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Objectives We aimed to evaluate the effects of acute and chronic aerobic exercise on cognitive function and depression levels in patients with Type 2 Diabetes Mellitus (T2DM) and the changes in related neurotrophic and metabotropic factors. Methods Sixteen female patients (age=57.5 ± 7.3) diagnosed with T2DM were included. A and B sections of the Trail Making Test (TMT) and Beck Depression Inventory (BDI) were used to assess executive function and depression states. Brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), irisin, total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), fasting plasma glucose, hemoglobin A1c, and high-density lipoprotein (HDL) cholesterol were analyzed in blood. Aerobic exercise intensity was applied at 50–70% of the maximal heart rate for 40 min/day, three days weekly on the treadmill. All evaluations were repeated after one exercise session, a 12-week exercise program, and after one year for follow-up. Results TMT-A (p=0.001) and TMT-B (p=0.002) values were increased following both acute and chronic exercise. BDI scores were decreased after long-term exercise (p=0.031). Measurement of metabolic parameters revealed positive changes in HDL cholesterol (p=0.044), TAS (p=0.005), and OSI (p=0.009) values ​​after chronic period exercise. No significant difference was found in BDNF (p=0.271), NGF (p=0.230), and irisin (p=0.101) values ​​after acute or chronic exercise, on the other hand. Conclusions Although aerobic exercise training had a positive effect on metabolic and cognitive outcomes, this effect was independent of neurotrophic and metabotropic factors. Regular and long-term aerobic exercise training has protective and regulatory functions in T2DM.

BACKGROUND: Sepsis is one of the leading causes of death in intensive care units worldwide. Vitamins C and E are natural antioxidants and anti-inflammatory agents. Suppressing the inflammation is an important treatment target because it plays a role in the pathophysiology of sepsis. The purpose of this study was to investigate the effect of vitamins C and E treatment in rats with sepsis-induced lung damage. METHODS: In this animal study, fecal intraperitoneal injection procedure (FIP) was performed on 30 of 40 rats included for creating a sepsis model. Rats were randomly assigned into four groups: Group 1, control group (no procedure was applied, n = 10), Group 2, FIP (untreated septic group n = 10), Group 3, FIP+vitC (treated with 500 mg/kg/day ascorbic acid, n = 10), and Group 4, FIP+vitE (treated with 300 mg/kg/day alpha-tocopherol, n = 10). Chest CT was performed in all rats and density of the lungs was measured by using Hounsfield unit (HU). Histopathological examination of lung damage was performed, and blood samples were collected for biochemical analysis. RESULTS: TNF-alpha, CRP, IL 1-beta, IL-6, and MDA plasma levels in groups treated with vitamin C or vitamin E were lower than in the FIP group. Histological scores in groups treated either with vitamin C or vitamin E were significantly lower as compared to those in the FIP group. The HU value of lung in groups treated wither with vitamin C or vitamin E were lower than that in the FIP group (p < 0.05). CONCLUSION: The rats treated either with vitamin C or E showed improved results for sepsis. We think that they can be used as adjuvant therapy for septic patients because of their effectivity and low costs (Tab. 3, Fig. 2, Ref. 27). Text in PDF www.elis.sk

SUMMARY OBJECTIVE: We aimed to determine which method gives the most consistent results between urethral monopolar cauterization and standard urethral partial ligation methods for the urethral obstruction model. METHODS: Thirty male rats were randomly divided into control, partial ligation, and monopolar cauterization groups. Six weeks after experimental procedures, the experimental groups were evaluated cystometrically, biochemically, and histologically. RESULTS: According to the cystometric results, bladder capacity, baseline bladder pressure, and compliance data of the monopolar cauterization group were higher than those of the partial ligation and monopolar cauterization groups (p

Background Autism is a complex neurobehavioral disorder that is associated with genetic and environmental factors. Patients with autism have altered gut microbiata, including higher frequency of bacteroidetes and clostridiales that produce of propionic acid (PPA) –a compound that is established as an autism-inducing agent. We hypothesized that lowering the PPA levels by regulating gut microbiata with ursodeoxycholic acid (UDCA) can regress the autism symptoms. Methods Thirty male Wistar albino rats were divided into three groups: controls, PPA-induced (5 days of intraperitoneal 250 mg/kg/day dosage) autism model receiving oral saline, and PPA-induced autism model receiving oral UDCA (100 mg/kg/day). Oral treatments were applied for 15 days. At the end of the 15th day, all rats underwent behavioral tests and MR spectroscopy. At the end of the study, all animals were sacrificed and brain tissue / blood samples were collected for histopathological and biochemical analyses. Results Sociability test, open field test and passive avoidance learning tests were impaired, similar to the autism behavioral pattern, in PPA recipients; however, results were closer to normal patterns in the PPA + UDCA group. Biochemically, MDA, TNF-alpha, IL-2, IL-17, NF-kB, lactate, NGF and NRF2 levels in brain tissues showed significant differences between controls and the PPA + Saline group, and between the PPA + Saline group and the PPA + UDCA group. Histopathology showed that PPA injection caused increased glial activity, neural body degeneration, decreased neural count and dysmorphic changes in hippocampal and cerebellar tissues. UDCA treatment significantly ameliorated these changes. Conclusion UDCA administration has ameliorating effects on PPA-induced autism-like behavioral, biochemical and histopathological changes in rats.

Alcohol use disorder (AUD) is the loss of a person's quality of life due to increased alcohol consumption and the failure of alcohol consumption control. In this study, the intra- and extracellular thiol-disulfide levels in people with AUD were compared with age-matched healthy controls. Forty male patients diagnosed with AUD and thirty healthy male individuals were included in the study. In addition to psychiatric and sociodemographic tests routine biochemical evaluations have been performed. The alcohol group had significantly higher Michigan Alcohol Screening Test (MAST), Beck Depression Inventory (BDI), and Beck Anxiety Inventory (BAI) scores compared to the control group. While there was a decrease in the intracellular GSH and extracellular native thiol levels in the blood of the alcohol group, GSSG and disulfide levels were increased, respectively. Subsequently, while there was an increase in the intracellular GSSG/GSH content levels in the alcohol group compared to the control group, the ratios of GSH/GSH+GSSG were decreased. These changes, indicative of oxidative stress, were observed both in blood serum and erythrocytes. Also, there was an increase in alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyltransferase (GGT) mean corpuscular volume (MCV), C-reactive protein (CRP) levels in the alcohol group in routine biochemical tests, while total protein, folic acid, ferritin and hemoglobin (HGB) levels were decreased. Our results suggest that increased intra- and extracellular GSSG/GSH % (disulfide/native thiol %) may serve as an indicator of developing oxidative stress in individuals with AUD.

We investigated the antioxidant and anti-ulcerogenic effects of fulvic acid (FA) on oxidative damage caused by water avoidance stress (WAS) in rat gastrointestinal mucosa. Three experimental groups were established: control (C), chronic stress (CS), and chronic stress + FA (CS + FA). After WAS, a single dose of FA was administered for 10 days to the CS + FA group. Samples of the pyloric region of the stomach were stained with hematoxylin and eosin (H & E) and periodic acid-Schiff (PAS). Immunohistochemical staining was performed for inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS). Total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) levels were measured biochemically. By light microscopy, we observed loss of gastric epithelial cells and greater polymorphonuclear cell migration into the mucosa in the CS group compared to the C group. We found intact epithelial cell structure and a thick superficial mucus layer in the CS + FA group compared to the CS group. These findings in the CS + FA group were similar to those for group C. iNOS staining was stronger in the CS group compared to the C group. TOS and OSI levels in the CS + FA group were decreased compared to the CS group, but TAS, SOD, GPx and CAT levels were increased. We found that WAS caused damage to epithelium and connective tissue of the stomach mucosa and that this damage was prevented by FA. Therefore, administration of FA appears to prevent stress induced damage to rat stomach.

The aim of our study is to investigate the dose-dependent biological system effect of hexagonal boron nitride (hBN) nanoparticles, which is directly produced nanoscale, in vivo. Wistar albino rats (n = 80) weighing 200-250 g were divided into eight groups (n = 10). The acute effects of hBN NPs (i.v) on the rats were investigated by measuring the biochemical, hematological parameters and oxidant-antioxidant status. The results show that no significant change was observed in the hematological and biochemical parameters when the control group and other low dose groups were compared, except for the 1600 and 3200 mu g/kg b.w. dose groups. Histological detection indicated that 1600 and 3200 mu g/kg hBN NPs treatment could induce significant damage in the liver, kidney, heart, spleen and pancreas. With the findings obtained, it can be seen that hBN NPs cannot be evaluated independently of particle morphology, and that the hBN NPs used in this study may be suitable for biomedical applications where low doses between 50 and 800 mu g/kg are not toxic. Eskiehir Technical University Scientific Research Projects Commission [19ADP163] This study was supported by Eskiehir Technical University Scientific Research Projects Commission. (Project No: 19ADP163). The authors would like to thank BORTEK Boron Technologies and Mechatronic Inc. for their material support and Dr. Umut SAVACI for his help to use Transmission Electron Microscopy (TEM) (Eskisehir Technical University, Turkey). WOS:000533059200001 2-s2.0-85085019778

Boric acid (BA) is an important mineral for plants in nature, animals and human to help metabolic functions. Boric acid has both positive and negative effects on biological systems. In the literature, there is no publication about boric acid effect on preimplantation mouse embryo about in vitro developments. The aim of the present work was to investigate the effects of different concentrations of boric acid added to prior in vitro cytotoxicity for beneficial doses and later the mouse embryo culture media for antioxidant levels, the embryo quality, in vitro development rate and related genes. Superovulated C57Bl6/6j female mice were sacrificed ~18 hours after human chorionic gonadotropin (hCG) injection. Single cell stage embryos were collected from the oviducts and the embryos were divided experiment groups and cultured in embryo medium supplemented BA+ in 5% CO2, 37°C until 96-120 h at the blastocyst stage. The blastocyst development rates of 0, DMSO, 10-2, 10-3, 10-4, and 10-5 ppm BA were 51.52% (34/66), 45.00% (9/20), 72.62% (36/49), 77.48% (41/53) and 81.15% (43/53), respectively. The in vitro development rates were significantly higher in the 10-2, 10-3, 10-4 ppm compared with 0 (control) (p) and 10-5 ppm BA significantly higher compared with control group (p). With these results, after determining the non-cytotoxic doses of BA, low doses influence embryo development by positively affecting in vitro development rates, embryo cell numbers, biochemical parameters, development at molecular level. Therefore, boric acid seems to play an important role on the in vitro embryo development.

Objectives: This article aims to explain the altered oxidative status and thiol/disulfide homeostasis before and after surgery in children with congenital heart disease (CHD). Methods: Blood samples were taken from the patients (n=50) before the operation (baseline), at the 1st hour, and at the 24th hour after the operation. Thiol-disulfide levels, total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), myeloperoxidase (MPO), ceruloplasmin, albumin, ischemia-modified albumin (IMA), and prolidase activities of all samples were measured. Preoperative oxygen saturation (SaO2) values and neutrophil/ lymphocyte ratios (NLR) were also measured. Results: Before the operation, TOS, OSI, MPO, ceruloplasmin, IMA, NRL, and disulfide levels were higher in the cyanotic group than in the acyanotic group. When the indicated three different time points were compared, the TOS, OSI levels, and MPO activities of the 24th hour were significantly lower than the baseline and 1st hour. In comparison, ceruloplasmin levels of 1st hour were significantly higher than of the baseline and 24th hour. Native thiol and total thiol levels in the baseline group were significantly lower than in the 1st and 24th hours. Disulfide levels of the 24th hour were significantly lower than of the baseline. Conclusions: The operation leads to changes in the thioldisulfide balance and oxidant status in CHD., Amaç: Bu makale konjenital kalp hastalığı (KKH) olan çocuklarda operasyon öncesi ve sonrası değişen oksidatif durum ve tiyol/disülfid homeostazını açıklamayı amaçlamaktadır. Yöntem: Hastalardan (n=50) operasyon öncesi (başlangıç), operasyon sonrası 1. saat ve 24. saatte kan örnekleri alındı. Bütün örneklerin tiyol-disulfid seviyeleri, total antioksidan durum (TAS), total oksidan durum (TOS), oksidatif stres indeksi (OSI), miyeloperoksidaz (MPO), seruloplazmin, albumin, iskemik modifiye albumin (IMA) ve prolidaz aktivitesi ölçüldü. Bunun yanı sıra operasyon öncesi oksijen saturasyon (SaO2) değeri ve nötrofil/lenfosit oranı (NLR) ölçüldü. Bulgular: Ameliyat öncesi siyanotik grubun TOS, OSI, MPO, seruloplazmin, IMA, NRL ve disülfid düzeyleri asiyanotik gruba göre daha yüksekti. Üç farklı zaman noktasını birbiriyle karşılaştırdığımızda 24. saatteki TOS, OSI seviyeleri ve MPO aktiviteleri başlangıç ve 1. saate göre anlamlı derecede düşük, 1. saat seruloplazmin seviyeleri ise başlangıç ve 24. saate göre anlamlı derecede yüksekti. Başlangıç grubunda doğal tiyol ve toplam tiyol düzeyleri 1. ve 24. saate göre anlamlı derecede düşüktü. 24. saatteki disülfid seviyeleri başlangıca göre önemli ölçüde düşüktü. Sonuç: Ameliyat, KKH’li çocuklarda tiyol-disülfid dengesinde ve oksidan durumunda değişikliklere yol açar.

Boric acid (BA) is used as an antioxidant and anti-inflammatory agent, and for regulating mitochondrial membrane potential in many disorders. We investigated the protective effects of BA against chronic ethanol toxicity in rat kidney. We used 32 male rats in four groups of eight: control (C), BA, ethanol (E), and ethanol + BA (E + BA). Kidney samples were taken for histology and biochemistry. Kidney injury was assessed using hematoxylin and eosin (H & E) and periodic acid-Schiff (PAS) staining. TUNEL and caspase-3 immunohistochemistry were used as indicators of apoptosis. We measured biochemical markers of ethanol induced oxidative stress in the kidneys including malondialdehyde (MDA), total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI). The E + BA group TOS, OSI and MDA levels decreased, whereas the TAS level increased compared to group E. Caspase-3 and TUNEL activity in the E + BA group were decreased compared to group E. BA acted as an antioxidant against renal tubule injury caused by chronic use of ethanol. BA protects against apoptosis in renal tubules by decreasing oxidative damage.

Background: Insulin resistance is associated with a pro-inflammatory state increasing the risk for complications in patients with type 2 diabetes mellitus (T2DM). In addition to its chronobiotic effects, the pineal hormone melatonin is also known to exert anti-inflammatory and antioxidant effects. Furthermore, melatonin was also suggested to affect insulin secretion and melatonin levels were reported to be decreased in T2DM patients Aims: The aim of this study was therefore to investigate the effect of melatonin on inflammation in diabetic rats and to study the possible involvement of the melatonin receptor, MT2. Materials and Methods: Male Sprague Dawley rats were randomly divided into four experimental groups (n = 10 per group):1) control, 2) streptozotocin/nicotinamid induced diabetes type 2 (T2DM), 3) T2DM treated with melatonin (500 µg/kg/day), and 4) T2DM treated with melatonin (500 µg/kg/day) and the selective MT2 receptor antagonist luzindole (0.25 g/kg/day). Blood samples were taken for biochemical parameters and various tissue samples (liver, adipose tissue, brain) were removed for immunohistochemistry (IHC), western blot (WB) and Q-PCR analyses, respectively. Results: Melatonin significantly reduced increased blood levels of liver transaminases (AST, ALT) and blood urea nitrogen (BUN) in diabetic rats. Furthermore, in liver and adipose tissue of treated rats, melatonin administration resulted in considerable lower expression of the increased inflammatory markers IL-1β, IL-6, TNF-α and NF-κB, as shown by reduction in RNA and protein levels. The MT2 receptor was only partly involved in the anti-inflammatory effects of melatonin. Conclusions: Our results suggest that melatonin has relevant anti-inflammatory effects in diabetic rats. Further studies in humans could prove the potential clinical benefit of melatonin supplementation in patients with T2DM.

Background: Hexagonal boron nitride nanoparticles (hBN NPs) are encouraging nanomaterials with unique chemical properties in medicine and biomedical fields. Until now, the optimal hBN NP's dosage and biochemical mechanism that can be used for in vivo systems has not been fully revealed. The main aim of this article is to reveal characteristics, serum and tissue interactions and any acute cytotoxic effect of different dose of hBN NPs for the first time. Methods: hBN NPs at concentrations varying between 50-3200 mu g/kg was administered by intravenous injection to Wistar albino rats (n = 80) divided into seven dosage and control groups. Blood and tissue samples were taken after 24 hours. Results: Our findings suggested that higher doses hBN NPs caused oxidative stress on the serum of rats dose-dependently. However, hBN NPs did not affect thiol/disulfide homeostasis on kidney, liver, spleen, pancreas and heart tissue of rats. Furthermore, hBN NPs increased serum disulfide formation by disrupting the thiol/disulfide balance in rats. Also, LOOH and MPO levels increased at high doses, while CAT levels decreased statistically. Conclusion: The results revealed that hBN NPs induce oxidative stress in a dose-dependent manner by modulating thiol/disulfide homeostasis in rats at higher concentrations Eskisehir Technical University Scientific Research Projects Commission [19ADP163] The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This study was supported by Eskis comma ehir Technical University Scientific Research Projects Commission [Project No: 19ADP163]. WOS:000636510600001 2-s2.0-85103183585 PubMed: 33754873

Fajlar organizmada humoral ve hucresel immun yaniti uyandirabilen yuksek immunojenik ozellige sahip molekullerdir ve potansiyel asi tasiyicisi olarak kullanilmaktadirlar. Bu calismada Hepatit B yuzey antijeni (HBsAg) tam molekul olarak M13 faj yuzeyinde fuzyon protein olarak ekprese edilmis ve rekombinant fajin antijenik etkisi BALB/cJ farelerinde incelenmistir. Farelerin yuksek dozda (10 12 ) rekombinant faj ile immunize edilmesinin normal faja kiyasla daha yuksek antikor yanitina neden oldugu gosterilmistir. BALB/cJ farelerinde elde edilen olumlu yanit sonrasi rekombinant fajin etkinligi Hepatit B virusu (HBV) transgenik farelerde ve hibrid farelerde (C57BL/6JXBALB/c) incelenmis ve ayrica etkisi aluminyum adjuvanti ve mineral yag adjuvanti gibi yaygin kullanimi olan adjuvantlarla karsilastirilmistir. Calismanin sonuclari BALB/cJ farelerin, HBV transgenik farelerin ve hibrid farelerin rekombinant faj ile immunizasyonunun antijene ozgu antikor yaniti olusturdugunu gostermistir. Sonuclar ayrica HBV tasiyicilarinda immun yanit olusturmak icin guclu adjuvantlarin kullanilmasi gerektigini de isaret etmektedir.

Abbasoglu, Semra/0000-0003-3467-9763; Oner-Iyidogan, Yildiz/0000-0001-6956-8794; Tuncdemir, Matem/0000-0002-5300-4449; KOCAK, Hikmet/0000-0003-1720-9102 WOS:000484049900002 PubMed ID: 30993920 Background. Apoptosis plays a major role in fatty liver disease. High-fat diets are related to the onset of fatty liver disease and hepatic oxidant-antioxidant imbalance. Curcumin and capsaicin are somewhat beneficial in reducing hepatic triglycerides; this is most likely because they are known to downregulate reactive oxygen species (ROS) and apoptosis. Objectives. The aim of this study was to investigate the effects of curcumin and capsaicin on apoptosis through the oxidative effect in an animal model of fatty liver disease. Material and methods. Male Sprague-Dawley rats were fed a normal control diet, a high-fat diet (HFD; 60% of total calories from fat), a HFD+curcumin (1.5 g curcumin/kg HFD), a HFD+capsaicin (0.15 g capsaicin/kg HFD), or a HFD+curcumin+capsaicin (1.5 g curcumin and 0.15 g capsaicin/kg HFD). Liver lysate levels of BAX, Bcl-2 and caspase-3 were determined via immunoblotting. Caspase-3 activity was measured with a colorimetric caspase-3 measurement kit. Total antioxidant status (TAS) and total oxidant status (TOS) were assayed using commercial kits. The generation of hepatic ROS was measured with fluorimetry. Fragmentation of DNA was detected using the TUNEL method. Results. High-fat diet caused increased expression of BAX and caspase-3, as well as increased TOS and caspase-3 activity, but decreased expression of Bcl-2. HFD+curcumin+capsaicin caused decreased BAX, caspase-3, TOS, and ROS levels as compared to HFD, but increased TAS and Bcl-2. A HFD +curcumin+capsaicin also decreased the number of TUNEL-positive cells. Conclusions. These results suggest that supplementation with curcumin and capsaicin balances the hepatic oxidant-antioxidant status and may have a protective role in the apoptotic process in an HFD-induced fatty liver model. Research Fund of Istanbul University, TurkeyIstanbul University [55331, BEK-2017-24926] This work was supported by the Research Fund of Istanbul University, Turkey, project No. 55331 and BEK-2017-24926.

Amaç: Çalışma, toksik olmayan bir ajan olan; antioksidan, antiapoptotik ve antiinflamatuvar özelliklere sahip fulvik asit (FA)’in kronik sudan kaçınma stresinin (KS) testis dokusunda oluşturduğu hasara karşı tedavi edici etkisinin araştırılmasıdır. Gereç ve Yöntem: Çalışmamızda 18 adet Sprague-Dawley erişkin erkek sıçan 3 eşit gruba ayrıldı: Kontrol (K), Kronik Stres (KS) ve Kronik Stres+Fulvik Asit (KS+FA). Testis dokusundan elde edilen histolojik kesitler Hematoksilen&Eozin (H&E) ve Toluidin mavisi (TM) ile boyandı; zonula okludens-1 (ZO-1), β-aktin ve indüklenebilir nitrik oksit sentaz (iNOS) immünohistokimya işaretlemeleri yapıldı. Biyokimyasal olarak dokulardaki total antioksidan seviyesi (TAS), total oksidan seviyesi (TOS), oksidatif stres indeksi (OSİ), katalaz (KAT), glutatyon peroksidaz (GPx) ve süperoksit dismutaz (SOD) düzeyleri ölçüldü. Bulgular: KS grubunda hasarlı seminifer tübüller, tunika albuginea komşuluğunda artmış mast hücre aktivitesi, tübül içerisinde artmış iNOS aktivitesi ve azalmış β-aktin ve ZO-1 aktivitesi gözlendi. Bu grupta ayrıca TOS ve OSI düzeylerinin arttığı; TAS, SOD, KAT ve GPx düzeylerinin azaldığı görüldü. KS+FA grubunda, fulvik asit kullanımıyla bu bulgularda iyileşme olduğu gözlendi. Sonuç: Bu bulgulara dayanarak fulvik asitin kronik stresin oluşturduğu testis hasarına karşı tedavi edici bir ajan olarak kullanılabileceği sonucuna varılmıştır.

The harmful use of alcohol is a worldwide problem involving all ages. This study aims to investigate chronic alcohol exposure related hepatotoxicity on the rat liver and possible hepatoprotective effects of boric acid. Rats were separated into 4 different groups: control, ethanol, ethanol+boric acid, and boric acid. We measured (i) malondialdehyde (MDA), total sialic acid (TSA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) levels, which are known to be the markers of alcohol damage; and also (ii) caspase-3, tumor necrosis factor-alpha (TNF-α), and the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) as the markers of apoptosis. In the ethanol group, MDA, TSA, and TNF-α levels increased whereas SOD and CAT levels decreased compared with the control group. Ethanol+boric acid group MDA, TSA, caspase-3, and TNF-α levels decreased whereas SOD and CAT levels increased compared with the ethanol group. Using histopathological evaluation of light microscope images, immunohistochemical caspase-3 and TNF-α activity in the ethanol+boric acid group were shown to be decreased compared with that in the ethanol group. Our results revealed that ethanol is capable of triggering oxidative stress and apoptosis in the rat liver. We propose that boric acid is an effective compound in protecting the rat liver against ethanol.

Alcohol consumption in pregnancy may cause fetal alcohol syndrome (FAS) in the infant. This study aims to investigate prenatal alcohol exposure related neuroapoptosis on the cerebral cortex tissues of newborn rats and possible neuroprotective effects of betaine, folic acid, and combined therapy. Pregnant rats were divided into five experimental groups: control, ethanol, ethanol + betaine, ethanol + folic acid, and ethanol + betaine + folic acid combined therapy groups. We measured cytochrome c release, caspase-3, calpain and cathepsin B and L. enzyme activities. In order to observe apoptotic cells in the early stages, TUNEL method was chosen together with histologic methods such as assessing the diameters of the apoptotic cells, their distribution in unit volume and volume proportion of cortical intact neuron nuclei. Calpain, caspase-3 activities, and cytochrome c levels were significantly increased in alcohol group while cathepsin B and L. activities were also found to be elevated albeit not statistically significant. These increases were significantly reversed by folic acid and betaine + folic acid treatments. While ethanol increased the number of apoptotic cells, this increase was prevented in ethanol + betaine and ethanol + betaine + folic acid groups. Morphometric examination showed that the mean diameter of apoptotic cells was increased with ethanol administration while this increase was reduced by betaine and betaine + folic acid treatments. We observed that ethanol is capable of triggering apoptotic cell death in the newborn rat brains. Furthermore, folic acid, betaine, and combined therapy of these supplements may reduce neuroapoptosis related to prenatal alcohol consumption, and might be effective on preventing fetal alcohol syndrome in infants.

To the best of our knowledge, this is the first study concerning the effect of boric acid (BA) administration on fetal alcohol syndrome (FAS). In this study, the aim was to investigate prenatal alcohol-induced oxidative stress on the cerebral cortex of newborn rat pups and assess the protective and beneficial effects of BA supplementation on rats with FAS. Pregnant rats were divided into three groups, namely the control, alcohol and alcohol + boric acid groups. As markers of alcohol-induced oxidative stress in the cerebral cortex of the newborn pups, malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) levels were measured. Although the MDA levels in the alcohol group were significantly increased compared with those in the control group (P

WOS: 000328658600043, PubMed ID: 24055552, Constitutes of the venom scorpion are a rich source of low molecular mass peptides which are toxic to various organisms, including man. Androctonus crassicauda is one of the scorpions from the Southeastern Anatolia of Turkey with public health importance. This work is focused on the investigation of biological effects of Acra3 peptide from Androctonus crassicauda. For this purpose, Acra3 isolated from crude venoms was tested for its cytotoxicity on BC3H1 mouse brain tumor cells using tetrazolium salt cleavage and lactate dehydrogenase activity assays. To determine whether the cytotoxic effects of Acra3 was related to the induction of apoptosis, the morphology of the cell's and the nuclear fragmentation was examined by using Acridin Orange staining and DNA fragmentation assay, respectively. Caspase 3 and caspase 9 activities were measured spectrophotometrically and flow cytometric assay was performed using Annexin-V FITC and Propidium Iodide staining. Furthermore toxic peptide Acra3 was used as an antigen for immunological studies. Results showed that Acra3 exerted very strong cytotoxic effect on BCH1 cells with an IC50 value of 5 mu g/ml. Exposure of the cells to 0.1 and 0.5 mu g/ml was resulted in very strong appearance of the apoptotic morphology in a dose dependent manner. On the other side, not any DNA fragmentation was observed after treatment of the cells. Caspase 3 and 9 activities were slightly decreased with Acra3. Results from flow cytometry and lactate dehydrogenase activity assays indicate that Acra3 exerts its effects by inducing a stronger necrosis than apoptosis in BC3H1 cells. To evaluate its immunogenicity, monoclonal antibody (MAb) specific for Acra3 antigen (5B9) was developed by hybridoma technology using spleen and lymph nodes of mice and immunoglobulin type of antibody was found to be IgM. We suggest that Acra3 may exert its effects by inducing both necrotic and apoptotic pathway in some way on mouse brain tumor cells. These findings will be useful for understanding the mechanism of cell death caused by venom in vitro. Anti-Acra3 monoclonal antibody can be further used as a bioactive tools for exploring the structure/function relationship and the pharmacological mechanism of scorpion peptide neurotoxins, Scientific and Technological Research Council of Turkey [TBAG-106T527], We would like to thank Dr. Hakan Caliskan and Dr. Umit Sirin from Biology Department of Eskisehir Osmangazi University, who collected scorpion used in this protocol. This work was financed by a grant from the Scientific and Technological Research Council of Turkey (TBAG-106T527) to the authors.

Despite effective vaccination programs in many countries, HBV infection is still a serious health problem throughout the world; more than 2 billion people have been infected with Hepatitis B virus (HBV). The serologic markers are crucial indicators in clinical diagnosis of HBV infection. The persistent presence of anti-HBc is associated with chronicity, and anti-HBe is an indicator for active viral replication. In the present study, two different hybridoma clones, 12E5 and 16F8, secreting anti-HBeAg and anti-HBc antibody were developed using hybridoma technology. BALB/c mice were immunized with HBe antigen (HBeAg), and monoclonal antibodies were generated from the spleen and lymph nodes of mice. Immunoglobulin types of antibodies were found to be IgG2a and IgG1, respectively. Monoclonal antibodies (MAbs) were produced in large scale, purified with affinity chromatography, and epitope analysis was performed. The results have shown that 12E5 and 16F8 monoclonal antibodies can be used for detection of HBcAg and HBeAg, indicating that they have the potential for use in clinical diagnosis.

In the present study, spleen and lymph nodes of mice were cryopreserved as a whole tissue and after thawing, membrane integrity of mononuclear cells was determined by trypan blue exclusion and PI staining. T and B lymphocytes, macrophages and dendritic cells have been isolated from both cryopreserved tissue and analyzed by Flow cytometry. BALB/c mice were immunized with Hepatitis e antigen (HBeAg) and spleen and lymph nodes of mice were cryopreserved for 3 to 10 months. The cells obtained from both tissue were applied to hybridoma technology to understand if the cells keep their viability and functionality. The cells were isolated and fused with F0 mouse myeloma cells and several antibody producing hybrid cells were developed. Results have shown that cryopreserved spleen and lymph nodes of mice can be efficiently used in hybridoma technology for the successful generation of monoclonal antibody producing hybrid cells.

Hepatitis B is a major public health problem worldwide, which may lead to chronic liver diseases such as cirrhosis and hepatocellular carcinoma. The hepatitis B core antigen (HBcAg) is one of the major viral proteins, which forms the inner core of hepatitis B virus (HBV) particles. In this study, filamentous bacteriophage M13 was genetically modified to display the polypeptides of HBcAg in order to develop an alternative carrier system. HBcAg gene was inserted into the minor coat protein (pIII) gene of M13, and HBcAg was expressed on the phage surface as a whole protein. Antigenicity and immunogenicity of HBcAg were tested by immunizing BALB/c mice three times with HBcAg-displaying recombinant phages. After successful immunization, one of the mice with high antibody titer to HBcAg was selected for fusion, and four monoclonal antibodies specific for HBcAg were developed. This result showed that HBcAg-displaying recombinant bacteriophages are immunogenic and can potentially be used for the development of monoclonal antibodies.

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European Biotechnology Congress -- SEP 28-OCT 01, 2011 -- Istanbul, TURKEY, WOS: 000295310800102, …, European Biotechnol Themat Network Assoc

Physicians recommend aspirin for prevention of heart attacks and stroke in people above the age of 40 years. In some cases, alcohol consumption accompanies aspirin intake. In this study, the in vitro effects of different doses of ethanol (50, 100, and 200 mM) and 100 microg/mL of aspirin and the possible protective role of betaine (0.5 and 1 mM) were investigated on rat cerebral synaptosomes. Synaptosomally enriched fractions, derived from Sprague Dawley rat brains, were incubated with ethanol and aspirin so as to measure sialic acid (SA), nitric oxide levels, and adenosine deaminase (ADA) activities, which are known to be the markers of alcohol damage. When combined with aspirin, ethanol increased SA levels compared with the control group at all doses, resulting in loss of SA residue from synaptosomal membrane. Betaine (0.5 mM) decreased SA levels with respect to the ethanol (200 mM) plus aspirin group (p.05), thereby preventing SA loss. Moreover, betaine reversed the destructive effects of ethanol by elevating reduced nitric oxide levels. Aspirin, when combined with all doses of ethanol, increased ADA activity, which is crucial for purine metabolism. ADA activities were also elevated in betaine-administered groups. We propose that betaine is an effective compound in protecting the rat brain synaptosomes against ethanol and aspirin together.

Coagulation proteases have increasingly recognized functions beyond hemostasis and thrombosis. Disruption of activated protein C (aPC) or insulin signaling impair function of podocytes and ultimately cause dysfunction of the glomerular filtration barrier and diabetic kidney disease (DKD). We here show that insulin and aPC converge on a common spliced-X-box binding protein-1 (sXBP1) signaling pathway to maintain endoplasmic reticulum (ER) homeostasis. Analogous to insulin, physiological levels of aPC maintain ER proteostasis in DKD. Accordingly, genetically impaired protein C activation exacerbates maladaptive ER response, whereas genetic or pharmacological restoration of aPC maintains ER proteostasis in DKD models. Importantly, in mice with podocyte-specific deficiency of insulin receptor (INSR), aPC selectively restores the activity of the cytoprotective ER-transcription factor sXBP1 by temporally targeting INSR downstream signaling intermediates, the regulatory subunits of PI3Kinase, p85α and p85β. Genome-wide mapping of condition-specific XBP1-transcriptional regulatory patterns confirmed that concordant unfolded protein response target genes are involved in maintenance of ER proteostasis by both insulin and aPC. Thus, aPC efficiently employs disengaged insulin signaling components to reconfigure ER signaling and restore proteostasis. These results identify ER reprogramming as a novel hormonelike function of coagulation proteases and demonstrate that targeting insulin signaling intermediates may be a feasible therapeutic approach ameliorating defective insulin signaling.