RESUMO
BACKGROUND: One of the most important side effects of contrast pharmaceutical agents, which are used very common in routine radiology practice, is contrast induced nephropathy. Even ischemia, oxidative stress and osmolality related cytotoxic effects are considered, the molecular mechanisms underlying this pathology have not been identified completely yet. OBJECTIVES: The aim of the current study was to reveal the role of oxidative stress and antioxidant enzymatic defence mechanisms in the aetiopathogenesis of contrast-induced nephropathy. We also studied possible alleviating effects of N-acetylcysteine (NAC), a potent antioxidant, to obtain extra information regarding the molecular mechanisms underlying this pathology. MATERIALS AND METHODS: This is an clinical-experimental study, This study was conducted of Istanbul/Turkey between September 15, 2012 and April 15, 2013. Three groups of male rats were randomly set up as a control group (C), a 100 mg/kg intraperitoneal NAC + 7 mL/kg contrast agent group (N + CIN) and a 7 mL/kg intraperitoneal contrast agent group (CIN). They were placed in individual metabolic cages 48 hours after agent administration to obtain 24-hour urine samples. Renal function tests (albumin, urea, creatinine, total protein) were conducted, oxidative stress parameters (Cu, Zn superoxide dismutase activity - Cu, Zn-SOD; advanced oxidation protein products - AOPP; protein carbonyls - PCO; total thiol groups - T-SH; and lipid hydroperoxides -LHP) were measured and tissues were analysed histopathologically. RESULTS: Compared with the control group, groups CIN and N + CIN had significantly higher urea and LHP levels (P < 0.05 and P < 0.001, respectively) and significantly lower Cu, Zn-SOD activity and creatinine clearance (P < 0.05). There was no statistically significant difference between the groups in PCO or AOPP levels despite differences in descriptive statistics. CONCLUSIONS: Contrast-agent-induced nephropathic changes are more closely related to the magnitude of lipid peroxidation than protein oxidation.
RESUMO
OBJECTIVES: YKL-40 is a glycoprotein, which is thought to play a role in inflammatory conditions and tissue remodeling. Although it has been investigated in numerous cancers, there is very limited knowledge about the role of YKL-40 in bladder cancer. In this study, our aim was to determine the levels of YKL-40 in the sera and urines of the patients with bladder cancer, and compare it to urinary bladder tumor antigen (BTA), a tumor marker that can be used in the diagnosis of bladder cancer. METHODS: The study was comprised of 2 major groups as 65 healthy controls and 67 patients with bladder cancer. The patient group was also divided into subgroups according to tumor stage and grade. Serum and urine YKL-40 levels and urine BTA levels in controls and patients were determined using commercially available enzyme-linked immunosorbent assay kits. RESULTS: Serum YKL-40 and urinary BTA levels were significantly elevated in patients and all patient subgroups compared to healthy controls. Urine YKL-40 levels, on the other hand, were significantly elevated in all subgroups except low stage (Ta) and low grade, compared to controls. Although serum YKL-40 levels could not differentiate any subgroup from one another, urinary BTA could only differentiate low stage (Ta) from all invasive (T1-T4) cancers. However, urine YKL-40 levels were significantly elevated in all invasive subgroups (T1, T2-T4, and T1-T4), compared to low stage (Ta). CONCLUSIONS: In summary, urine YKL-40 levels can be used to assist BTA in the diagnosis of bladder cancer as a marker for early invasiveness and thus help determine its treatment regimen.
