Taha Abdulkadir Coban

Serum YKL-40/chitinase 3-like protein 1 level is an independent predictor of atherosclerosis development in patients with obstructive sleep apnea syndrome.

OBJECTIVE The inflammatory process plays an important role in the development of cardiovascular complications in patients with obstructive sleep apnea syndrome (OSAS). YKL-40/chitinase 3-like protein 1 is a novel biomarker of systemic inflammation. This study aimed to investigate whether carotid intima-media thickness (CIMT), a useful marker for early atherosclerosis, is associated with serum YKL-40/chitinase 3-like protein 1 levels in patients with normotensive and nondiabetic OSAS. METHODS The study included 40 OSAS patients and 40 age- sex- and body mass index-matched healthy controls. Serum YKL-40 levels were detected by enzyme-linked immunosorbent assay. CIMT was measured by B-mode ultrasound. RESULTS The patients with OSAS had significantly increased CIMT and higher YKL-40 and high sensitivity C-reactive protein (hsCRP) levels than those of the controls. CIMT was strongly correlated with serum YKL-40 levels (r=0.694, p<0.001), hsCRP (r=0.622, p<0.001), age (r=0.525, p=0.001), and weakly correlated with apnea-hypopnea index (AHI) (r=0.365, p=0.021) and the percentage of recording time spent (PRTS) of oxygen saturation<90% (r=0.488, p=0.001). Moreover, it was detected that serum YKL-40 levels were strongly correlated with AHI (r=0.617, p<0.001), and weakly correlated with SaO2<90% of PRTS (r=0.394, p=0.012) and hsCRP (r=0.486, p=0.001). In multiple regression analyses, age and serum levels of YKL-40 and hsCRP were found to be independent predictors of CIMT. CONCLUSION In patients with OSAS, CIMT was increased. This increase was associated with serum YKL-40 level. Increased serum level of YKL-40 may be an early predictor of atherosclerosis development in patients with OSAS.

Effects of nimesulide on the small intestine mucositis induced by methotrexate in rats

Intestinal mucositis is one of the major problems in the patients receiving cancer treatment. Nimesulide is a drug with antioxidant, antiinflammatory and antiulcer features. We aimed to investigate the effect of nimesulide on the small intestine mucositis induced by methotrexate (MTX) in rats. Experimental animals were divided into the control group, MTX group (MTXG) and nimesulide+MTX administered group (NMTXG) with eight rats per group. The control and MTXG groups were given distilled water by gavage and the NMTXG was given nimesulide 100 mg/kg orally. After one hour, the NMTXG and MTXG rat groups were administered oral MTX 5 mg/kg. This procedure was repeated once a day for 15 days and the rats were sacrificed. The duodenum and jejunum of each rat was removed for the assessment of biochemical markers and histopathological evaluation. Malondialdehyde (MDA) and myeloperoxidase (MPO) levels were significantly higher in the duodenal and jejunal tissues of the animals which received MTX, compared to the control and NMTXG (P<0.001). Also, the levels of total glutathione (tGSH), glutathione reductase (GSHRd), glutathione peroxidase (GSHPx), catalase (CAT) and superoxide dismutase (SOD) were significantly lower in the MTXG (P<0.001) compared to other groups. MTX led to villus and crypt epithelial damage and inflammation containing marked PMNL and eosinophils in the intestinal tissues histopathologically. Whereas, there was only mild irregularities in the villus structures of the NMTXG. Nimesulide protected the small intestines against damage by MTX. Intestinal mucositis caused by MTX may be preventable by co-administered nimesulide.

Susceptibility of cord blood antioxidant enzymes glutathione reductase, glutathione peroxidase and glutathione S-transferase to different antibiotics: in vitro approach

Cord blood has numerous facilities for life and used in many different areas. Cord blood contains many different catalytic proteins including antioxidant enzymes. Here we purified human cord blood glutathione reductase (hcbGR), glutathione S-transferase (hcbGST) and human cord blood glutathione peroxidase (hcbGPx) from human cord blood erythrocytes and analyzed the inhibition effects of the antibiotics incorporating cefuroxime, ceftriaxone, ceftizoxime and cefoperazone, on these enzymes. KI values for the drugs ranged from 10.42 to 28.72 µM for hcbGR, 32.7 to 244.8 µM for hcbGPx, and 32.39 to 267.3 µM for hcbGST. Cefuroxime caused the highest inhibition on all enzymes with KI values of 10.42, 32.39, 32.7 µM for hcbGR, hcbGST, and hcbGPx, respectively. All drugs displayed non-competitive inhibition regardless of their structures. Since these drugs are often used during pregnancy, identification of possible undesired impacts on various parameters has a great importance for pharmacological and medical applications.

Does myo-inositol oxygenase, the only enzyme to catalyze myo-inositol in vivo, play a role in the etiology of polycystic ovarian syndrome?

Abstract In polycystic ovary syndrome (PCOS), myo-inositol (MI) supplements have shown many beneficial effects. In this study, therefore, we aimed to investigate the serum level of myo-inositol oxygenase (MIOX), which is the only enzyme catalyzing MI in vivo, in patients with PCOS. Serum MIOX enzyme levels and other laboratory parameters were compared between sixty patients, who were diagnosed with PCOS for the first time, and sixty healthy individuals at similar age and sex. MIOX serum levels were not different between two groups (p = 0.7428). MIOX median and 95% CI were 19.4 and 10.6–39.1 in the control group and 16.4 and 7.6–46.2 in the patient group respectively. Demographic data, biochemical and hematological parameters, hormone parameters were not different except from the lymphocyte count between the two groups. Lymphocyte count was higher in the patient group. Although the ratio of LH/FSH was higher in the patient group, it was not statistically significant. Our results suggest that serum MIOX levels do not change in PCOS. It was, therefore, concluded that MI deficiency observed in PCOS was not related to the level of MIOX enzyme which cleaves MI.

Effects of Hippophae rhamnoides extract on oxidative mucosal injury induced by cisplatin in rat jejunum

Objectives: We aimed to assess the effect of Hippophae rhamnoides extract (HR) on oxidative stress induced by cisplatin (Cis) in rat small intestine tissue by evaluating the biochemical and gene expression levels and histopathological changes. Materials and Methods: The control group and Cis group received distilled water, while the HR25+cisplatin (HR25+Cis) group and the HR50+cisplatin (HR50+Cis) group were given HR 25 and 50 mg/kg, respectively, orally for seven days. HR25+Cis, HR50+Cis, Cis groups were injected with a single dose of intraperitoneal cisplatin on the first day. After sacrifice, the jejunum of each rat was removed for the assessment of oxidants and antioxidants. Analyses of the gene expression (for IL-1s and TNF-α) and histopathological changes evaluated. Results: HR significantly inhibited the increase of oxidants and the decrease of antioxidants caused by cisplatin in the jejunal tissue. IL-1β and TNF-α gene expression levels were almost the same in both the HR50+Cis and the control groups. HR better prevented increase of the serum levels of IL-1β and TNF-α in animals at 50 mg/kg dose compared to 25 mg/kg dose. We confirmed that HR prevented the histopathological changes caused by cisplatin. Conclusions: It was concluded that oxidative stress caused by cisplatin may be preventable by coadministered HR.

Can thıamıne pyrophosphate prevent desflurane ınduced hepatotoxıcıty ın rats

PURPOSE To investigate the effects of thiamine pyrophosphate (TPP) against desflurane induced hepatotoxicity. METHODS Thirty experimental animals were divided into groups as healthy (HG), desflurane control (DCG) , TPP and desflurane group (TDG). 20 mg/kg TPP was injected to intraperitoneally TDG. After one hour of TPP administration, desflurane was applied for two hours. After 24 hours, liver tissues of the animals killed with decapitation were removed. The oxidant/antioxidant levels and ALT, AST and LDH activities were measured. The histopathological examinations were performed in the liver tissues for all rats. RESULTS Notwithstanding the levels of oxidants and liver enzymes were significantly increased (p<0.0001), antioxidant levels were significantly decreased in DCG (p<0.0001). On contrary to the antioxidant parameters were increased (p<0.05) the oxidant parameters and liver enzymes were decreased in TDG (p<0.0001). Whereas multiple prominent, congestion, hemorrhage and dilatation were observed in sinusoids and lymphocyte-rich inflammation results in the centrilobular and portal areas of liver tissue in DCG, these findings were observed less frequently in TDG. CONCLUSİON : Thiamine pyrophosphate prevented liver oxidative damage induced with desflurane and may be useful in prophylaxis of desflurane induced hepatotoxicity.