pain, and glomerulonephritis. The pathogenesis of HSP has not been clearly identified. Oxidative damage has a role in the pathogenesis of most cases. AIM: This study aimed to evaluate changes of oxidative stress by studying parameters like superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) in an attempt to identify the role of oxidative stress in HSP from another perspective. MATERIALS AND METHODS: This study enrolled 23 pediatric patients (ten girls and thirteen boys) diagnosed with HSP who were under follow-up at Sutcu Imam University School of Medicine Department of Pediatrics between 2014 and 2016 and twenty healthy children as the control group. The parents of all subjects gave informed consent to participate in the study. In the HSP group, the beginning season of the illness and the systemic involvement during follow-up were determined. Blood specimens were obtained at presentation before any treatment was started. SOD, CAT activities, and MDA values in erythrocyte and plasma samples were compared between the patient group and the healthy children. RESULTS: Twenty-three patients with HSP (13 males, 10 females) and 20 healthy children participated in this study. The mean age of the HSP cases was 8.21±3.78 years (range 2-16 years) and of the controls was 8.6±4.2 (range 3-14 years). The mean MDA value was 2.95±0.71 nmol/ml in the patient group and 2.67±0.66 nmol/ml in the control group (p=0.787). The mean level of the CAT enzyme was 1.32±0.35 U/g Hb in the patient group and 7.8±1.74 U/g Hb in the control group (p=0.001). The mean levels of the SOD enzyme were 3.06±0.85 U/g Hb in the patient group and 0.97±0.36 U/g Hb in the control group (p=0.001). CONCLUSIONS: Although high MDA levels support the role of lipid peroxidation in the pathogenesis of HSP, statistical significance was not reached owing to a limited number of our patients. The reduced CAT enzyme activity is consistent with the findings of previous reports. This finding supports the notion that oxidative stress can play a role in the pathogenesis of HSP. KEYPOINTS: Our findings support the notion that oxidative stress can play a role in the pathogenesis of HSP.

Diagnostic Performance of Erythropoietin and Erythropoietin Receptors Levels in Children with Attention Deficit Hyperactivity Disorder.

OBJECTIVE: Attention deficit hyperactivity disorder (ADHD) is a heterogeneous, highly heritable, a common childhood neurobehavioural disorder resulting from complex gene-gene and gene-environment interactions. The erythropoietin (Epo)/erythropoietin receptors (EpoR) system turned out to have additional important functions in nonhematopoietic tissue. In this study, we aimed to investigate the levels of Epo and and EpoR, and also their diagnostic values in children with ADHD. METHODS: A total of 70 children were included in the study, 35 drug-naive patients with ADHD (age: 6-12 years; male/female: 20/15) and 35 healthy controls (age: 6-12 years; male/female: 22/13). Serum Epo and EpoR levels was determined using a commercial sandwich enzyme-linked immunosorbent assay kit. RESULTS: The results indicated that the levels of Epo decreased in patients with ADHD compared to control (p < 0.05). On the other hand, EpoR levels increased in these patients (p < 0.05). Furthermore, the ratio of Epo/EpoR was significantly lower in ADHD patients than controls (p < 0.05). Receiver operator characteristic curve analysis showed high diagnostic performance for Epo and EpoR, areas under curve were 0.980 and 1.000, respectively. CONCLUSION: This is the first report to investigate the association between serum Epo and EpoR levels in ADHD patients. Our results indicated that Epo may play a role in the etiology of ADHD, and Epo therapy may be beneficial in these disorders if given in addition to the routine treatment of children with ADHD. Furthermore, our results reveal possible diagnostic value of Epo and EpoR.

Investigation of the Effects of Octreotide Agent on Oxidative Stress, 8-Hydroxy Deoxyguanosine in Experimental Hepatic Carcinogenesis Rat Model.

INTRODUCTION: 2-AAF and DEN are well-known liver toxicants commonly used to stimulate tumors in laboratory animals. AIM: The aim of this study was to investigate the effect of octreotide on DEN-induced and 2-AAF-supplemented hepatocarcinogenesis in Wistar albino rats. MATERIALS AND METHODS: In this study, 64 Wistar albino rats were divided into 8 groups. DEN (175 mg/kg) initiated and 2-AAF (20 mg/kg) promoted liver carcinogenesis in rats. The tumor growth inhibitor octreotide (300 µg/kg) was used. Rats were sacrificed at the end of experiment and their liver tissues were taken for the study. SOD, GSH-Px, CAT activities, NO and MDA levels were measured spectrophotometrically. Also, Hsp70 and 8-OHdG was measured by the ELISA method. RESULTS: In group 7, MDA, 8-OHdG, and Hsp70 levels were significantly increased. In addition, SOD, GSH-Px activity was significantly reduced in this group. MDA, 8-OHdG and Hsp70 levels were significantly reduced in Group 8, which received octreotide for treatment. CONCLUSION: DEN and 2-AAF cause very serious liver damage. Octreotide protects the liver from carcinogenesis, increases the activity of cellular antioxidant enzymes and helps reduce DNA damage. Therefore, octreotide may be an inhibitor in tumor cells and may reduce oxidative stress.

The Role of Natural Antioxidants Against Reactive Oxygen Species Produced by Cadmium Toxicity: A Review.

Cadmium (Cd) is a significant ecotoxic heavy metal that adversely affects all biological processes of humans, animals and plants. Exposure to acute and chronic Cd damages many organs in humans and animals (e.g. lung, liver, brain, kidney, and testes). In humans, the Cd concentration at birth is zero, but because the biological half-life is long (about 30 years in humans), the concentration increases with age. The industrial developments of the last century have significantly increased the use of this metal. Especially in developing countries, this consumption is higher. Oxidative stress is the imbalance between antioxidants and oxidants. Cd increases reactive oxygen species (ROS) production and causes oxidative stress. Excess cellular levels of ROS cause damage to proteins, nucleic acids, lipids, membranes and organelles. This damage has been associated with various diseases. These include cancer, hypertension, ischemia/perfusion, cardiovascular diseases, chronic obstructive pulmonary disease, diabetes, insulin resistance, acute respiratory distress syndrome, idiopathic pulmonary fibrosis, asthma, skin diseases, chronic kidney disease, eye diseases, neurodegenerative diseases (amyotrophic lateral sclerosis, Parkinson's disease, Alzheimer's disease, and Huntington disease). Natural antioxidants are popular drugs that are used by the majority of people and have few side effects. Natural antioxidants play an important role in reducing free radicals caused by Cd toxicity. Our goal in this review is to establish the relationship between Cd and oxidative stress and to discuss the role of natural antioxidants in reducing Cd toxicity.

A study of chewing muscles: Age-related changes in type I collagen and matrix metalloproteinase-2 expression.

OBJECTIVE: In this study, the aim was to investigate the biochemical, physiological and histological changes that occur in masticatory muscles of the masticatory system with aging. DESIGN: In this study, 14 BALB/c mice were used. Animals were divided into two equal groups of seven. Group I was organized as the group of young animals (n = 7) and Group II as the group of adult animals (n = 7). After routine histological follow-up was performed, the tissues were embedded in paraffin. 4-5 µm thick cross-sections were taken from paraffin-embedded tissues and they were stained with Haemotoxylin and Eosin Type I collagen and Matrix metalloproteinase-2 (MMP-2) immunohistochemically. RESULTS: It was observed that there was a decrease and shrinking in blood vessels due to aging. In young mice, Type I collagen and MMP-2 immunoreactivity in the masseter muscle tissue showed low staining, while Type I collagen and MMP-2 immunoreactivity in the temporal muscle tissue showed moderate staining. Type I collagen and MMP-2 immunoreactivity were significantly higher in the masseter and temporal muscles of elderly mice (p = 0.001). In the H-score evaluation, MMP-2 immune reactivity was significantly lower in young mice than in older mice (p = 0.001). CONCLUSION: It was determined that severe pain complications and functional losses are likely to occur with the increase of degeneration due to aging of masticator muscles.