Neutrophil gelatinase-associated lipocalin as a screening test in prostate cancer.

OBJECTIVE: Prostate specific antigen (PSA) with digital rectal examination is used for diagnosis of prostate cancer (PCa), where definite diagnosis can only be made by prostate biopsy. Recently neutrophil gelatinase-associated lipocalin (NGAL), a lipocalin family member glycoprotein, come into prominence as a cancer biomarker. This study is aimed to test serum NGAL as a diagnostic biomarker for PCa and discriminate PCa from benign prostatic hyperplasia (BPH). MATERIAL AND METHODS: In this prospective study, 90 patients who underwent transrectal ultrasound-guided 12-core prostate biopsy between May 2015 and September 2015, were evaluated. Histopathologically diagnosed 45 PCa and 45 BPH patients were enrolled in this study. Serum NGAL and PSA levels of all participants were measured, then these data were evaluated by statistical programs. RESULTS: When sensitivity fixed to 80% specificity of NGAL was better than PSA (49%, 31% respectively). Receiver operating characteristic (ROC) curve analysis showed that NGAL alone or its combined use with PSA have better area under curve (AUC) results than PSA alone (0.662, 0.693, and 0.623 respectively). CONCLUSION: In conclusion NGAL gave promising results such as increased sensitivity and a better AUC values in order to distinguish PCa from BPH. NGAL showed a potential to be a non-invasive biomarker which may decrease the number of unnecessary biopsies.

Diagnostic value of microRNAs in prostate cancer patients with prostate specific antigen (PSA) levels between 2, and 10 ng/mL.

OBJECTIVE: Prostate specific antigen (PSA), used for the early diagnosis of prostate cancer (PCa), is one of the best tumour markers known so far. However, in situations when PSA is between 2-10 ng/mL, which is named as grey zone, PSA falls short of distinguishing benign prostate diseases from PCa. On the other hand, it was demonstrated in many previous studies that microRNA (miRNA) could be a marker for cancer. Therefore, in this study, it was aimed to enhance the diagnostic power of PSA, especially with grey zone patients, by the use of miRNA. MATERIAL AND METHODS: Ninety-four patients included in the study were divided into three groups as "control group" (n=44, PSA=2-10 ng/mL and benign), "PCa 1 group" (n=37, PSA=2-10 ng/mL), and "PCa 2 group" (n=13, PSA >10 ng/mL), according to their pathological results and PSA levels. Free PSA (fPSA) and total PSA (T-PSA) levels were measured with chemiluminometric sandwich immunoassay method. Expressions of miRNAs were analyzed using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) method. The most appropriate specificity, sensitivity and prediction values were found by drawing the receiver operating characteristic (ROC) curves of total PSA, free/total PSA (f/T PSA) ratio, and miRNAs, and the diagnostic powers were compared with each other. RESULTS: Diagnostic powers of the f/T PSA ratio and miRNA were compared in PCa 1 and the control groups to determine the marker with higher area under the curve (AUC). It was shown that the diagnostic power of the combination of miR-16-5p and f/T PSA was higher than that obtained when they were used separately. CONCLUSION: As a result, while making the the discrimination between benign and malignant prostate in patients with grey zone, it was determined that the combination of miR-16-5p and f/T PSA was more valuable than T-PSA or f/T PSA alone. It was thought that diagnostic role of miRNAs in the early diagnosis of the different stages of PCa needed to be examined in further studies with larger groups.

Erythropoietin may attenuate lung inflammation in a rat model of meconium aspiration syndrome.

BACKGROUND: Inflammation is believed to play a key role in the pathophysiology of meconium aspiration syndrome (MAS). PURPOSE OF THE STUDY: The objective was to determine whether the recombinant human Erythropoietin (rhEPO) pretreatment could attenuate meconium-induced inflammation. MATERIALS AND METHODS: In this study, 24 ventilated adult male rats were studied to examine the effects of recombinant human EPO (rhEPO) on meconium-induced inflammation. Seventeen rats were instilled with human meconium (1.5 mL/kg, 65 mg/mL) intratracheally and ventilated for 3 hours. rhEPO (1000 U/kg) (n = 9) or saline (n = 8) was given to the animals. Seven rats that were ventilated and not instilled with meconium served as a sham-controlled group. Analysis of the blood gases, interleukin (IL)-1ß, IL-6, IL-8, and tumor necrosis factor (TNF)-α in blood and bronchoalveolar lavage (BAL) fluid samples, and lung tissue myeloperoxidase levels were performed. RESULTS: Intrapulmonary instillation of meconium resulted in the increase of TNF-α (p = 0.005 and p < 0.001, respectively) and IL-8 concentrations (p < 0.001 and p < 0.001, respectively) in BAL fluid in the EPO + meconium and saline + meconium groups compared with the sham-controlled group. rhEPO pretreatment prevented the increase of BAL fluid IL-1ß, IL-6, and IL-8 levels (p < 0.001, p = 0.021, and p = 0.005, respectively), and serum IL-6 levels (p = 0.036). CONCLUSION: rhEPO pretreatment is associated with improved BAL fluid and serum cytokine levels. Pretreatment with rhEPO might reduce the risk of developing of meconium-induced derangements.

The impact of hypoxemia on serum total and free prostate-specific antigen levels in patients with chronic obstructive pulmonary disease.

Prostate-specific antigen (PSA) is the most important biochemical marker in the diagnosis and follow-up of patients with prostate cancer. In recent years, a relationship between PSA levels and hypoxic conditions has been described. However, no study has investigated the PSA levels in patients with chronic obstructive pulmonary disease (COPD). The aim of the present study was to investigate the impact of hypoxemia on serum total (tPSA) and free PSA (fPSA) levels in patients with COPD. Between January 2010 and January 2014, 95 male patients who hospitalized for acute exacerbations of COPD and 80 control subjects were enrolled in the study. Serum tPSA and fPSA levels and f/tPSA ratios were determined in all patients on the first day of hospitalization (exacerbation) and 7 days after the treatment (stable state). Statistical analysis included paired t test and Mann-Whitney U test. No statistically significant differences were found between COPD and control groups with regard to the baseline characteristics, except for smoking status. The levels of serum tPSA and fPSA during exacerbation of COPD were significantly higher than the levels of the stable period (p < 0.01), whereas f/tPSA ratio did not change (p > 0.05). Hypoxemia during acute exacerbation of COPD can cause a rise in serum tPSA and fPSA levels, but f/tPSA ratio is not affected. Acute exacerbation of COPD may be added to list of the events in which PSA measurements must be interpreted with caution.

Lack of nephrotoxicity of gadopentetate dimeglumine-enhanced non-vascular MRI and MRI without contrast agent in patients at high-risk for acute kidney injury.

BACKGROUND: Gadolinium chelates (GCs) have been traditionally considered as non-nephrotoxic magnetic resonance imaging (MRI) contrast materials. However, it has been suggested in some recent articles that GCs may have a nephrotoxic potential, but most of these reports are retrospective. However, the evaluated contrast agents, their doses, and the tests used to determine the kidney function were not consistent across studies. We aimed to investigate the effect of magnetic field and an MRI contrast agent, gadopentetate dimeglumine (GD), on renal functions in patients at high risk for acute kidney injury (AKI). MATERIAL AND METHODS: We designed a prospective case-control study with 2 age- and sex-matched groups of patients at high-risk for AKI (n=72 for each group). Patients in Group 1 received a fixed dose of (0.2 mmol/kg) GD-enhanced non-vascular MRI and patients in Group 2 received MRI without GD. Before the MRI and at 6, 24, 72, and 168 hours after the MRI, biochemical tests, estimated glomerular filtration rate (eGFR), albumin/creatinine ratio in spot urine, and early AKI biomarkers (cystatin C, N-Acetyl-Glucosaminidase [NAG], Neutrophil gelatinase-associated lipocalin [NGAL]) were measured. RESULTS: Serum creatinine, albumin/creatinine ratio, and eGFR were not different between Group 1 and 2 (p>0.05). There were no significant changes in renal function tests and AKI biomarkers (∆serum creatinine, ∆albumin/creatinine ratio, ∆GFR, ∆cystatin C, ∆NAG, and ∆NGAL) for either groups 6, 24, 72, and 168 hours after the procedures (p>0.05). CONCLUSIONS: MRI without contrast agent and non-vascular contrast-enhanced (GD, 0.2 mmol/kg) MRI are not nephrotoxic procedures for patients at high risk for AKI.

Does the MRI or MRI contrast medium gadopentetate dimeglumine change the oxidant and antioxidant status in humans?

BACKGROUND: It has become evident that gadolinium-based contrast agents (GBCA) may have nephrotoxic potential. Oxidative stress is one of the most important pathways in the pathogenesis of iodinated contrast-induced nephropathy. PURPOSE: To investigate the effects of static magnetic fields and gadopentetate dimeglumine (Magnevist(®)) on oxidant/antioxidant status via measurement of total antioxidant capacity (TAC), total oxidant status (TOS), and serum malondialdehide (MDA). MATERIAL AND METHODS: Two age- and sex-matched groups of patients not under oxidative stress conditions that underwent magnetic resonance imaging (MRI) were recruited to this study. While contrast-enhanced (Magnevist(®), 0.2 mmol/kg) MRI was performed in group 1, MRI without GBCA was performed in group 2. Fasting blood glucose, C-reactive protein, serum creatinine, liver enzymes, uric acid, and lipid parameters were examined in all patients. Peripheral venous blood samples in order to determine TAC, TOS, and MDA were collected before and 6, 24, and 72 h after the MRI procedures. The TOS:TAC ratio was used as the oxidative stress index (OSI). Patients were followed up to 72 h. RESULTS: There were no significant changes in serum TAC, TOS, and MDA levels (Δ(serum TAC), Δ(serum TOS), and Δ(MDA)) in either group 6, 24, or 72 h after the procedures (P > 0.05). Furthermore, OSI did not change after the procedures in either group (P > 0.05). CONCLUSION: Magnetic field and gadopentetate dimeglumine (Magnevist(®)) do not change the oxidant or antioxidant status at a dose of 0.2 mmol/kg.

The effects of pentoxifylline on lung inflammation in a rat model of meconium aspiration syndrome.

To examine the effects of pentoxifylline (PTX) on regional pulmonary and systemic inflammation after meconium aspiration, we studied 26 anesthetized and ventilated adult rats for 3 hours. Seventeen rats were instilled with human meconium (1.5 mL/kg, 65 mg/mL) intratracheally. After instillation of meconium, PTX (20 mg/kg, i.a.; n = 9) or saline (n = 8) was given to the subjects. Nine rats that were ventilated and not instilled with meconium served as sham group. Meconium instillation resulted in increased bronchoalveolar lavage (BAL) fluid tumor necrosis factor-α (TNF-α; P = 0.004 and P = 0.002, respectively), protein (P = 0.005 and P = 0.001, respectively) levels, and arterial oxygenation index (OI) in PTX and saline groups. PTX treatment prevented the increase of BAL fluid TNF-α, protein concentrations, and OI in the meconium-instilled lungs but had no statistically significant effect. These results indicate that meconium aspiration induces severe inflammation in the lung. PTX treatment affects the TNF-α production in the lungs and it may attenuate meconium-induced derangements.

Antioxidant capacity of breast milk of mothers who delivered prematurely is higher than that of mothers who delivered at term.

BACKGROUND: The total antioxidant capacity of plasma of preterm infants has been suggested to be lower than that of term infants. The objective of this study was to compare the total antioxidant capacity of the breast milk of mothers who delivered prematurely with that of mothers who delivered at term. MATERIALS AND METHODS: A total of 71 breast milk samples were collected, 41 from mothers who delivered preterm (27 to 37 weeks) and 30 from mothers who delivered at term (38 to 42 weeks). RESULTS: The mean total antioxidant capacity of the breast milk of mothers who delivered prematurely was higher (2.19 ± 0.88 mmol/L) than that of mothers who delivered at term (1.7 ± 0.86 mmol/L) (p = 0.024). CONCLUSION: Breastfeeding may protect preterm infants against oxidative stress and related disorders in the neonatal period.

The effect of CO2 pneumoperitoneum on serum prostate-specific antigen levels in patients undergoing laparoscopic cholecystectomy.

BACKGROUND: Recently, several studies have shown an elevation of serum prostate-specific antigen (PSA) levels after the events associated with presumed pelvic ischemia. Although it has been shown that CO2 pneumoperitoneum during laparoscopic surgery causes splanchnic ischemia, no study has investigated the PSA levels after this procedure. This study aimed to evaluate the effects of CO2 pneumoperitoneum on serum total PSA (tPSA) and free PSA (fPSA) levels in patients undergoing laparoscopic cholecystectomy. METHODS: This study involved 30 men who underwent elective laparoscopic cholecystectomy. Serum tPSA and fPSA levels and f/tPSA ratios were determined the day before surgery (baseline), immediately before insufflation, after desufflation, and 24 hours and 7 days after surgery. RESULTS: Serum tPSA and fPSA values after desufflation and 24 hours after surgery were significantly higher than the values before insufflation and at baseline (P<0.01), whereas the f/tPSA ratio did not change (P>0.05). PSA levels decreased to baseline levels after 7 days. CONCLUSIONS: Our study showed that CO2 pneumoperitoneum during laparoscopic surgery can cause a rise in serum tPSA and fPSA levels. We think that CO2 pneumoperitoneum during laparoscopic surgery should be added to list of the events in which PSA measurements must be interpreted with caution.

Plasma visfatin level in lean women with PCOS: relation to proinflammatory markers and insulin resistance.

OBJECTIVES: The present study was undertaken to investigate the association between plasma visfatin concentrations and inflammatory markers such as interleukin-6 (IL-6) and high-sensitive C-reactive protein (hsCRP) in company with several metabolic parameters in lean women with polycystic ovary syndrome (PCOS). METHODS: The study group consisted of 21 lean women with PCOS (BMI 20.74 +/- 1.74 kg/m(2)) and 15 healthy, normally menstruating women (BMI 20.85 +/- 2.08 kg/m(2) control group). PCOS was defined according to the Rotterdam criteria. Visfatin, IL-6, hsCRP, hyperandrogenism markers and metabolic markers were examined in all PCOS and control women. RESULTS: Plasma visfatin level in the PCOS group was higher than that in the control group. Plasma hsCRP and IL-6 levels in PCOS group were similar with the control group. Plasma visfatin levels were positively associated with total cholesterol, high density lipoprotein, hirsutism score, total testosterone and FAI. Plasma visfatin level was negatively associated with SHBG. However, there were no correlation between plasma visfatin level and IL-6 and hsCRP. In multivariate regression analyses, only FAI and high density lipoprotein-cholesterol (HDL-C) showed a significant association with serum visfatin. CONCLUSION: Our data indicates that plasma visfatin levels are associated with HDL-C and markers of hyperandrogenism, but it is not associated with proinflammatory markers and insulin resistance in lean women with PCOS.

The correlation of thrombolysis in myocardial infarction frame count with insulin resistance in patients with slow coronary flow.

BACKGROUND: It has been reported that coronary endothelial dysfunction plays an important pathogenetic role in patients with slow coronary flow (SCF). Insulin resistance is defined as impairment of insulin-stimulated glucose and/or lipid metabolism, while endothelial dysfunction is defined as paradoxical or inadequate endothelial-mediated vasodilation. In this study, we aimed to evaluate insulin resistance in patients with SCF. METHODS: The study population included 25 patients with SCF and 28 healthy controls. Insulin resistance was estimated via homeostasis model assessment insulin resistance index (HOMA-IR). RESULTS: Patients with SCF had higher high-sensitive C-reactive protein (hs-CRP) and HOMA-IR scores (P<0.05) than controls. Mean thrombolysis in myocardial infarction frame count had significant correlation with hs-CRP, fasting plasma insulin levels and HOMA-IR score (r=0.566, P<0.05; r=0.883, P<0.05; r=0.884, P<0.05, respectively). CONCLUSION: In patients with SCF, thrombolysis in myocardial infarction frame counts and hs-CRP are correlated with increased insulin resistance and thus, it can be suggested that insulin resistance and inflammation may, in part, have a role in the pathogenesis of SCF.

The importance of macroprolactinemia in the differential diagnosis of hyperprolactinemic patients.

OBJECTIVE: Hypersecretion of prolactin (PRL) by lactotroph cells of the anterior pituitary may lead to hyperprolactinemia in physiological or pathological conditions. However, some of the patients may present with another cause of hyperprolactinemia, described by various authors as macroprolactinemia. PATIENTS AND METHODS: The clinical, radiological and biochemical assessment of 124 patients were carefully evaluated for differential diagnosis in light of the literature. Macroprolactinemia was assessed by the polyethylene glycol (PEG) method in all of the patients, with high PRL level but without significant symptomatology, presenting to our clinic between 2004 and 2006. RESULTS: The sera from 124 patients with hyperprolactinemia were screened for macroprolactinemia using the PEG method and macroprolactinemia was detected in 10 patients (8%). The average age of the patients was 35 years (range 23-46). Nine of the ten patients were female (90%) and one was male (10%). All of the patients had MRI. An intrasellar mass and stalk lipoma were found in three of the ten patients (30%). CONCLUSIONS: In conclusion, macroprolactinemia should be taken into consideration as a probable cause of high serum prolactin levels to avoid repeated hormone assessments, neuroradiological examinations and unnecessary medical and surgical treatments.

Are glutathione S-transferase gene polymorphisms linked to neonatal jaundice?

Glutathione S-transferases (GSTs) are a major group of phase II detoxification enzymes involved in the metabolism of both endogenous and xenobiotic compounds. In addition to their catalytic function in detoxification, GSTs participate in binding to nonsubstrate ligands such as bilirubin. Ligandin, which is one of the principal hepatic-binding proteins, is also a member of the GST family. The aim of the present study was to investigate the possible relationship between neonatal jaundice and the GST gene polymorphisms. The study cohort consisted of a patient group of 116 newborns (plasma bilirubin levels > or = 15 mg/dl) and a control group of 54 newborns (plasma bilirubin levels <13 mg/dl). In the patient group, the null genotype frequencies in GSTM1 and GSTT1 were 52.6 and 19%, respectively; in the control group, these were 63 and 27.8%, respectively. The frequencies of GSTM1 and GSTT1 were similar in the patient and control groups (p > 0.05). Total bilirubin levels were found to be significantly higher in patients with the GSTM1 null genotype than in patients with the GSTM1 wild genotype (p = 0.042). There was no statistically significant difference in total bilirubin levels between patients with the null GSTT1 genotype and those with the wild GSTT1 genotype. It is conceivable that there is a relation between GSTM1 gene polymorphism and total bilirubin levels in neonatal jaundice. We suggest that GSTM1 gene polymorphisms may affect ligandin functions in hepatocytes, which are important in bilirubin transportation. Consequently, patients with the GSTM1 null genotype may have higher total levels of bilirubin.

The frequency of UDP-glucuronosyltransferase 1A1 promoter region (TA)7 polymorphism in newborns and it's relation with jaundice.

Increased bilirubin formation and decreased bilirubin conjugation play an important role in the pathogenesis of the newborn jaundice. Although physiologic jaundice is seen in most of the newborns, there are many risk factors that affect the severity and duration of hyperbilirubinemia. The latest studies showed that the frequency and severity of neonatal jaundice have been increased when mutations of the gene coding UDP-glucuronosyltransferase(UGT)1A1 coexist with other risk factors. Healthy term newborns weighing over 2500 g. were included in this study. The patient group consisted of 107 newborns either with total bilirubin level over 15 mg dl(-1) within 7 days or 5 mg dl(-1) after 15 days of age. The control group consisted of 55 newborns with bilirubin levels in physiological ranges. We investigated the frequency of promoter region [thymine-adenine(TA)]7 polymorphism in UGT1A1 gene. Factors which might cause pathologic and prolonged jaundice with coexisting polymorphism were also investigated. UGT1A1 6/7 genotype was found to be 11% in patient group and 13% in the control group. The difference between patient and control groups was not statistically significant. (TA)7 allele frequency was 0.069 and it is concluded that UGT1A1 promoter region polymorphism was not a risk factor for neonatal jaundice.

Leukotriene C4 synthase A-444C gene polymorphism in patients with allergic rhinitis.

OBJECTIVE: To determine the frequency of leukotriene C4 synthase A-444C polymorphism in allergic rhinitis patients. STUDY DESIGN AND SETTING: A prospective, randomized, case-controlled study. Blood samples were obtained from 85 patients with allergic rhinitis and 95 healthy individuals. After the extraction of DNA from the blood samples, the leukotriene C4 synthase A-444C polymorphism was studied by a real-time polymerase chain reaction method. RESULTS: The AC and CC genotype frequencies were statistically higher in the study group (P = 0.048 and P = 0.037, respectively). In addition, the AC polymorphism carried an increased risk of developing allergic rhinitis (odds ratio = 2.18, 95% confidence interval, 1.173-4.053, P = 0.014). CONCLUSION: The C allele of the leukotriene C4 synthase gene increases the risk of developing allergic rhinitis. SIGNIFICANCE: The leukotriene C4 synthase A-444C gene polymorphism is important in susceptibility to allergic rhinitis and this is the first study of this gene polymorphism in allergic rhinitis. EBM RATING: B-3b.

Serum leptin levels in patients with allergic rhinitis.

OBJECTIVE: To investigate the serum leptin levels in patients with allergic rhinitis during the symptomatic period. STUDY DESIGN AND SETTING: A randomized, prospective study was performed on 26 adult patients with allergic rhinitis and 20 control subjects with similar age, sex and body mass index in a tertiary otolaryngology center. RESULTS: Leptin levels were 28.8 +/- 14.1 ng/mL in the patients with allergic rhinitis, and 20.8 +/- 13.5 ng/mL in the control group respectively. The difference between the groups was statistically significant (p = 0.04). CONCLUSION: Serum leptin levels were found to be significantly higher in patients with allergic rhinitis in symptomatic period. SIGNIFICANCE: Apart from its primary role in the regulation of body weight and energy expenditure, leptin may have a role in the inflammatory process of the allergic rhinitis.

Elevated plasma endothelin-1 levels in coronary sinus during rapid right atrial pacing in patients with slow coronary flow.

The aim of the study was to evaluate whether there was an imbalance between endothelin-1 (ET-1) and nitric oxide (NOx) release and diffuse atherosclerotic changes existed in patients with slow coronary flow (SCF). Baseline and post-atrial pacing coronary sinus ET-1 and NOx levels were measured in 19 patients with SCF (11 female, 56 +/- 9 years) and in 14 control subjects (nine female, 54 +/- 7 years). All patients underwent subsequent intravascular ultrasound (IVUS) investigation at the same setting with right atrial pacing. Baseline arterial (12.4 +/- 9.9 vs. 6.3 +/- 5.1 pg/ml, P<0.005) and coronary sinus (12.2 +/- 11.1 vs. 6.4 +/- 6.9 pg/ml, P<0.005) ET-1 plasma levels were higher in patients than in controls. After atrial pacing, concentration of ET-1 level from coronary sinus (24.7 +/- 14.6) significantly increased as compared to baseline (12.4 +/- 9.9, P<0.0001) and control levels (5.3 +/- 6.3, P<0.0001). Additionally, coronary sinus ET-1 level increased significantly with atrial pacing compared to femoral artery ET-1 level (16.3 +/- 8.5, P<0.005) in patients with SCF. After atrial pacing, the femoral artery ET-1 level also increased in patients compared to control level (P<0.0001). No significant differences in arterial and coronary sinus NOx plasma levels were found between the two groups, both at baseline and after pacing. Upon IVUS investigation, the common finding was longitudinally extended massive calcification throughout the epicardial arteries in patients with SCF. Mean intimal thickness was 0.59 +/- 0.18 mm. The data of this study suggest that increased ET-1 levels and insufficient NOx response, as well as the pathological data of IVUS may be associated with coronary microvascular dysfunction and may be the manifestation of early diffuse epicardial atherosclerosis in these patients with SCF.

Apolipoprotein E gene polymorphism and serum lipids in patients with superficial fungal disease.

Superficial mycosis, including dermatophytic infections, tinea versicolor, and cutaneous candidiasis is mostly limited to the outer layers of the skin, nails, and mucous membranes. In this study, Apolipoprotein E (ApoE) polymorphism and lipoprotein cholesterol concentrations were compared between 42 patients with superficial fungal disease and 27 control subjects. Both the patients and controls were found to be normolipemic. The patients with superficial fungal disease had significantly higher concentrations of high-density cholesterol (HDL) compared to the control group (p=0.0462). However, there was no difference in the serum triglyceride, low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) cholesterol concentrations. A significantly higher incidence of heterozygosity E2/3 was found in the patients (p=0.0228), and significantly lower incidence of homozygosity E3/3 in all patients, and those with candidiasis and dermatophytosis (p=0.0139, 0.0194 and 0.0337, respectively) compared to the control group. The E3/4 genotype differences between patients and controls were not statistically significant. There were slight differences in the allele frequencies between the two groups, but these did not reach statistically significant levels. It was concluded that the presence of apoE2/3 genotype, high HDL-cholesterol levels and the absence of apoE3/3 genotype can be regarded as risk factors for superficial fungal disease, especially dermatophytosis.

Changes in antioxidant enzyme activity and malondialdehyde level in patients with age-related macular degeneration.

Age-related macular degeneration is the leading cause of legal blindness in the developed world, and yet its pathogenesis remains poorly understood. Oxidative stress may play a major role in the etiology and pathogenesis of age-related disorders such as age-related macular degeneration. Catalase is an antioxidant enzyme which plays an important role in the detoxification of free oxygen radicals. Malondialdehyde is a marker that shows free radical damage. We have measured the erythrocyte activity of catalase and the serum level of malondialdehyde in 30 patients with age-related macular degeneration and 60 healthy subjects. Patients with age-related macular degeneration showed significantly lower catalase activity compared to healthy subjects (p = 0.002). Plasma malondialdehyde level of the patient group was significantly higher than that of the controls (p = 0.038).

The protective effects of acetylsalicylic acid on free radical production in cisplatin induced nephrotoxicity: an experimental rat model.

Cisplatin-induced nephrotoxicity is closely associated with an increase in lipid peroxidation. In several previous reports it was claimed that acetylsalicylic acid (ASA) shows its therapeutic potential as a free radical scavenger. The aim of the study was to investigate effects of ASA on cisplatin induced nephrotoxicity in an experimental rat model. Control animals (n:7) were administered 1 mL saline solution intraperitoneal (i.p.). Cisplatin group (n:7) was treated with a single dose of cisplatin i.p. (6 mg/kg), ASA group (n:7) was treated with i.p. (2.5 mg/kg) per day during the study, cisplatin plus ASA group (n:7) was administered single dose cisplatin i.p. (6 mg/kg) plus ASA (2.5 mg/kg) during 5 days. At the end of the study, Catalase (CAT), Glutathione Peroxidase (GSH-Px), Superoxide Dismutase (SOD), Nitric Oxide Synthase (NOS) enzymes activities and Malondialdehyde (MDA), Antioxidant Potential (AOP) levels were measured in both erythrocytes and renal tissues. Urea and creatinine levels and renal tissue necrosis in cisplatin plus ASA group were significantly lower than cisplatin group (p = 0.000, p = 0.014, p = 0.015). SODr activities and MDAr levels of cisplatin plus ASA group were also significantly lower than cisplatin group (p = 0.000, p = 0.029). These results show that cisplatin and ASA combination decreases the levels of urea and creatinine, reduces necrosis and improves antioxidant enzyme activities, MDA and AOP in rat kidney.