Assumptions surrounding the kidney as a target for accumulation of ochratoxin A (OTA) are addressed because the contribution of the toxin in blood seems invariably to have been ignored. Adult rats were maintained for several weeks on toxin-contaminated feed. Using standard perfusion techniques, animals were anaesthetised, a blood sample was taken, one kidney was ligated, and the other kidney perfused with physiological saline in situ under normal blood pressure. Comparative analysis of OTA in pairs of kidneys showed marked reduction in the perfused organ in the range 37%–98% (mean 75%), demonstrating the general efficiency of perfusion supported also by histology, and implying a major role of blood in the total OTA content of kidney. Translation of OTA values in plasma to whole blood, and its predicted contribution as a 25% vascular compartment in kidney gave values similar to those in non-perfused kidneys. Thus, apparent ‘accumulation’ of OTA in kidney is due to binding to plasma proteins and long half-life in plasma. Attention should be re-focused on whole animal pharmacokinetics during chronic OTA exposure. Similar principles may be applied to DNA-OTA adducts which are now recognised as occurring in blood; application could also extend to other nephrotoxins such as aristolochic acid. Thus, at least, quantitative reassessment in urological tissues seems necessary in attributing adducts specifically as markers of potentially-tumourigenic exposure.

In this study, the diabetogenic effects of long term Ochratoxin A (OTA) administration in rats were investigated, and its role in the etiology of diabetes mellitus (DM) was examined utilizing 42 female Wistar rats for these purposes. The rats were divided into three different study and control groups according to the duration of the OTA administration. The rats received 45 μg OTA daily in their feed for 6, 9 and 24 weeks, respectively. Three control groups were also used for the same time periods. Blood and pancreatic tissue samples were collected during the necropsy at the end of the 6, 9 and 24 weeks. The plasma values of insulin, glucagon and glucose were determined for the study and control groups. Pancreatic lesions were evaluated via histopathological examination and insulin and glucagon expression in these lesions was subsequently determined using immunohistochemical methods. Statistically significant decreases in insulin levels were observed, in contrast to increases in blood glucagon and glucose levels. Histopathological examinations revealed slight to moderate degeneration in Langerhans islet cells in all OTA-treated groups. Immunohistochemistry of pancreatic tissue revealed decreased insulin and increased glucagon expression. This study demonstrated that OTA may cause pancreatic damage in the Langerhans islet and predispose rats to DM.

Bu çalışmada, Antalya İli’nde yetiştirilen gökkuşağı alabalığı kültür popülasyonundan büyüme hormonu I geni izole ve karakterize edilmiştir. Bu amaçla kültür popülasyonundan 10 birey örnek olarak alınmıştır. Örneklenen balıkların kas dokularından toplam DNA izole edilmiştir. Polimeraz zincir reaksiyonunda kullanılmak üzere primerler dizayn edilmiş ve hedef gen bölgesi çoğaltılmıştır. İzole edilen genin dizi analizi yapılmış ve 4591 nükleotitten oluştuğu tespit edilmiştir. Referans diziye kıyasla 2 transisyonel, 14 transversiyonel ve 38 insersiyonel baza karşılık gelen 54 nükleotitten oluşan mutasyon bulunmuştur. Tüm nükleotit farklılıkları genin intron bölgelerinde tespit edilmiştir. Genin intron bölgelerinde yer alan putatif hormon yanıt elemanları (HRE) değerlendirildiğinde ise daha önce raporlanan dizi ile tamamen uyumlu olduğu görülmüştür. Elde edilen veriler filogenetik ve gen aktarım çalışmalarında kullanılabilecek niteliktedir.