Evaluation of Serum Paraoxonase, Myeloperoxidase, and HDL-Cholesterol Levels in Acute Myeloid Leukemia.

Inflammation and oxidative stress play a significant role in the pathogenesis of acute myeloid leukemia. While myeloperoxidase carries pro-oxidant effects, HDL-cholesterol and paraoxonase have antioxidant properties. Therefore, we evaluated serum paraoxonase, myeloperoxidase, and HDL-cholesterol levels in cases with acute myeloid leukemia. Myeloperoxidase, paraoxonase, and HDL-cholesterol levels in 40 acute myeloid leukemia patients and 18 healthy individuals were determined. The relationship between these parameters and other prognostic factors, as well as their association with response to chemotherapy, was investigated. Myeloperoxidase levels were higher, while paraoxonase and HDL-cholesterol levels were lower in acute myeloid leukemia cases compared to the control group (p < 0.001, p < 0.001, p = 0.006, respectively). The myeloperoxidase level was significantly negatively correlated with paraoxonase and HDL-c levels (r = - 0.64, p < 0.001; r = - 0.27, p = 0.02, respectively). Paraoxonase level was positively correlated with HDL level (r = 0.34, p = 0.04). Lactate dehydrogenase level was negatively correlated with HDL-c and paraoxonase levels and positively correlated with myeloperoxidase level (r = - 0.37, p = 0.019; r = - 0.35, p = 0.04; r = 0.45, p = 0.03, respectively). Following complete remission induction treatment, cases with complete remission had lower myeloperoxidase levels and higher HDL-cholesterol and paraoxonase levels compared to other cases (p = 0.03, p = 0.01, p = 0.04, respectively). Myeloperoxidase levels are higher, while paraoxonase and HDL-cholesterol levels are lower in acute myeloid leukemia cases. The obtained findings emphasize the potential importance of inflammation and oxidative stress in the pathogenesis of acute myeloid leukemia. These parameters can be used as biomarkers for prognosis prediction and prediction of response to chemotherapy.

Role of TGF-ß1 and PDGF-B in Crimean-Congo hemorrhagic fever in Eastern Anatolia Region in Turkey.

BACKGROUND & OBJECTIVES: In this study, we aimed to investigate the relationship between serum TGF-ß1 and PDGF-B levels with the pathogenesis, clinical course and prognosis of adult Crimean-Congo hemorrhagic fever (CCHF) patients. METHODS: 50 adult patients and 30 healthy individuals as a control group were included in the study, who were followed up and treated with the diagnosis of CCHF at the Atatürk University Faculty of Medicine Infectious Diseases and Clinical Microbiology Clinic, between March 2017 and September 2019 in Eastern Anatolia Region in Turkey. Blood samples were taken from patients on the first day of their hospitalization and on the sixth day of their complaints. TGF-ß1 and serum PDGF-B levels were studied by ELISA method using commercial kits, from serum samples taken from CCHF patient group and individuals in healthy control group and stored at -80°C. RESULTS: While the serum TGF- ß1 levels of patients with CCHF were found to be significantly higher on the sixth day of their complaints compared to the first day of hospitalization (42.33 ± 15.42, 28.40 ± 7.06, p = 0.001, respectively), the serum PGDF-B levels were found to be significantly lower on the sixth day of their complaints compared to those measured on the day of hospitalization (62.14 ± 19.75, 93.96 ± 20.02, respectively, p = 0.001). INTERPRETATION & CONCLUSION: Serum TGF-ß1 levels are higher and PDGF-B levels are lower in CCHF patients with severe disease, indicating that serum TGF-ß1 and PDGF-B play an important role in the pathogenesis of CCHF.

The protective efficacy of Quercetin and Naringenin against radiation-related submandibular gland injury in female rats: A histopathological, immunohistochemical, and biochemical study.

OBJECTIVE: In this study, we aimed to reveal the effectiveness of Quercetin and Naringenin in preventing radiotherapy-associated submandibular gland injury. DESIGN: The study was conducted using 48 adult female Sprague Dawley rats. The rats were randomly assigned into six groups of eight animals each. Group 1 represented the control group. The rats received only Naringenin was regarded as Group 2, received only Quercetine was regarded as Group 3. The rats exposed to radiotheraphy at a dose of 15 Gy was regarded as Group 4. Rats in group 5 were received Naringenin at a dose of 50 mg/kg daily for one week prior to radiotheraphy exposition while rats in group 6 was received Quercetine at a dose of 50 mg/kg daily for one week prior to radiotheraphy. Rats were sacrificed after radiotheraphy and submandibular glands were dissected for biochemical and immunohistochemical evaluations. RESULTS: Quercetin and Naringenin were found to have protective effect against radiation-induced damage. Naringenin and Quercetin increased the levels of Superoxide dismutase, Catalase, Glutathione Peroxidase, Glutathione and Total antioxidant status while decreasing the levels of Myeloperoxidase and Total oxidant status. Also, these agents inhibited the expression of Tumor Necrosis Factor-α and 8-hydroxy 2-deoxyguanosine immunohistochemically. CONCLUSIONS: With their powerful antioxidant and anti-inflammatory effects, Naringenin and Quercetin exhibit histopathological, immunochemical, and biochemical protection against radiation-related submandibular gland injury. In addition, Quercetin was found to be superior to Naringenin in terms of this efficacy.

The hepato-renal protective potential of walnut seed skin extract against acute renal ischemia/reperfusion damage.

Acute kidney damage is defined as a sudden change in kidney functions that prevents the removal of nitrogenous wastes from the body, thus disrupting the body's fluid and electrolyte balance. When acute kidney injury occurs, the kidneys and liver are most affected in the body. Agents used in the treatment of acute kidney injury often have nonsteroidal anti-inflammatory properties that can produce toxic effects on the gastrointestinal tract and kidneys. Natural antioxidants can be recommended as an alternative to existing treatment or in combination to protect tissues against these toxic effects. Therefore, we conducted our current study on whether walnut seed skin (WSS) extract might have hepato-renal protective effects in kidney-damaged Sprague-Dawley rats. This study is the first to use walnut seed skin extract in liver and kidney tissues in renal ischemia/reperfusion (IR) injury. Female Sprague-Dawley rats were randomly divided into three groups: Healty control (HC), renal IR (50 min ischemia - 3 h reperfusion), and renal IR + 450 mg/kg/p.o. WSS extract (the rats were treated with WSS extract orally once 1 h before the IR procedure). For this purpose, blood, liver and kidney tissues of rats were used. In serum samples, aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), urea and creatinine values were determined separately for the administration groups. We also performed histopathological studies on liver and kidney tissues. Finally, gene markers (endothelial nitric oxide synthase (eNOS), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), Caspase-4 and Caspase-9) determined to evaluate the anti-oxidant, anti-inflammatory and apoptotic effect of walnut seed skin were measured by q-RT PCR method. As a result of the study it was determined that pre-application of WSS extract improved the deteriorated serum parameters in rats with renal ischemia. In the histopathological analysis results, it was observed that WSS had a protective effect on kidney and liver tissue. In studies on gene expression, although there were different and contradictory results for liver and kidney tissue, we determined that WSS was more protective on liver tissue. In conclusion, the healing potential of WSS in renal and hepatic tissues seems to act by inhibiting the inflammatory response, oxidative stress and apoptosis. Therefore, the potential of this extract is remarkable and may serve as a potential therapeutic that may protect against acute organ damages due to renal IR.

Could VEGF-D level have a role in clinical risk scoring, estimation of thrombus burden, and treatment in acute pulmonary thromboembolism?

OBJECTIVE: Pulmonary embolism (PE) is usually a complication of deep vein thrombosis and is an important cause of mortality and morbidity. Vascular endothelial growth factor D (VEGF-D) is a secretory protein that plays a role in the remodelling of blood vessels and the lymphatic system. This study aimed to determine the relationship between VEGF-D level and clinical risk scoring in patients with PE. METHODS: The study included 117 patients admitted for PE that were divided into four groups: high-risk patients (n = 35), high-intermediate-risk patients (n = 30), low-intermediate-risk patients (n = 24), and low-risk patients (n = 28). Plasma VEGF-D was measured from peripheral venous blood samples (5 mL) using a commercial enzyme-linked immunosorbent assay (ELISA) kit. Pulmonary Artery Obstruction Index (PAOI) was calculated from CT angiography imaging. RESULTS: There was no significant difference in troponin-I and NT-proBNP levels between the high-intermediate-risk and high-risk PE patients (P = .134, .146). VEGF-D and PAOI levels were found to be statistically significantly higher in high-risk patients compared with high-intermediate-risk patients (P = .016, .001). VEGF-D level was moderately correlated with mean pulmonary artery pressure and PAOI (r = .481, P = .01; r = .404, P = .01). In ROC curve analysis, a cut-off of 370.1 pg/mL for VEGF-D had 91.4% sensitivity and 67% specificity in the differentiation of high-intermediate-risk and high-risk PE patients. CONCLUSION: This study showed that plasma VEGF-D level was more reliable than troponin-I and NT-proBNP in clinical risk scoring and demonstrating thrombus burden. VEGF-D can be used as a biomarker in clinical risk scoring and estimation of thrombus burden in patients with acute PE.

Evaluation of the relationship between macrophage migration inhibitory factor level and clinical course in patients with COVID-19 pneumonia.

The COVID-19 pandemic, which has ravaged our world for more than a year, still shapes our agenda with a scale of intensity that fluctuates over time. In our study, we aimed to determine the correlation between serum migration inhibitory factor (MIF) level and disease severity in COVID-19 with different prognoses. Between 15 October 2020 and 20 January 2021, 110 patients over the age of 18 who were diagnosed with COVID-19 and 40 volunteer healthcare personnel were included in our study. MIF levels were measured by enzyme-linked immunosorbent assay. In the comparison of serum MIF values in the patient and control group, it was observed that the MIF level was significantly higher in patients with both moderate and severe COVID-19 levels compared to the control group (p = 0.001, 0.001). In the comparison of serum MIF values of moderate to severe COVID-19 patients, it was observed that MIF level was higher in severe patients (p = 0.001). In the receiver operating characteristic curve analysis performed to differentiate between severe and moderate COVID-19 patients with MIF levels, the area under the curve was observed as 0.78. When the cutoff value of the MIF level was taken as 4.455 ng/ml, the sensitivity was 83% and the specificity was 62%. Failure to adequately balance the pro-inflammatory cytokines synthesized in COVID-19 with anti-inflammatory effect is the most important reason for the aggravation of the disease course. Playing a role in pro-inflammatory cytokine synthesis, MIF can provide important information about the disease prognosis in the early period.

Determination of Pentraxin-3, Interleukin-8 and Vascular Endothelial Growth Factor Levels in Patients with Gastric Adenocarcinoma.

INTRODUCTION AND AIM: The purpose of this study was to determine the value, in terms of diagnosis, resectability and prognosis of pentraxin-3 (PTX3), interleukin-8 (IL-8) and vascular endothelial growth factor (VEGF) in cases of gastric adenocarcinoma, an important condition both worldwide and in Turkey, and to determine their levels in order to contribute to elucidating the pathogenesis of the disease. MATERIALS AND METHODS: Serum was separated from blood specimens collected from 45 patients diagnosed with gastric adenocarcinoma and from a 30-member healthy control group. Serum PTX3, IL-8 and VEGF levels were studied by ELISA method. RESULTS: Serum PTX3 values differed significantly between the patient group and the control group (p <0.05). Serum IL-8 values also differed significantly between the patient group and the control group (p <0.05). A significant difference was also observed between serum VEGF values in the patient group and the control group (p <0.05). Significant correlation was determined between serum PTX3 and VEGF (p <0.01; r=0.833), between serum PTX3 and IL-8 (p <0.01; r=0.818), and between serum VEGF and IL-8 (p <0.01; r=0.803), measurements when the entire study population was evaluated irrespectively of groups. CONCLUSION: Serum PTX3, IL-8 and VEGF levels decreased in cases of gastric adenocarcinoma compared to the control group, and their levels affected one another.
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Is Metrnl an Adipokine Involved in the Anti-inflammatory Response to Acute Exacerbations of COPD?

PURPOSE: Chronic obstructive pulmonary disease (COPD) is a common lung disease characterized by airflow limitation and systemic inflammation. Recently, there has been growing interest in adipose tissue-mediated inflammation in the pathogenesis of COPD. The aim of our study was to determine the relationships between a new adipocytokine, meteorin-like protein (Metrnl), and acute exacerbations of COPD, smoking, and comorbidities. MATERIALS AND METHODS: The study included 313 patients aged 40-65 years in four groups: Group 1: ex-smokers (≥ 20 pack-years) with COPD hospitalized for COPD exacerbation (n = 133), Group 2: current-smokers (≥ 20 pack-years) without COPD (n = 60), Group 3: ex-smokers (≥ 20 pack-years) without COPD (n = 60), and Group 4: never-smokers without COPD (n = 60). Peripheral venous blood samples (5 cc) were collected from all participants. Plasma Metrnl levels were measured using commercial enzyme-linked immunosorbent assay (ELISA) kit. RESULTS: Mean Metrnl levels were 28.45 ± 11.27 ng/ml in Group 1, 24.34 ± 4.38 ng/ml in Group 2, 18.84 ± 3.8 ng/ml in Group 3, and 19.44 ± 3.92 ng/ml in Group 4. Group 1 had significantly higher mean Metrnl level compared to the other groups (p = 0.006, p = 0.001, p = 0.001). Metrnl level was also significantly higher in Group 2 when compared with Groups 3 and 4 (p = 0.001, p = 0.005). Group 1 patients with diabetes mellitus and coronary artery disease showed significantly lower Metrnl levels compared to other patients in the group (p = 0.001, p = 0.001). CONCLUSION: The high Metrnl level in COPD exacerbations and active smoking may be important in balancing the inflammatory response. However, plasma Metrnl levels were found to be lower in COPD patients with comorbidities.

Protective effect of gallic acid against cisplatin-induced ototoxicity in rats / Efeito protetor do ácido gálico contra a ototoxicidade induzida por cisplatina em ratos

Abstract Introduction: Cisplatin is an antineoplastic agent widely used in the treatment of a variety of cancers. Ototoxicity is one of the main side-effects restricting the use of cisplatin. Objective: The purpose of this study was to investigate the protective efficacy of gallic acid, in biochemical, functional and histopathological terms, against ototoxicity induced by cisplatin. Methods: Twenty-eight female Sprague Dawley rats were included. Rats were randomly assigned into four groups of seven animals each. Cisplatin group received a single intraperitoneal dose of 15 mg/kg cisplatin. Gallic acid group received intraperitoneal gallic acid at 100 mg/kg for five consecutive days. Cisplatin + gallic acid group received intraperitoneal gallic acid at 100 mg/kg for five consecutive days and a single intraperitoneal dose of 15 mg/kg cisplatin at 3rd day. A control group received 1 mL intraperitoneal saline solution for five consecutive days. Prior to drug administration, all rats were exposed to the distortion product otoacoustic emissions test. The test was repeated on the 6th day of the study. All rats were then sacrificed; the cochleas were removed and set aside for biochemical and histopathological analyses. Results: In cisplatin group, Day 6 signal noise ratio values were significantly lower than those of the other groups. Also, malondialdehyde levels in cochlear tissues were significantly higher, superoxide dismutase and glutathione peroxidase activities were significantly lower compared to the control group. Histopathologic evaluation revealed erosion in the stria vascularis, degeneration and edema in the connective tissue layer in endothelial cells, impairment of outer hair cells and a decrease in the number of these calls. In the cisplatin + gallic acid group, this biochemical, histopathological and functional changes were reversed. Conclusion: In the light of our findings, we think that gallic acid may have played a protective role against cisplatin-induced ototoxicity in rats, as indicated by the distortion product otoacoustic emissions test results, biochemical findings and immunohistochemical analyses.

Resumo Introdução: A cisplatina é um agente antineoplásico amplamente usado no tratamento de vários tipos de câncer. A ototoxicidade é um dos principais efeitos colaterais que restringem o uso da cisplatina. Objetivo: O objetivo deste estudo foi investigar a eficácia protetora do ácido gálico, em termos bioquímicos, funcionais e histopatológicos, contra a ototoxicidade induzida por cisplatina. Método: Vinte e oito ratas Sprague-Dawley foram incluídas. As ratas foram distribuídas aleatoriamente em quatro grupos de sete animais cada. O grupo cisplatina recebeu uma única dose intraperitoneal de 15 mg/kg de cisplatina. O grupo ácido gálico recebeu ácido gálico via intraperitoneal a uma dose de 100 mg/kg durante cinco dias consecutivos. O grupo cisplatina + ácido gálico recebeu ácido gálico via intraperitoneal a uma dose de 100 mg/kg durante cinco dias consecutivos e uma única dose intraperitoneal de 15 mg/kg de cisplatina no terceiro dia. O grupo controle recebeu 1 mL de solução salina via intraperitoneal por cinco dias consecutivos. Antes da administração do fármaco, todos os ratos foram expostos ao teste de emissões otoacústicas - produto de distorção. O teste foi repetido no sexto dia do estudo. Todos os ratos foram então sacrificados; as cócleas foram removidas e reservadas para análises bioquímicas e histopatológicas. Resultados: No grupo cisplatina, os valores da relação sinal-ruído do dia 6 foram significativamente mais baixos aos dos outros grupos. Além disso, os níveis de malondialdeído nos tecidos cocleares foram significativamente mais altos, e as atividades de superóxido dismutase e glutatione peroxidase foram significativamente mais baixas em comparação com o grupo controle. A avaliação histopatológica revelou erosão na estria vascular, degeneração e edema na camada de tecido conjuntivo em células endoteliais, comprometimento das células ciliadas externas e diminuição do número dessas células. No grupo cisplatina + ácido gálico, estas alterações bioquímicas, histopatológicas e funcionais foram revertidas. Conclusão: Tendo em vista os nossos achados, consideramos que o ácido gálico pode ter desempenhado um papel protetor contra a ototoxicidade induzida por cisplatina em ratas, conforme indicado pelos resultados do teste emissões otoacústicas - produto de distorção, achados bioquímicos e análises imuno-histoquímicas.

Levosimendan ameliorates cisplatin-induced ototoxicity: Rat model.

OBJECTIVES: Cisplatin is employed for chemotherapeutic purposes in several types of adult and pediatric cancer. However, side-effects including nephrotoxicity, ototoxicity, gastrointestinal effects and neuropathy restrict the use of the drug due to their adverse impacts on quality of life. This study aimed to determine whether levosimendan exhibits a protective effect against cisplatin-related ototoxicity in a rat model by means of functional, biochemical and histochemical analysis. METHODS: The study was employed with 24 female Sprague Dawley rats. After distortion product otoacoustic emissions (DPOAE) tests applied to all rats, rats were randomly assigned into four groups of six animals each. A single intraperitoneal 15 mg/kg dose of cisplatin was administered to Cisplatin group. Levosimendan group received intraperitoneal levosimendan at a dose of 100 mg/kg for five consecutive days. Cisplatin + Levosimendan group received intraperitoneal levosimendan at a dose of 100 mg/kg for five consecutive days and a single intraperitoneal dose of 15 mg/kg cisplatin at 3rd day of the study. Control group received 8 mL/kg/day intraperitoneal saline solution for five consecutive days. The DPOAE test was repeated on the 6th day of the study. All rats were then sacrificed, the cochleas were removed and set aside for biochemical and histopathological analyses. RESULTS: A significant increase in levels of Malondialdehyde (MDA) and significantly lower activities of superoxide dismutase (SOD) and Glutathione peroxidase (GPx) were observed at rats of cisplatin group. Administration of levosimendan showed significantly lower cochlear MDA levels, while SOD and GPx activities both increased significantly. The DPOAE test performed at 6th day of the study showed a significant impairment in the signal-noise ratio (SNR) levels of rats in Cisplatin group. The SNR levels of rats treated with levosimendan were significantly higher than those of cisplatin group and were similar to those of the control group. Cisplatin impaired the cochlear structure and a severe Caspase 3 and 8-hydroxy-2' -deoxyguanosine (8-OHdG) immunopositivity was observed at cochlea of the rats of cisplatin group. Administration of levosimendan protected the structure of cochlea and there was a mild Caspase 3 and 8OHdG immunopositivity. CONCLUSION: Our data demonstrate that levosimendan protects hearing against cisplatin-induced ototoxicity and obviates cellular degeneration. It also significantly reduces oxidative stress and apoptosis, probable mechanisms involved in ototoxicity.

Protective effect of gallic acid against cisplatin-induced ototoxicity in rats.

INTRODUCTION: Cisplatin is an antineoplastic agent widely used in the treatment of a variety of cancers. Ototoxicity is one of the main side-effects restricting the use of cisplatin. OBJECTIVE: The purpose of this study was to investigate the protective efficacy of gallic acid, in biochemical, functional and histopathological terms, against ototoxicity induced by cisplatin. METHODS: Twenty-eight female Sprague Dawley rats were included. Rats were randomly assigned into four groups of seven animals each. Cisplatin group received a single intraperitoneal dose of 15mg/kg cisplatin. Gallic acid group received intraperitoneal gallic acid at 100mg/kg for five consecutive days. Cisplatin+gallic acid group received intraperitoneal gallic acid at 100mg/kg for five consecutive days and a single intraperitoneal dose of 15mg/kg cisplatin at 3rd day. A control group received 1mL intraperitoneal saline solution for five consecutive days. Prior to drug administration, all rats were exposed to the distortion product otoacoustic emissions test. The test was repeated on the 6th day of the study. All rats were then sacrificed; the cochleas were removed and set aside for biochemical and histopathological analyses. RESULTS: In cisplatin group, Day 6 signal noise ratio values were significantly lower than those of the other groups. Also, malondialdehyde levels in cochlear tissues were significantly higher, superoxide dismutase and glutathione peroxidase activities were significantly lower compared to the control group. Histopathologic evaluation revealed erosion in the stria vascularis, degeneration and edema in the connective tissue layer in endothelial cells, impairment of outer hair cells and a decrease in the number of these calls. In the cisplatin+gallic acid group, this biochemical, histopathological and functional changes were reversed. CONCLUSION: In the light of our findings, we think that gallic acid may have played a protective role against cisplatin-induced ototoxicity in rats, as indicated by the distortion product otoacoustic emissions test results, biochemical findings and immunohistochemical analyses.

The effect of restorative materials on cytokines in gingival crevicular fluid.

OBJECTIVE: Composition of the restorative materials may cause inflammatory responses by monocyte activation and changes in the levels of cytokine released from different cells. Interleukin-6 (IL-6), interleukin-8 (IL-8) and Tumor necrosis factor alpha (TNF-α) are important cytokine for evaluating of the inflammatory process. The aim of this study was to evaluate the different restorative materials used in class V cavities effect on gingival crevicular fluid inflammatory cytokine levels. DESIGN: 60 individuals having Class V carious cavities participated in the study. Cavities were restored with FiltekZ250, DyractXP, Fuji IX, Cavex avalloy restorative materials. Changes in clinical and biochemical parameters were evaluated before restorations, seven and 21days after restorations. Contralateral tooth intact enamel surface was determined as control side. Periotron8000 device was used for detection of GCF volume. Cytokine level of GCF was evaluated by Human ELISA kits. Data were analyzed using Mann-Whitney U test and Wilcoxon signed ranks test. The correlations between clinical parameters and biochemical parameters were examined by Spearman's rank correlation analysis. RESULTS: After restorative treatments PI and GI scores were decreased compared with baseline evaluations. There was a significant difference in GCF levels between experimental and control sites in all groups. GCF IL-6 levels in all groups except Filtek Z250, GCF IL-8 levels in all groups except Fuji IX, GCF TNF-α level in only Fuji IX showed significant differences between experimental and control sites. CONCLUSIONS: The obtained data supported that all of the tested materials caused changes in GCF cytokine levels.

Carnitine and Adiponectin Levels in Breast Cancer after Radiotherapy.

In this study, serum carnitine (CRNT) and adiponectin (APN) levels and the correlation of these parameters in patients with breast cancer before and after treatment with radiotherapy (RT) were determined. MATERIALS AND METHODS: Serum adiponectin and carnitine levels were assessed in 58 patients with breast carcinoma and 30 control subjects. Serum carnitine and APN levels were determined using a specific enzyme-linked immunosorbent assay. RESULTS: While serum carnitine level was significantly lower in the patients with breast cancer after RT compared with the control group and before treatment (p=0.002 and p=0.019, respectively), serum APN level was significantly higher than in the control group and before treatment ( p=0.003 and p=0.027, respectively). Carnitine level showed a negative correlation with APN level in the patients after RT (r= -0.626, p= 0.001). There was no correlation between carnitine and APN levels in subjects of control group and before treatment. Also, neither carnitine nor APN levels demonstrated correlation other parameters. CONCLUSIONS: Results suggest that increased serum adiponectin and decreased carnitine levels in breast cancer after RT than control group. Carnitine level showed a negative correlation with APN level in the patient with breast cancer after RT. While carnitine, HDL-C and total cholesterol levels are decreased, trygliceride and LDL-C levels are increased in patients than control group. In addition, serum APN concentration was inversely correlated with serum carnitine levels. Furthermore, increased serum APN level in breast cancer after RT might be associated with hypocarnitinemia.

Lecithin: cholesterol acyltransferase and na(+)-k(+)-ATPase activity in patients with breast cancer.

PURPOSE: The aim of this study was to determine whether plasma lecithin:cholesterol acyltransferase (pLCAT) and erythrocyte membrane Na(+)-K(+)-ATPase ase (emNaKATPs) activity have a correlation in breast cancer. This study compared these parameters at time points before and after treatment with radiotherapy. METHODS: The levels of pLCAT and emNaKATPs were assessed in 30 patients with breast carcinoma and 20 control subjects. While emNaKATPs was measured with spectrophotometric method, pLCAT levels was measured using a specific enzyme-linked immunosorbent assay. RESULTS: pLCAT levels, both before and after radiotherapy, were found to be decreased in breast cancer patients than in the controls groups (p<0.001 and p<0.001, respectively). Also, pLCAT levels after radiotherapy were found to be decreased in breast cancer patients than the pLCAT levels before radiotherapy (p<0.001). The emNaKATPs activity were higher in the control group than in the breast cancer patients before/after radiotherapy (RT) (p<0.001 and p<0.001, respectively). At the same time, emNaKATPs activity before RT was higher in the breast cancer patients than emNaKATPs activity after RT (p<0.001). There was a significant correlation between pLCAT and emNaKATPs activity in breast cancer patients receiving radiotherapy (r=0.63, p<0.001), but no correlation between in breast cancer patients before RT and control group (r=0.023, p>0.05). CONCLUSION: The results of the present study demonstrated that decreased pLCAT and emNaKATPs activity levels in breast cancer patients after/before RT than control group. In addition, decreased emNaKATPs activity in breast cancer patients receiving radiotherapy may be due to decreased pLCAT concentrations and RT beam. In our opinion, altered activities of pLCAT and emNaKATPs are linked to the treatment effect of radiotherapy. These data may clarify the development of cell membrane dysfunction and lipid metabolism in breast cancer patients receiving radiotherapy.