Aflatoxin exposure in viral hepatitis patients in Turkey.

Background/aims: Hepatocellular carcinoma is the fifth most common cancer and a major public health problem worldwide. Differences in distribution of hepatocellular carcinoma incidence are probably due to different levels of exposure to hepatocellular carcinoma risk factors: chronic infections with hepatitis B virus (HBV) and aflatoxin exposure in developing countries, and smoking and alcohol abuse in developed countries. Aflatoxin is one of the most important of the environmental toxins that contribute to the pathogenesis of hepatocellular carcinoma, especially in the regions where dietary foodstuffs (peanuts, corn, Brazil nuts, pistachios, spices and figs) are highly contaminated.

The effect of K-ATP channel blockage during erythropoietin treatment in renal ischemia-reperfusion injury.

ATP dependent K channels (K-ATP) take part in the Erythropoietin (EPO) induced cardioprotection but these channel activations have role in cytoprotective role of EPO in the renal ischemia reperfusion (IR) damage is still unknown. For this purpose rats were pretreated with EPO (500 IU/kg) and/or K-ATP channel blocker glibenclamide (40 mM/kg) i.p.

Midkine secretion protects Hep3B cells from cadmium induced cellular damage.

Aim: To evaluate role of midkine secretion during Cadmium (Cd) exposure in the human hepatocyte cell line Hep3B cells.

Methods: Different dosages of Cd (0.5-1-5-10 microg/mL) were applied to Hep3B cells and their effects to apoptosis, lactate dehydrogenase (LDH) leakage and midkine secretion were evaluated as time dependent manner.

Erythropoietin attenuates hydrogen peroxide-induced damage of hepatocytes.

Background/aims: High levels of hydrogen peroxide (H2O2) are observed during inflammatory and ischemic states of the liver and usually lead to cellular dysfunction and cytotoxicity. Recently, it has been reported that erythropoietin and mitochondrial K (ATP) channel openers have a protective effect via a pharmacological preconditioning action during ischemia reperfusion injury of the liver and heart. However, it remains unclear as to whether K (ATP) channel blockers can reduce the protective effect of erythropoietin in the H2O2-induced injury of hepatocytes.