Durrin Ozlem Dabak

Effects of testosterone on orchiectomy-induced oxidative damage in the rat hippocampus

The aim of this study was to investigate the morphological changes of the hippocampus after orchiectomy and the protective effects of testosterone on these changes. Animals were divided into 3 groups. The rats in group I were used for sham-orchiectomy. Orchiectomy was performed on the rats in group II. The rats in group III were administrated testosterone propionate 0.5mg/kg/day for 30 days after the orchiectomy. Some of the hippocampal tissues were used for determination of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) enzyme activities, and malondialdehyde (MDA) levels. The remaining hippocampal tissue specimens were stained with routine histological methods and examined under the light microscope. Additionally, the samples were immunohistochemically stained by using avidin-biotin-peroxidase for determination of bax immunoreactivity. The SOD and GSH-Px enzyme activities of the hippocampus were decreased, and MDA levels were increased in group II rats compared to the sham-orchiectomy group. In the light microscopic evaluation of the tissue specimens from group II, significant increases were detected in the number of picnotic cells and in bax immunoreactivity compared to the sham-orchiectomy group. However, an increase was observed in activities of SOD and GSH-Px enzymes and a decrease of the MDA levels in animals with orchiectomy, but having externally administered testosterone. It was determined that the increase of bax immunoreactivity and histopathological changes in this group were regressed by testosterone. The results of our study revealed that orchiectomy-induced oxidative damage and morphological changes in the hippocampal tissue were suppressed by testosterone.

Determination of ghrelin immunoreactivity in kidney tissues of diabetic rats.

Backgrounds/Aims. Ghrelin, a recently discovered hormone, is released largely from stomach and might affect insulin secretion and glucose metabolism. The aim of this study was to determine the immunohistochemical localization of ghrelin in streptozotocin-induced diabetic rat kidneys. Methods. Fifty-four adult male Wistar rats were used in this study. All rats were divided into nine groups according to three time points of the study (2, 4, and 6 weeks) as control group, control group given 0.1 M phosphate-citrate, and diabetic group given 50 mg/kg streptozotocin intraperitoneally. The rats in all groups were decapitated at the end of 2, 4, and 6 weeks of the study. The kidneys of the rats were removed, and tissue samples were processed by using routine paraffin techniques. The samples were immunohistochemically stained using avidin-biotin-peroxidase method for ghrelin immunoreactivity. Results. There were no differences of ghrelin immunoreactivity between the control groups. Ghrelin immunoreactivity was observed in both distal tubulus and collecting ducts in the diabetic groups, while it was detected only in distal tubules of the control groups. The intensity of ghrelin immunoreactivity was increased at 4 and 6 weeks of the study in the diabetic groups. Conclusion. Increased ghrelin immunoreactivity in the diabetic rat kidney tissues suggests that ghrelin may contribute to the pathophysiological mechanism of diabetic nephropathy.

Effects of Vitamin D3 (Cholecalciferol) on Adriamycin-Induced Nephrotoxicity

Although immune-mediated pathogenesis in adriamycin (ADR)-induced nephropathy has been proposed recently, studies are lacking about the effects of immunmodulators, such as vitamin D, on ADR-induced nephrotoxicity. We hypothesized that vitamin D3 (cholecalciferol) would be beneficial on ADR‐induced nephropathy because of its immunmodulatory properties. Eighteen male Wistar rats were divided into three groups (n = 6): group 1 (control), group 2 (single ADR injection intravenously), and group 3 (similar single ADR injection intravenously + daily oral cholecalciferol for 21 days) were used in the study. A single high dose of ADR resulted in increased urinary protein: creatinine ratio for all three weeks of the experiment in both groups 2 and 3 compared with the controls. Histological examination of the kidney tissue revealed distinct tubular lesions as tubular necrosis, hyaline casts in tubular lumen, tubular degeneration, tubular dilatation, and tubular vacuolization in group 2 compared with group 1. These tubular lesions were significantly reduced in group 3 compared to group 2. The results of this study indicate that cholecalciferol causes satisfactory tubulointerstitial recovery in ADR-induced nephrotoxicity in rats.

Effects of silymarin on methotrexate-induced nephrotoxicity in rats

Abstract Methotrexate (MTX) is widely used in the treatment of various malignancies and nononcological diseases but its use has been limited by its nephrotoxicity. Silymarin (SLY), a natural flavonoid, has been reported to have antioxidant, anti-inflammatory and anti-apoptotic effects. This study was carried out to determine whether SLY exerts a protective effect against MTX-induced nephrotoxicity. Rats were divided into six groups: Group 1 (saline, i.p., single injection), Group 2 (0.5% carboxymethyl cellulose (CMC), by gavage once daily for five consecutive days), Group 3 (SLY, 300 mg/kg per day, i.p. for five consecutive days), Group 4 (MTX, 20 mg/kg, i.p., single injection), Group 5 (MTX + CMC similarly as groups 2 and 4) and Group 6 (MTX + CMC + SLY similarly as groups 2, 3 and 4). Histopathologic alterations including apoptotic changes of the kidney were evaluated. MTX injection exhibited dilated Bowman’s space, inflammatory cell infiltration, glomerular and peritubular vascular congestion and swelling of renal tubular epithelium cells. Apoptotic cell death was also markedly increased in renal tubules after MTX administration. SLY treatment resulted in statistically significant amelioration in the histological alterations and reduced the number of TUNEL-positive cells as compared with the MTX treated rats (p < 0.05). In conclusion, SLY treatment leads to a reduction on MTX-induced renal damage in rats. Since SLY is safe and acceptable for human consumption, further studies to define the exact mechanism of the protecting effect of SLY on MTX-induced nephrotoxicity and the optimum dosage of this compound would be useful.

Immunolocalization of TGF-β2 in the rat thymus during late stages of prenatal development

The aim of this study was to investigate the immunolocalization of transforming growth factor beta (TGF-beta2) in rat thymic stromal cells and thymocytes and investigate the roles of TGF-beta2 in thymopoiesis during the late stages of fetal development. Twelve adult pregnant female Wistar rats weighing 250-270 g were used in this study. The rats were killed by cervical dislocation on gestation days 16 (GD16), 18 (GD18) and 20 (GD20). Fetal thymus glands were prepared and examined by an immunohistochemical technique to reveal binding of an anti-TGF-beta2 rabbit polyclonal antibody. The thymic primordium was surrounded with a connective tissue capsule at GD16 and at this stage TGF-beta2 immunoreactivity was not observed. At GD18, the connective tissue capsule had formed septa which subdivided the tissue into lobules and at this stage TGF-beta2 immunolocalization was detected in the capsule and in thymocytes. Lobulation was more evident at GD20 and TGF-beta2 immunoreactivity of thymocytes was more extensive than on GD18. Results indicate that TGF-beta2 may play an important role in the organization or development of thymocytes in the late stages of thymopoiesis.

The investigation of effect of alpha lipoic acid against damage on neonatal rat lung to maternal tobacco smoke exposure

Graphical abstract

Gebelikte Tütün Dumanı Maruziyetinin Anne Sıçan Akciğer Dokusunda Meydana Getirdiği Değişiklikler Üzerine Alfa Lipoik Asitin Etkilerinin İncelenmesi

Amac: Calismamizda gebelikte tutun dumanina maruz kalan anne sicanlarin akciger dokusunda meydana gelen degisiklikler uzerine alfa lipoik asitin etkilerinin deneysel sican modeli uzerinde arastirilmasi amaclandi. Yontemler: Calismada 28 adet disi Sprague-Dawley cinsi sicanlar kullanildi. Gebe sicanlar; Kontrol grubu, Tutun dumani (TD) grubu, Tutun dumani + Alfa lipoik asit (TD+ALA) grubu ve Alfa lipoik asit (ALA) grubu olmak uzere rastgele dort esit gruba ayrildi. TD ve TD+ALA grubundaki sicanlar ciftlesmeden once sekiz hafta ve gebelik suresince gunde iki saat tutun dumanina maruz birakildi. TD+ALA ve ALA grubundaki sicanlara ise ciftlesmeden once sekiz hafta ve gebelik suresince gun asiri oral gavaj yolu ile 20 mg/kg dozunda alfa lipoik asit verildi. Deneyin sonunda sicanlar dekapite edilerek akciger dokulari cikarildi ve histolojik, biyokimyasal ve immunohistokimyasal metotlar uygulandi. Bulgular: TD grubuna ait akciger kesitlerinde inflamatuar hucre artisi, konjesyon, odem, hemoraji gibi histopatolojik bulgular gozlendi. ALA uygulamasiyla bu histopatalojik bulgularda istatistiksel olarak anlamli oranda duzelmeler izlendi. TD grubunda VEGF immunreaktivitesinin kontrol grubuna gore anlamli artis gosterdigi, TD+ALA grubunda ise TD grubuna gore VEGF immunreaktivitesinin anlamli derecede azaldigi belirlendi. TD grubunda MDA degerlerinin kontrole gore anlamli derecede arttigi, TD+ALA grubunda ise TD grubuna gore anlamli derecede azaldigi gozlendi. Sonuc: Tutun dumaninin gebe sican akcigerinde yol actigi oksidatif hasarin, alfa lipoik asit tedavisinin antioksidan etkileri ile kismen engellendigi belirlendi.

Protective effects of vitamin D3 against d-galactosamine-induced liver injury in rats

In this study, we examined liver damage induced by d-galactosamine (d-GaIN) and the protective effects of vitamin D3 in relation to d-GaIN toxicity. Twenty Wistar albino rats were used in this study. The rats were divided into four groups. Group I rats were used as the control group. Group II rats were given a single intraperitoneal injection of d-GaIN. Group III rats were given a single intraperitoneal injection of d-GaIN, intramuscular vitamin D3 for five days. Group IV rats were given intramuscular vitamin D3 for five days. All of rats were euthanized by cervical decapitation on the fifth day of experiment. Upon completion of the experiment, a midsaggital incision was performed, and the livers of all rats were removed and fixed. The livers were processed to perform TUNEL technique and histochemical staining. During the microscope examination, we observed inflamatory cell infiltration, sinusoidal dilatation, and apoptotic bodies due to d-GaIN exposure. In addition, glycogen content of the group II hepatocytes was significantly decreased. Vitamin D3 treatment provided better structural apperance of the livers in group III. TUNEL positive cells were extremly pervasive in the group II livers. The study found group III TUNEL positive cells at a reduced rate in relation to group II due to vitamin D3 treatment. This findings indicate that d-GaIN causes inflamation in the liver. This inflamation triggers the apoptotic process gradually. Vitamin D3 has potency to decrease the severity of d-GaIN-caused structural liver damage.