Evaluation of the Relationship Between Mobile Phone Usage and miRNA-574-5p and miRNA-30C-5p Levels in Thyroid Cancer Patients.

Objectives: This study aimed to evaluate the relationship between mobile phone usage and miRNA-574-5p and miRNA-30C-5p levels in patients diagnosed with differentiated thyroid cancer (DTC). Methods: Fifty patients diagnosed with DTC and 50 healthy volunteers were included in the study. miRNA-574-5p and miRNA-30C-5p gene expression levels in the blood of all subjects were analyzed by real time-polymerase chain reaction, and a questionnaire including various questions was administered to both groups. Results: Although there was a 7.60-fold increase in miRNA-30C-5p gene expression levels in the patient group compared with the control group, it was not found to be statistically significant. Considering the miRNA-574-5p gene expression levels, although there was a 2.96-fold increase in the patient group compared with the control group, no significant relationship was found. In our study, 85% of our patients were using mobile phones with internet access, whereas 98% of our healthy volunteers were using mobile phones (p<0.05). While 53.5% of the patients had their mobile phones with them while they were sleeping, this rate was 83.7% in healthy volunteers (p<0.05). However, 93.9% of the healthy volunteers did not have a Wi-Fi device in their bedrooms, and this rate was 75% in the patient group (p<0.05). Conclusion: Although miRNA-30C-5p and miRNA-574-5p gene expression levels were higher in patients than in healthy volunteers, the differences were not statistically significant. Although there was no significant difference in miRNA levels, we believe that due to the higher rate of Wi-Fi device presence in bedrooms in patients compared with healthy volunteers, the effects of electromagnetic radiation on the thyroid can be reduced by paying attention to this simple change.

Investigation of Early Growth Response Protein (EGR) Levels in Patients with Fibromyalgia Syndrome: A Cross-Sectional Study.

BACKGROUND: Fibromyalgia is a soft tissue rheumatism characterized by chronic and widespread musculoskeletal pain at specific points in the body. OBJECTIVES: In this study, we aimed to investigate the relationship between Early Growth Response (EGR1, EGR2, and EGR3) protein levels in patients with Fibromyalgia Syndrome (FMS) and healthy controls. METHODS: In our studies, 76 FMS patient group and 78 healthy control group who were newly diagnosed with primary FMS according to the 2010 American College of Rheumatology criteria for fibromyalgia in Sivas Cumhuriyet University Hospital, Physical Therapy, and Rehabilitation were used. Venous blood samples were taken from both groups for the measurement of EGR1, EGR2, and EGR3 protein plasma levels, and protein levels were determined using ELISA methods. Statistical parametric test assumptions were compared using the Independent Student's t-test. In addition, specificity, sensitivity, and AUC values were calculated with the ROC curve. RESULTS: The relationship between plasma EGR1 protein levels of FMS patients and control groups was statistically significant (p=0.001). CONCLUSION: EGR1 protein levels were found to be lower in the patient group diagnosed with FMS compared to the control group. It has been suggested that EGR1 protein levels can be important in the diagnosis of FMS disease.

In Silico and In Vitro Studies of Novel Azomethines on DNA Repair Genes in Gastric Cell Lines.

We herein report the determination of the cytotoxic activity and expression profiles of some DNA repair genes of newly synthesized azomethines in the gastric cancer cell line (AGS). The studied novel compounds were synthesized by a condensation reaction and received compounds were characterized by 1H and 13C NMR spectroscopy methods. Furthermore, they were applied to the AGS cell line at eight different concentrations (0.1-50 µg/mL). Anticancer activities were determined using the MTT method. Expression levels of ATR, ERCC1, TOP2A, and ABCB1 genes were determined by the RT-PCR method. Biochemical parameters were also examined. The interaction of proteins with other proteins was investigated with the String v11 program. The IC50 values of compounds 1, 2, and 3 obtained after 72 h were 23.10, 8.93, and 1.58 µg/mL, respectively. The results demonstrate that the cytotoxic activity of compound 3 on AGS cancer cells is higher in comparison with other molecules. It was determined that the expression levels of ATR, TOP2A, and ABCB1 genes in compounds 1, 2, and 3 were decreased compared to the control group. In addition, it was determined that ERCC1 gene expression increased in compound 3, decreased in compound 2, and remained unchanged in compound 1 (p < 0.001). In AGS gastric cancer cells, a 64% decrease was detected for GST levels in compound 1, while a 38% decrease in GSH levels in compound 2. In addition, compounds 1-3 were examined at the molecular level with computational techniques and the docking studies revealed 4LN0 as a target protein.

A Significant Association Between rs2295190 Polymorphism of the ESR1 Gene and Fibromyalgia Syndrome.

Fibromyalgia syndrome (FMS) is a multifactorial disease characterized by chronic diffuse pain. Genetic factors are also involved in the etiology. However, there is not enough information on the genetic factors that play a role in the pathogenesis of FMS. The aim of this study is to investigate the relationship between estrogen receptor 1 gene (ESR1) 594G>A (rs2228480) and 325C>G (rs2295190) polymorphisms and fibromyalgia syndrome (FMS). A total of 294 women, 146 of who were FMS patients and 148 of whom were healthy controls, were enrolled in the study. The instruments used to collect data from patients included patient follow-up form, Visual Analogue Scale (VAS), and Fibromyalgia Impact Questionnaire (FIQ). Genotyping of ESR1 594G>A and 325C>G polymorphisms in the extracted DNA samples was performed using an RT-PCR device and TaqMan hydrolysis probes. It was found that, for rs2295190 polymorphism, patients with CG and GG genotypes versus CC genotypes showed a decreased risk for FMS (OR: 0.442; 95% CI: 0.234-0.833). But there were no significant differences were found in the genotype distribution of  rs2228480 polymorphism between the FMS patients and controls. The intragroup evaluation of FMS patients revealed no significant association between symptoms, pain score, FIQ score, and polymorphisms (p>0.05). We are of the opinion that there is a significant association between ESR1 rs2295190 polymorphism and FMS and that this polymorphism may be protective against FMS. However, there is a need for comprehensive studies on different populations to obtain clearer data as well as further studies to elucidate the possible mechanism of association.

Potassium Ion Channel Protein (KCNH) Levels in Patients with Fibromyalgia Syndrome.

Although there is not yet full clarity of the pathogenesis of fibromyalgia syndrome (FM), central sensitization is considered to be responsible. The purpose of this study was to measure the plasma levels of potassium ion channel proteins (human KCNH2, KCNH6 and KCNH7) in FM patients and healthy control subjects. The study sample includes 76 newly diagnosed FM patients and 79 healthy individuals. Venous blood samples were taken to measure the plasma levels of KCNH2, KCNH6 and KCNH7. Pain severity in FM patients was assessed using a visual analog scale (VAS). Bioinformatics analysis was performed using the STRING v 11 Protein interaction tool. Age, gender and body mass index were seen to be similar in both groups. In comparisons between FM and control groups, KCNH2 plasma levels was found to be significantly lower in the FM group. No significant correlation was found between plasma levels of KCNH2, KCNH6 and KCNH7 protein levels and VAS score of patients with FM. The KCNH2 protein had a high homology score with 9 proteins. The plasma levels of KCNH2 FM patients were found to be lower than those of the healthy control subjects, no difference was determined in respect of the plasma levels of KCNH6 and KCNH7. These results may be of use in guiding future studies on the pathogenesis of FM.

High levels of cathepsin S and cystatin C in patients with fibromyalgia syndrome.

OBJECTIVES: Although the etiopathogenesis of fibromyalgia syndrome (FM) is not yet clear, central sensitization is thought to be responsible for the pathogenesis of FM. The aim of this study was to compare the serum cathepsin S (CatS) and cystatin C (CysC) levels between patients with FM and healthy control subjects. METHODS: This study was conducted in the Physical Medicine and Rehabilitation Clinic between January 2019 and October 2019. The study included 145 FM patients newly diagnosed with primary FM according to the 2010 American College of Rheumatology criteria and 129 healthy volunteers. The age, gender, and body mass index (BMI) of the participants were recorded. Venous blood samples were collected from both groups for the measurement of the levels of serum CatS and CysC. The functional status of FM patients was evaluated using the Fibromyalgia Impact Questionnaire (FIQ). RESULTS: No statistically significant difference was determined between the patient and control groups in terms of age, gender, and BMI (P > .05). A comparison of the serum CatS and CysC levels of the FM and control groups revealed a statistically significant difference (P = .001). No correlation was determined between FIQ and serum CatS and CysC levels (P > .05). CONCLUSION: Serum CatS and CysC levels were found to be higher in FM patients. However, there was no correlation between the functional status of FM patients and serum CatS and CysC levels. These results can be of guidance for further clinical studies of the etiopathogenesis and treatment of FM.

Serum Calcitonin Gene-Related Peptide and Receptor Protein Levels in Patients With Fibromyalgia Syndrome: A Cross-Sectional Study.

OBJECTIVES: This study aims to compare the serum calcitonin gene-related peptide (CGRP) and CGRP receptor protein levels between patients with fibromyalgia syndrome (FM) and healthy control subjects. PATIENTS AND METHODS: The study included 88 patients (7 males, 81 females; mean age 44.5±9.1 years; range, 20 to 72 years) newly-diagnosed with FM according to the 2010 American College of Rheumatology criteria and 88 healthy volunteers (6 males, 82 females; mean age 43.0±6.1 years; range, 20 to 57 years). Venous blood samples were collected from both groups for the measurement of the levels of serum CGRP and CGRP receptor proteins (receptor component protein [RCP], receptor activity modifying protein 1 [RAMP 1] and calcitonin receptor-like receptor [CLR]). RESULTS: A comparison of the serum CGRP, CLR and RCP levels of the FM and control groups revealed a statistically significant difference (p=0.001, p=0.005, p=0.001, respectively). The difference between the groups in respect of the serum RAMP 1 levels was not statistically significant (p=0.107). CONCLUSION: The serum CGRP, CLR and RCP levels were found to be higher in the FM patients, but no difference was determined between the FM patients and the healthy control group in respect of the RAMP 1 level. These results can be of guidance for further clinical studies of the etiopathogenesis and treatment of FM.

Comparison of Beta-2 Adrenergic Receptor Gene Polymorphisms Between Patients with Fibromyalgia Syndrome and Healthy Controls.

OBJECTIVES: This study aims to compare the beta-2 adrenergic receptor (ADRB2) gene polymorphisms of patients with fibromyalgia syndrome (FMS) with those of healthy control subjects, and to investigate the possible relationship between symptoms of FMS and polymorphisms of the ADRB2 gene. PATIENTS AND METHODS: The study included 170 females (mean age 47.8±10.3 years; range, 21 to 75 years) diagnosed with FMS according to the 2010 American College of Rheumatology criteria and 170 healthy females (mean age 47.2±8.8 years; range, 20 to 72 years) as the control group. Several clinical symptoms of the participants related to FMS were questioned and recorded. The visual analog scale (VAS) and Fibromyalgia Impact Questionnaire (FIQ) scores of the fibromyalgia group were recorded. In both groups, the ADRB2 (rs1042717) single-nucleotide polymorphism was detected by way of a real-time polymerase chain reaction. The wild-type (Guanine/Guanine), the mutant type (Adenine/Adenine) and heterozygous type (Adenine/Guanine) were detected. The sample power was calculated considering the minor allele frequency. RESULTS: The comparison of the ADRB2 gene polymorphism between patients with FMS and the control subjects showed that the groups were similar in terms of ADBR2 gene polymorphism and genotype (p>0.05). There was no significant difference in terms of genotype when the ADRB2 gene polymorphisms in patients with FMS were compared in terms of clinical symptoms, VAS and FIQ scores (p>0.05). CONCLUSION: Beta-2 adrenergic receptor (rs1042717) gene polymorphisms and genotype distribution are no different between patients with FMS and healthy individuals. ADRB2 gene polymorphisms in patients with FMS have no effect on clinical symptoms and VAS and FIQ scores. The results of the present study will light the way for future research into ADRB2 gene polymorphisms in the pathogenesis of FMS.

Significant association between MDM2 T309G polymorphism and colorectal cancer.

PURPOSE: The Murine double minute 2 (MDM2) gene plays a crucial role in regulating and suppressing the function of apoptotic pathway. We investigated the relationship between MDM2 gene SNP309 (T309G) (rs2279744) polymorphism and colorectal cancer (CRC) in a Turkish population. METHODS: The polymorphism T309G (rs2279744) in the MDM2 gene was studied in patients with colorectal cancer (n=135) and healthy control subjects (n=145) using the polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) method. The findings were evaluated using logistic regression and x2 tests. RESULTS: When CRC cases and controls were evaluated based on different habits and family cancer histories, a statistically significant relationship was found between CRC and alcohol consumption (x2=4.07, p=0.044). Cancer cases and controls had statistically significant different family histories of cancer (x2=6.82, p=0.009). There was also significant difference in TG genotype distribution in the MDM2 T309G polymorphism between those with and without cancer (OR=1.98, 95% CI=1.98-3.91, x2=4.00, p=0.045). CONCLUSIONS: The SNP309 polymorphism of the MDM2 gene is associated with increased CRC risk in the Turkish population.

Role of SOD2 Ala16Val polymorphism in primary brain tumors.

The present study aimed to investigate the possible association between the genetic polymorphism of the enzyme superoxide dismutase 2 (SOD2, also known as manganese-dependent SOD), Ala16Val (rs4880), and primary brain tumor risk in the Turkish population. Frequency of the SOD2 gene rs4880 polymorphism was identified in 225 Turkish individuals (120 controls and 105 patients with primary brain tumor) by polymerase chain reaction-restriction fragment length polymorphism. Subject demographics and clinical characteristics were also recorded. The findings were evaluated using logistic regression and χ2 tests. Logistic regression analysis indicated that smoking did not increase the risk for primary brain tumor [odds ratio (OR)=0.77, 95% confidence interval (CI)= 0.44-1.33, χ2=0.352, P=0.860]. Similarly, there was no statistically significant difference in the family history of cancer incidence between the control subjects and the primary brain tumor patients (OR=0.81, 95% CI=0.39-1.71, χ2=0.340, P=0.560). There was no significant association of the histopathological type, genotype/allele frequencies and inheritance models of tumor with the gene variants among the patients with primary brain tumor. In summary, the results of the present study indicated that the Ala16Val polymorphism of the SOD2 gene was not associated with primary brain tumor risk in the Turkish population studied.

The effects of colostrum on some biochemical parameters in the experimental intoxication of rats with paracetamol.

In the current study, the possible prophylactic and therapeutic effects of colostrum (COL) on acute organ injury caused by paracetamol (PAR) in rats were evaluated. Within the scope of this study, a 2-month-old male (150-200 g) 70 Wistar Albino rat was used and a total of seven groups were designed. The first group (CNT) was maintained for control purposes. The second group (COL-1) was given COL for 1 day, at a dose of 500 mg/kg at 6-h intervals, and blood and tissue sampling was performed at 24 h. The third group (COL-7) received COL for 7 days, at a dose of 500 mg/kg at 6-h intervals on day 1 and at a daily dose of 500 mg/kg on the following days, and blood and tissue samples were taken at the end of seventh day. The fourth group (PAR-1) was administered with PAR at a dose of 1.0 g/kg bw and was blood and tissue sampled at 24 h. The fifth group (PAR-7) received PAR at a dose of 1.0 g/kg bw on day 1 and was blood and tissue was removed at the end of day 7. The sixth group (PAR+COL-1) was administered with a combination of PAR (1 g/kg bw) and COL (500 mg/kg at 6-h intervals), and blood and tissue samples were collected at 24 h. The seventh group (PAR+COL-7) received 1.0 g/kg bw of PAR on day 1 and was given COL throughout the 7-day study period (at a dose of 500 mg/kg at 6-h intervals on day 1 and at a daily dose of 500 mg/kg on the following days). In the seventh group, blood and tissue samples were taken at the end of seventh day. Alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), glucose, creatinine, triglyceride, total bilirubin, total protein and albumin levels/activities were analysed in the serum samples. The malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) levels/activities, known as oxidative stress parameters, were assayed for tissue homogenates and blood (erythrocytes/plasma); in addition, enzyme activities of GSH S-transferase (GST), cytochrome P4502E1 (CYP2E1), NADH-cytochrome b5 reductase (CYTB5), glucose-6-phosphate dehydrogenase (G6PD), NADPH-cytochrome P450 C reductase (CYTC) and glutathione (GSH) levels/activities defined as drug metabolising parameters were measured in liver homogenates. In result, it was determined that PAR caused significant alterations in some biochemical and lipid peroxidation parameters and the activities/levels of drug metabolising parameters in the liver and that COL normalised some of these parameters and reduced PAR-induced tissue damage.

Significant Association of the MDM2 T309G Polymorphism with Breast Cancer Risk in a Turkish Population

Background: Breast cancer is a leading cause of death in women worldwide. Genetic polymorphisms have been reported to be important etiological factors. Murine double minute 2 (MDM2) T309G interacts with p53 and mutations in p53 are present in approximately 50% of all cancers. However, it has been reported that effect of the polymorphism on breast cancer risk may vary in different populations. Here, we therefore investigated whether there is an association between MDM2 T309G (rs2279744) polymorphism and breast cancer in a Turkish population. Materials and Methods: We analysed 110 patients with breast cancer and 138 matched? controls. For genotyping, polymerase chain reaction and restriction length fragment polymorphism methods were used. Results: A significant difference was observed between case and control groups with regard to the distribution of the MDM2 T309G polymorphism (p<0.05). There was a significantly higher frequency of the TT genotype in the control group (p=0.028; OR, 2.42; 95% CI, 1.09-5.37). However, we did not find any relationships among tumor grade and metastasis status and this polymorphism. Conclusion: This study indicates that the MDM2 T309G polymorphism GG genotype and the TG+GG combination may be risk factors for breast cancer in our Turkish population.

Investigation of the association between the MDM2 T309G polymorphism and gastric cancer.

Murine double minute clone 2 oncoprotein (MDM2) is a key component in the regulation of the tumour suppressor p53. The association between the MDM2 polymorphism and gastric cancer (GC) has been investigated in Turkish population. In the present case-control study, the aim was to investigate the association between genetic polymorphisms of the MDM2 gene (a major regulator of p53 function) and primary GC risk in a Turkish population. The polymorphism, T309G (rs2279744) in the MDM2 gene was determined in patients with GC (n=65) and in healthy control subjects (n=67) using the polymerase chain reaction-restriction fragment length polymorphism method. The findings were evaluated using logistic regression and χ2 tests. No statistically significant differences were observed between the control subjects and patients with GC regarding smoking status. A comparison between GC cases and control subjects indicated a statistically significant difference for family history of cancer [odds ratio (OR)=0.17; 95% confidence interval (CI), 0.05-0.56; χ2=0.19; P=0.01]. A significant difference was identified in the GG genotype distribution between GC patients and control subjects (OR=4.58; 95% CI, 1.18-17.79; P=0.022). Thus, the results of the present study indicate that the MDM2 gene T309G intron (GG) genotype may be an important risk factor for GC development in the Turkish population.

The Diagnostic Value of the Correlation between Serum Anti-p53 Antibody and Positron Emission Tomography Parameters in Lung Cancer.

OBJECTIVE: Mutations in the p53 gene are the most commonly observed genetic abnormalities in malignancies. The purpose of this study was to assess the diagnostic value of serum anti-p53 antibody (Ab) along with the correlation between serum anti-p53 Ab level and quantitative positron emission tomography (PET) parameters such as maximum standardized uptake value (SUVmax), SUVave, metabolic tumor volume, total lesion glycolysis (TLG) and tumor size. METHODS: Serum anti-p53 Ab level was studied in three groups. Patients who underwent 18F-fluorodeoxyglucose (FDG) PET/computed tomography (CT) imaging for staging of previously diagnosed lung cancer constituted the first group, while patients who underwent 18F-FDG PET/CT imaging for evaluation of suspicious pulmonary nodules detected on thorax CT and did not show pathologic FDG accumulation (NAPN=pulmonary nodule with non avid-FDG) were enrolled in the second group. The third group consisted of healthy volunteers. RESULTS: Twenty-eight patients with lung cancer (median age: 62.5, range: 39-77years), 28 patients with NAPN (median age: 65, range: 33-79 years), and 24 healthy volunteers (median age: 62, range: 44-74 years) were enrolled in the study. The serum anti-p53 Ab level was low in healthy volunteers while it was higher in both lung cancer patients and NAPN patients (p<0.05). When serum anti-p53 Ab level and PET parameters were evaluated, there was no significant correlation between serum anti-p53 Ab level and SUVmax, SUVave, TLG, tumor volume and tumor size of patients with lung cancer (p>0.05). Besides, there was no significant difference between serum anti-p53 Ab level and lesion size of NAPN patients (p>0.05). CONCLUSION: It was determined that serum anti-p53 Ab levels are not significantly correlated with PET parameters, and that serum anti-p53 Ab levels increase in any benign or malignant lung parenchyma pathology as compared to healthy volunteers. These results indicate that this Ab cannot be used as a predictor of malignancy in a lung lesion.

The acute and chronic toxic effect of cypermethrin, propetamphos, and their combinations in rats.

This study was aimed at determining the acute and chronic toxic effects of cypermethrin, propetamphos, and combined cypermethrin and propetamphos. Four groups, each comprising 10 animals, were established for the acute (a) and chronic (b) toxicity trials, and in total, 80 male Wistar albino rats were used. In the acute toxicity trial, the first group was maintained for control purposes, and groups 2a, 3a, and 4a were administered only once with 80 mg/kg.bw of cypermethrin, 25 mg/kg.bw of propetamphos and 80 mg/kg.bw of cypermethrin combined with 25 mg/kg.bw of propetamphos, respectively, by gavage directly into the stomach. In the chronic toxicity trial, the first group was also maintained for control purposes, while groups 2b, 3b, and 4b were administered daily with 12 mg/kg.bw of cypermethrin, 4 mg/kg.bw of propetamphos, and 12 mg/kg.bw of cypermethrin combined with 4 mg/kg.bw of propetamphos respectively, by gavage directly into the stomach for 60 days. Blood and tissue (liver, kidney, brain, spleen, and testis) samples were taken 24 h after pesticide administration in the acute toxicity trial and at the end of day 60 in the chronic toxicity trial. Oxidative stress (MDA, NO, SOD, CAT, GSH-Px, and G6PD) parameters, serum biochemical parameters (glucose, triglyceride, cholesterol, HDL, LDL, BUN, creatinine, AST, ALT, ALP, protein, and albumin) and hepatic drug-metabolizing parameters (CYP2E1, CYPB5, CYTC, GST, and GSH) were investigated in the samples. When administered either alone or in combination, both pesticides inhibited the antioxidant enzymes and increased MDA and NO levels. For the drug-metabolizing parameters investigated, particularly in the chronic period, either increase (CYP2E1, CYPB5, and CYTC) or decrease (GST and GSH) was observed. Furthermore, some negative changes were detected in the serum biochemical parameters. In result, cypermethrin and propetamphos combinations and long-term exposure to these combinations produced a greater toxic effect than the administration of these insecticides alone. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1415-1429, 2016.

The toxic effect of cypermethrin, amitraz and combinations of cypermethrin-amitraz in rats.

In this study, the effects of cypermethrin (CYP), amitraz (AMT) and combined cypermethrin-amitraz (CYP-AMT) on some serum biochemical, oxidative stress and drug-metabolising parameters were investigated in male Wistar albino rats. CYP, AMT and combined CYP-AMT were administered at doses of 80 mg kg(-1) bw(-1) of CYP and 170 mg kg(-1) bw(-1) of AMT for 1 day (single dose), and at doses of 12 mg kg(-1) bw(-1) of CYP and 25 mg kg(-1) bw(-1) of AMT for 40 days by oral gavage. Oxidative stress (malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glucose-6-phosphate dehydrogenase (G6PD)), serum biochemical (glucose, triglyceride, cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL), blood urea nitrogen (BUN), creatinine, asparatate amino transferase (AST), alanine amino transferase (ALT), alkaline phosphatase (ALP), total protein, albumin) in blood/tissues (liver, kidney, brain, spleen and testis) and hepatic drug-metabolising (cytochrome P450 2E1 (CYP2E1), NADH-cytochrome b5 reductase (CYPb5), NADPH-cytochrome c reductase/NADPH cytocrome P450 reductase (CYTC), glutathione S-transferase (GST), glutathione (GSH)) parameters were measured in liver samples taken on days 1 and 40. In result, it was determined that CYP, AMT and their combinations led to significant changes in the parameters investigated, and it was ascertained that long-term exposure to insecticides and the administration of insecticide combinations produced greater toxic effects in comparison with the administration of insecticides alone.

Investigation of wound healing in rat lung tissues in the postpartum period.

To assess the wound healing capabilities of damaged lung tissue in the postpartum period, we investigated the parameters related to wound healing in a rat model of lung damage. Rats were divided into six groups: IA, IB, II, IIIA, IIIB and IV (n=7 in each group). Group IA included rats not in the postpartum period that were sacrificed on the third day after lung injury, group IB included rats not in the postpartum period that were sacrificed on the tenth day after lung injury, group II included rats not in the postpartum period that did not receive lung injury, group IIIA included rats in the postpartum period that were sacrificed on the third day after lung injury, group IIIB included rats in the postpartum period that were sacrificed on the tenth day after lung injury and group IV included rats in the postpartum period without lung injury. Wound healing was evaluated histopathologically and measurements of hydroxyproline levels, serum alanine and glutamine were taken. A significant difference in serum alanine levels was evident between groups IA and IIIA. Significant differences were also observed between serum alanine and glutamine levels in groups IB and IIIB. In conclusion, we demonstrated that serum alanine levels were reduced in the postpartum period following lung injury, which may be expected to negatively impact wound healing in this period. The administration of exogenous alanine for traumatic events occurring during the postpartum period may thus contribute positively to wound healing capabilities during this period.

Myeloperoxidase G-463A polymorphism and risk of lung and prostate cancer in a Turkish population.

Myeloperoxidase (MPO) is a phase I enzyme that can bioactivate many specific procarcinogens, including polycyclic aromatic hydrocarbons and aromatic amines. The MPO gene contains a common single nucleotide polymorphism, for which the -463G>A substitution within the promoter region has been shown to reduce MPO expression and activity. We investigated the association between the MPO -463G>A polymorphism and lung and prostate cancer in a Turkish population. MPO genotypes in the study populations were determined using polymerase chain reaction-based restriction fragment length polymorphism assay. The allelic frequency was significantly different between the cases and controls for lung cancer (p=0.02), but not prostate cancer (p=0.30). No significant difference was noted between the lung and prostate cancer cases and control populations in terms of genotype distribution (p=0.07, p=0.53, respectively). Control groups of lung and prostate cancer were in Hardy-Weinberg equilibrium (p=0.87 and p=0.41, respectively). To determine the protective effect against lung cancer among individuals with the -463A allele, G/A and A/A genotypes were combined. Comparison of the G/G and G/A + A/A genotypes between the lung cancer cases and control groups showed a statistically significant relationship (p=0.032, OR=0.60, 95% CI 0.38-0.95). No gender-specific difference was found in terms of genotype distribution between the lung cancer patients and the controls (female, p=0.20; male, p=0.34). In the case of smokers, a difference in genotype distribution between the lung cancer patients and the controls was statistically significant (p=0.02), although this difference was not statistically significant for non-smokers (p=0.90). Overall, no statistically significant difference was found between the prostate cancer cases and the controls in terms of genotype combination (p=0.46, OR=0.83, 95% CI 0.51-1.36). Additionally, in smokers and non-smokers, no significant relationship was determined between the prostate cancer patients and the control population (p=0.21, p=0.91, respectively). These results suggest that the MPO -463A allele significantly contributes to a protective effect overall and in smokers against lung cancer.

AXIN2 polymorphism and its association with prostate cancer in a Turkish population.

Polymorphism of AXIN2, a component of Wnt signaling, has been shown to play a role in tumorigenesis and dysregulated in cancer cells. In order to find out if AXIN2 polymorphism is a risk factor for prostate cancer, we analyzed eight polymorphic regions of this gene in 84 patients with prostate cancer and compared the results with 100 healthy controls in a Turkish population using PCR-RFLP methods. The genotype frequencies and risk factors of prostate cancer and control groups were analyzed by Chi-square test. We found a statistically significant result between prostate cancer risk and AXIN2 Intron2-956+16A/G (rs35285779) SNP. The frequency of the homozygous G/G (0%) and heterozygous A/G (18%) genotypes was significantly less in patients with prostate cancer than in healthy controls (7 and 32%, respectively) (P<0.05) for this SNP. When compared with the wild-type A/A genotype of the controls, prostate cancer patients with the A/G and G/G genotype showed reduced risk of cancer; the adjusted odds ratio (OR) for patients with the homozygous G/G genotype was 0.87 (95% CI: 0.81-0.95) and for heterozygous A/G genotype was 0.42 (95% CI: 0.20-0.85). We found no statistically significant association between controls and prostate cancer for other seven SNPs of AXIN2 including Exon1-148 C/T (rs2240308), Exon1-432 T/C (rs2240308), Exon5-1365 G/A (rs9915936), Exon5-1386 C/T (rs1133683), Intron5-1712+19 T/G, Exon7-2062 C/T, and Intron7-2141+73 G/A (rs4072245) (P>0.05). These results suggest that the AXIN2 Intron2 rs35285779 SNP is associated with development of prostate cancer as a protective SNP, while an association between other seven SNPs of the AXIN2 and risk of prostate cancer was not observed.

Sulfotransferase 1A1 Arg(213)His polymorphism and prostate cancer risk.

Sulfotransferase 1A1 (SULT1A1) is a member of the sulfotransferase family that plays an important role in the biotransformation of numerous carcinogenic and mutagenic compounds through sulfation. A transition, G to A at position 638, in the SULT1A1 gene, results in the Arg(213)His change. This single nucleotide polymorphism reduces the activity and thermostability of the SULT1A1 enzyme. In the present study, the relationship between the SULT1A1 Arg(213)His polymorphism and prostate cancer was investigated using PCR-RFLP. No significant difference in genotype and allele distribution was noted between the prostate cancer and control populations (P=0.072; P=0.099, respectively). The risk of prostate cancer in individuals carrying the SULT1A1(*)2 allele (His(213) allele) was determined by combining the SULT1A1(*)1/SULT1A1(*)2 (Arg/His(213)) and SULT1A1(*)2/SULT1A1(*)2 (His/His(213)) genotypes. No association was observed between SULT1A1 Arg(213)His polymorphism and prostate cancer incidence (P=0.24; OR, 1.36; 95% CI, 0.84-2.25). However, the His(213) allele was found to increase the risk of prostate cancer by 1.36-fold. In smoker and non-smoker populations, no significant relationship was determined between the prostate cancer and control population (P=0.45; P=0.34, respectively).