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Resveratrol (RES) is a polyphenol with antioxidant, anti-inflammatory, and many other physiological effects on tissues. In the present study, the effect of resveratrol in hyperoxaluria driven nephrolithiasis/nephrocalcinosis is investigated. Wistar-Albino rats of 250–300 g (male, n = 24) were included in the present study. The rats were randomized into three groups: Group 1 consisted of the controls (n = 8), Group 2 of hyperoxaluria (1% ethylene glycol (EG), n = 8), and Group 3 of the treatment (1% EG + 10 mg/kg of RES, n = 8) group. At the beginning and fifth week of the study, two rats from each group were placed in metabolic cages for 24 h and their urine was collected. At the end of the study, the rats were killed and their blood was collected from the vena cava inferior. The right kidneys of the rats were used for biochemical and the left ones for immunohistochemical analyzes. Malondialdehyde (MDA), catalase, urea, calcium, oxalate, and creatinine clearance were studied in the blood, urine, and kidney tissues. Moreover, routine histological evaluation, and p38-MAPK and NFkB immunohistochemical analyses were conducted. In the hyperoxaluria group, urinary oxalate levels were higher than the control group; yet, lower in the treatment group compared to hyperoxaluria group (p

The aim of the current study was to investigate the probable protective effects of Pentoxifylline (PTX) and Alpha Lipoic Acid (ALA), which display anti-oxidative efficacy against hepatotoxicity and nephrotoxicity, those being the major side effects of Methotrexate (MTX). Rats were divided into four groups: a control group; MTX (20mg/kg/day) group; MTX+PTX (20mg/kg/day+50mg/kg/day) group; and an MTX+ALA (20mg/kg/day+100mg/kg/day) group. At the end of the experiment, biochemical, histochemical and immunohistochemical analyses were performed on liver and kidney tissues of rats. We determined Glutathione Peroxidase (GSH-Px), Superoxide Dismutase (SOD), Catalase (CAT), Malondialdehyde (MDA), Nitric Oxide (NO) and Xanthine Oxidase (XO) levels in the liver and kidney. Moreover, Gamma Glutamyl Transferase (GGT), Direct Bilirubin (DBil), Blood Urea Nitrogen (BUN), and urea levels were measured in the serum. The histochemical evaluation revealed a significant decrease in MTX caused damage in the PTX- and ALA-treated groups (especially in ALA group). On the other hand, the immune staining of iNOS and TNF-α were observed most densely in the MTX group, while the density decreased in the PTX- and ALA-administered groups. We determined increased GGT, BUN, urea and levels of CAT, MDA, NO, and XO values in both groups, while GSH-Px (an increase in liver tissue) and DBil levels were decreased in the group that received MTX. However, we determined decreased SOD levels in liver tissue. In the PTX and ALA groups, the levels of GGT, BUN and urea as well as the levels of CAT, MDA, NO and XO decreased (SOD increased in the liver tissue), and the levels of GSH-Px and DBil increased. In conclusion, it can be stated that, although ALA is more effective in preventing the toxic effects of MTX on the liver and kidney, PTX also has a preventive effect. As a result, we can readily suggest that ALA and PTX can have protective effects by decreasing MDA, NO, BUN and urea values as antioxidants against MTX-induced damage in liver and kidney of rats.

Amaç: Fosfatlı gübrelerde, deterjanlarda ve rafine petrol türevlerinde bulunan kadmiyum, 1817 yılında keşfedilmiş toksik ağır bir metaldir ve sigaranın majör bileşenlerinden biridir. Selenyum serbest radikallerin üretimini azaltmak ve önlemek için gerekli olan, doymamış yağ asitlerinden türeyen ve peroksitleri yok ettiği düşünülen bir elementtir. Melatonin, pineal bezin majör hormonudur. Organizma, serbest radikallerin neden olduğu hücre hasarını önlemek için antioksidan savunma sistemi geliştirir. Bu çalışmada, kadmiyumun vücutta dokularda birikerek oluşturduğu toksisite üzerine Selenyum (Se) ve Melatoninin etkisinin belirlenmesi amaçlandı. Gereç-Yöntem: Deney grupları; her grupta 8 dişi sıçan olmak üzere, kontrol (Grup I), Kadmiyum (Grup II), Melatonin (Grup III), Selenyum (Grup IV), Kadmiyum+Melatonin (Grup V), Kadmiyum+Selenyum (Grup VI), Melatonin+Selenyum (Grup VII) ve Kadmiyum+Melatonin+Selenyum (Grup VIII) şeklinde düzenlendi. Kadmiyum (2 mg/kg/gün; gavajla), Melatonin (3 mg/kg/gün; intraperitoneal) 30 gün boyunca günde bir kez, selenyum ise 5'er gün arayla 30 günde 6 kez uygulandı. Deney sonunda over, tuba uterina ve uterus dokuları alınarak, bir kısmı histokimyasal ve immünohistokimyasal değerlendirme için %10'luk nötral formaldehit içerisine, diğer kısmı ise biyokimyasal çalışma için fosfat tamponu içerisine ve kan örnekleri apopitotik hücre ve DNA fragmantasyonu tayini için EDTA'lı tüplere alındı. Bulgular, Sonuç ve Tartışma: Çalışmamızın sonunda kadmiyum verilmesine bağlı olarak over, tuba uterina ve uterus dokularında MDA düzeyleri kontrol grubuna göre artış gözlendi. GSPx ve CAT aktivite değerlerinde de artış saptandı. Grup III, VII ve VIII' de benzer parametreler gözlendi. Grup V ve VI' da ise antioksidanların etkisi ile lipid peroksidasyon engellenerek MDA, GSPx ve CAT düzeylerinin kadmiyuma göre düştüğü tespit edildi. DNA ladder kit ile yapılan analizler sonucunda sadece kadmiyum verilen grupta DNA fragmantasyonu ve buna bağlı olarak apopitotik hücre artışı gözlendi. Histolojik ve immünohistokimyasal bulgularımızda biyokimyasal analizler ve DNA ladder değerlerine paralel sonuçlar elde edildi. Kadmiyum grubunun bütün dokularında hasar (overlerin foliküllerinde dejenerasyon, hemorajik alanlar, mononükleer hücre infiltrasyonu ve bağ dokusu artışı; tuba uterina'nın epitelinde dejenerasyon ve tübüllerinde dejenerasyon; uterusun epitelinde dejenerasyon, endometriyum tabakasında dilate alanlar ve endometriyal bezlerde dejenerasyon), E-kaderin, NCAM sentezinde artış ve dokularda yüksek MT-3 birikimi gözlendi. Grup VI ve VIII' de anlamlı histopatolojik düzelmeler gözlemlendi, ancak grup V'te herhangi bir düzelme tespit edilemedi. Kadmiyumun dişi genital sistem organlarında hasar meydana getirdiğini, selenyumun dokuları bu hasardan korurken Melatoninin herhangi bir koruyucu ya da düzeltici etkisi olmadığı gözlendi. Melatoninin koruyucu bir etki gösterememesinin sebebini dişi sıçanların hormonal değişimlerine ve Melatoninin uzun süreli kullanımına bağlı olabileceği düşünüldü. Çalışmamızın kadmiyum tedavisine ya da korumasına katkı sağlamasını ve yeni tedavi yollarına basamak teşkil etmesini umuyoruz. Aim: Cadmium which is discovered in 1817 is a toxic heavy metal and found in phosphate fertilizers, detergents and refined petroleum and it's one of the major components of cigarette smoking. Selenium is an element, derived from unsaturated fatty acids, thought to degrade peroxides and needed to reduce - prevent the production of free radicals. Melatonin is the major hormone of the pineal gland and it is develops an antioxidant defense system to prevent cell damage caused by free radicals in organism. In our study, it was aimed to determine whether Selenium and Melatonin show antioxidant properties on the toxicity that cadmium accumulates on tissues in the body. Material Method: Experimental groups; Control (Group I), Cadmium (Cd) (Group II), Melatonin (Group III), Selenium (Group IV), Cadmium+Melatonin (Group V), Cadmium+Selenium (Group VI), Melatonin+Selenium (Group VII) and Cadmium + Melatonin + Selenium (Group VIII) were arranged to be8 female rats in each group. Cadmium (2 mg / kg / daywith gavage), Melatonin (3 mg / kg / day, intraperitoneal)30 days were applied once a day and seleneium wasapplied 6 times in 30 days, 5 days a day. At the end ofthe experiment, over, tuba uterine and uterus tissues weretaken. Some of the receiving tissues were in 10% neutralformaldehyde for histochemical and immunohistochemicalevaluation and the other were in phosphate buffer forbiochemical study and bloods were taken into the EDTAtube for apoptotic cell and DNA fragmentation assay.Results and Discussion: At the end of our study, MDAlevels were increased in the over, tubal uterine anduterine tissues according to the cadmium administrationgroup and also increase in GSPx and CAT activity valueswas detected, similar parameters were also observed ingroup III, group VII, group VIII. But in group V and groupVI, were found to inhibit lipid peroxidation of antioxidantsand decrease MDA, GSPx and CAT levels comparedto cadmium. As a result of the analysis with DNA ladderkit, DNA fragmentation and consequently apoptotic cellsnumber were observed only in the cadmium-administeredgroup. Histological and immunohistochemical findingsgave parallel results to biochemical analyzes and DNAladder values. in all the tissues of the cadmium group were observed; High MT-3 accumulation, damage (degeneration of ovarian follicles, haemorrhagic areas, mononuclear cell infiltration and increased connective tissue; degeneration in tuba uterina epithelium and degeneration in tubules; degeneration in the uterine epithelium, dilate fields in the endometrium layer and degeneration in the endometrial glands) and increase in E-cadherin, NCAM synthesis. When significant improvements were observed in group VI and group VIII, there were no improvement in the group V. We have seen that cadmium brings damage to the female genital system organs and while selenium has protective effect for tissues from this damage, Melatonin has not a protective or corrective effect but we think, the cause of this event because of to hormonal changes of female rats and the long-term use of Melatonin. At last, we hope that our work will contribute to cadmium treatment or protection and will provide a stepping stone to new ways of treatment.

The purpose of this study was to provide a morphologic description and assessment on the formation level of the sural nerve (SN) and its components. Also we aimed to reveal histological features of the SN components. An anatomical study of the formation of the SN was carried out on 100 limbs from 50 embalmed foetuses. The results showed that the SN was formed by the union of the medial sural cutaneous nerve (MSCN) and the peroneal communicating branch (PCB) in 71% of the cases (Type A); the MSCN and PCB are branches of the tibial and common peroneal nerve (CPN) or lateral sural cutaneous nerves (LSCN), respectively. Formation level of the SN was at the distal third of the leg in 43% of the cases, at the middle third of the leg in 46% of the cases, and at the upper third of the leg in 11% of the cases. The PCB originated in the CPN in 68% and the PCB originated in the LSCN in 3% of the cases. The SN was formed only by the MSCN in 20% of the cases (Type B). Type C was divided into four subgroups: in the first group the PCB and fibres of the posterior femoral cutaneous nerve joined the MSCN in 4% of cases; in the second group the MSCN, PCB, and sciatic nerve did not unite and coursed separately in 1% of cases; in the third group the SN arose directly from the sciatic nerve alone and the MSCN made a little contribution in 2% of cases; and in the fourth group the PCB, fibres of the sciatic nerve, and the MSCN formed the SN in 1% of the cases. The SN was formed only by the PCB in 1% of the cases (Type D). Distances of the formation level of the SN to the intercondylar line and the lateral malleolus were measured and also noted. A detailed knowledge of the anatomy of the SN and its contributing nerves are important in many interventional procedures.