The effects of walnut supplementation on hippocampal NMDA receptor subunits NR2A and NR2B of rats.

OBJECTIVES: Walnuts contain numerous selected dietary factors that have an impact on brain functions, especially learning and memory formation in the hippocampus. Hippocampal N-methyl d-aspartate receptors (NMDARs) are involved in the formation of cognitive functions. In this study, we aimed to investigate the molecular effects of walnut supplementation on the hippocampal expressions of NMDARs involved in cognitive functions and lipid peroxidation levels in rats. METHODS: The male Sprague-Dawley rats (6 months old, n = 24) were fed with a walnut-supplemented diet (6% walnut diet, n = 12) and a control diet (rat food, n = 12) as ad libitum for 8 weeks. At the end of this period, NMDAR subunits NR2A and NR2B in the hippocampi were assayed by western blotting. Lipid peroxidation levels were measured using the thiobarbituric acid. RESULTS: The expression of NR2A and NR2B was elevated in the walnut-supplemented rats compared with the control group (P < 0.05). In addition, the levels of lipid peroxidation in the walnut-supplemented group were significantly decreased compared with the control group. DISCUSSION: We suggested that walnut supplementation may have protective effects against the decline of cognitive functions by regulating NMDAR and lipid peroxidation levels in the hippocampus. The study provides evidence that selected dietary factors (polyunsaturated fatty acids, melatonin, vitamin E, and flavonoids) within walnut may help to trigger hippocampal neuronal signal transduction for the formation of learning and memory.

The association of plasma oxidative status and inflammation with the development of atrial fibrillation in patients presenting with ST elevation myocardial infarction.

Atrial fibrillation (AF) is the most common supraventricular arrhythmia following ST elevation myocardial infarction (STEMI). Oxidative stress and inflammation may cause structural and electrical remodeling in the atria making these critical processes in the pathology of AF. In this study, we aimed to evaluate the association between total oxidative status (TOS), total antioxidative capacity (TAC) and high-sensitivity C-reactive protein (hs-CRP) in the development of AF in patients presenting with STEMI. This prospective cohort study consisted of 346 patients with STEMI. Serum TAC and TOS were assessed by Erel's method. Patients were divided into two groups: those with and those without AF. Predictors of AF were determined by multivariate regression analysis. In the present study, 9.5% of patients developed AF. In the patients with AF, plasma TOS and oxidative stress index (OSI) values were significantly higher and plasma TAC levels were significantly lower compared to those without AF (p = .003, p = .002, p < .0001, respectively). Multivariate regression analysis results showed that, female gender (Odds ratio [OR] = 3.07; 95% Confidence Interval [CI] = 1.26-7.47; p = .01), left atrial diameter (OR =1.28; 95% CI =1.12-1.47; p < .0001), hs-CRP (OR =1.02; 95% CI =1.00-1.03; p = .001) and OSI (OR =1.10; 95% CI =1.04-1.18; p = .001) were associated with the development of AF in patients presenting with STEMI. The main finding of this study is that oxidative stress and inflammation parameters were associated with the development of AF in patients presenting with STEMI. Other independent predictors of AF were female gender, left atrial diameter and hs-CRP.

Endometrial flushing αVß3 integrin, glycodelin and PGF2α levels for evaluating endometrial receptivity in women with polycystic ovary syndrome, myoma uteri and endometrioma.

The aim of this cross-sectional study is to compare endometrial flushing fluid levels of αVß3 integrin, glycodelin and PGF2α during the midluteal phase of the menstrual cycle of women with polycystic ovary syndrome (PCOS, n = 20), myoma uteri (n = 20) and endometrioma (n = 19) with the healthy controls (n = 20). After collecting samples at the midluteal phase of ovulatory volunteers and storing them at -80 °C, αVß3 integrin, glycodelin and PGF2α levels were analyzed using ELISA. The mean ages of the groups were 28.90 ± 5.45, 37.25 ± 2.73, 32.84 ± 6.62 and 32.15 ± 5.18 in PCOS, myoma uteri, endometrioma and control groups, respectively. The αVß3 integrin level (ng/ml) was statistically significantly higher in endometrioma group (9.70 ± 1.72, p < 0.05) as compared to myoma uteri and control groups. Similarly, glycodelin level (ng/ml) was significantly higher in endometrioma group (341.04 ± 93.32) than PCOS (p < 0.01), myoma uteri (p < 0.001) and healthy subjects (p < 0.001). Moreover, PGF2α level (350.04 ± 464.50 ng/ml) was significantly higher in PCOS group relative to myoma uteri (p < 0.001), endometrioma (p < 0.05) and control (p < 0.05) groups. In conclusion, αVß3 integrin level was significantly higher in endometrioma subjects than those with myoma uteri and control groups; glycodelin level was significantly higher in endometrioma group than other three groups, and lastly, PCOS patients had significantly higher PGF2α levels than those patients with myoma uteri, endometrioma and controls.

The Effects of Adjuvant Endocrine Treatment on Serum Leptin, Serum Adiponectin and Body Composition in Patients with Breast Cancer: The Izmir Oncology Group (IZOG) Study.

BACKGROUND: A limited number of studies have been conducted on the effects of hormonal therapy with tamoxifen (TMX) or aromatase inhibitors (AIs) on plasma levels of leptin and adiponectin, as well as body composition in breast cancer (BC) patients. Therefore, we aimed to analyze the relationship between adipocytokines and body composition as well as the effects of TMX and AIs on plasma adiponectin, leptin, leptin/adiponectin ratio (LAR) and body composition. METHODS: Patients were treated with either TMX or AI according to their menopausal status after adjuvant radiotherapy. Changes in body composition and serum leptin and adiponectin levels were evaluated. We recorded the type of hormonal therapy, BMI, waist/hip ratio (WHR), leptin and adiponectin levels at study entry, and after 6 and 12 months. RESULTS: From baseline to the 6- and 12-month follow-ups, there were statistically significant increases in WHR (p = 0.003), fat mass (p = 0.041), and serum leptin (p < 0.001) and adiponectin levels (p < 0.001). The changes in body composition and serum leptin and adiponectin levels were similar in TMX and AI groups. A statistically significant decrease was found in total body water and LAR (p < 0.001). Although weight and body fat percentage increased, such increases were not statistically significant. A positive correlation was found between baseline BMI and serum leptin levels. This correlation was maintained at 6 and 12 months. The negative correlation found between serum adiponectin levels at baseline and baseline BMI did not last throughout the study. CONCLUSION: In this study, increased leptin and adiponectin levels and a decreased LAR were found in both AI and TMX groups. These changes might have occurred through both mechanisms of hormonal therapy and body composition changes. Therefore, AIs and TMX may exert their protective effects for BC patients by decreasing LAR rather than affecting leptin or adiponectin alone.

Effects of long-term pre- and post-natal exposure to 2.45 GHz wireless devices on developing male rat kidney.

PURPOSE: The aim of the present study was to investigate oxidative stress and apoptosis in kidney tissues of male Wistar rats that pre- and postnatally exposed to wireless electromagnetic field (EMF) with an internet frequency of 2.45 GHz for a long time. METHODS: The study was conducted in three groups of rats which were pre-natal, post-natal. and sham exposed groups. Oxidative stress markers and histological evaluation of kidney tissues were studied. RESULTS: Renal tissue malondialdehyde (MDA) and total oxidant (TOS) levels of pre-natal group were high and total antioxidant (TAS) and superoxide dismutase (SOD) levels were low. Spot urine NAG/creatinine ratio was significantly higher in pre- and post-natal groups (p < 0.001). Tubular injury was detected in most of the specimens in post-natal groups. Immunohistochemical analysis showed low-intensity staining with Bax in cortex, high-intensity staining with Bcl-2 in cortical and medullar areas of pre-natal group (p values, 0.000, 0.002, 0.000, respectively) when compared with sham group. Bcl2/Bax staining intensity ratios of medullar and cortical area was higher in pre-natal group than sham group (p = 0.018, p = 0.011). CONCLUSION: Based on this study, it is thought that chronic pre- and post-natal period exposure to wireless internet frequency of EMF may cause chronic kidney damages; staying away from EMF source in especially pregnancy and early childhood period may reduce negative effects of exposure on kidney.

The Red Blood Cell Acetylcholinesterase Levels of Depressive Patients with Suicidal Behavior in an Agricultural Area.

Long-term exposure to organophosphate pesticides (OPs) without acute poisoning can lead to various OPs. Environmental exposure to organophosphate pesticides may be associated with depression and suicide attempts in a population living in a rural agricultural area. Patients (n = 149) suffering from major depressive disorder (with and without attempted suicide) and a control group of healthy individuals (n = 64) who had been living in the same rural district for at least 1 year were selected. Red blood cell acetylcholine esterase (RBC-AChE) activity was examined as the basis of evaluating the degree of chronic environmental exposure to OPs residues. There were negative association between RBC-AChE activity levels and suicide attempts, the number of past suicide attempts and hopelessness levels in the depressive patients. The results of the study may support the idea that environmental exposure to OPs may be associated with mental health in individuals living in agricultural districts who are not farmers or working in occupations with access to OPs.

The protective effect of Capparis ovata on 6-mercaptopurine-induced hepatotoxicity and oxidative stress in rats.

Capparis ovata is a member of Capparidacaeae family has been used in phytomedicine with a lot of positive effects such as an antioxidative, antihyperlipidemic, anti-inflammatory, and antihepatotoxic agent. The aim of this study was to research the protective effect of C. ovata on 6-mercaptopurine (6-MP) induced to hepatotoxicity and oxidative stress in rats. The rats were divided into 4 groups: control, 6-MP, C. ovataovate, and 6-MP + C. ovata. A complete blood count was performed, liver function test and antioxidant enzymes levels such as superoxide dismutase, glutathione peroxidase, catalase, and malondialdehyde were measured in blood before and after a 14-day test period. White blood cell and platelet counts were lower in the 6-MP group than other 3 groups (P < 0.005). Hepatic transaminase levels were higher in 6-MP group than the 3 groups (P < 0.05). Superoxide dismutase, glutathione peroxidase, and CAT levels were lower and malondialdehyde was higher in blood samples in 6-MP group than other 3 groups (P < 0.005). In conclusion, our tests were showed that C. ovata may be useful in patients receiving 6-MP therapy to prevent hepatotoxicity and in order to maintain uninterrupted therapy possibly reducing the risk of relapse. Although additional studies ensure that Capparis does not affect 6-MP antileukemic activity. We believe these results are important contribution to the literature.

Evaluation of total oxidative status and total antioxidant capacity in patients with endemic fluorosis.

The objective of the present study was to determine the plasma total oxidative status (TOS) and total antioxidant capacity (TAC) in patients with endemic fluorosis. A total of 79 (35 males and 44 females; mean age 44.0 ± 11.9 years) patients with endemic fluorosis and 55 (23 males and 32 females; mean age 48.3 ± 8.5 years) age-, sex- and body mass index-matched healthy controls were included in this study. The urine fluoride levels and plasma TOS and TAC levels were measured. The urine fluoride levels of fluorosis patients were significantly higher than control subjects as expected (1.91 ± 0.15 vs. 0.49 ± 0.13 mg/L, respectively; p < 0.001). TOS was significantly higher in fluorosis group than in control group (17.55 ± 3.82 vs. 15.06 ± 4.31 µmol H(2)O(2) Eq/L, respectively; p = 0.001). TAC was significantly lower in fluorosis group than in control group (1.60 ± 0.36 vs. 1.82 ± 0.51 mmol Trolox Eq/L, respectively; p = 0.004). Oxidative stress index (OSI) was significantly higher in fluorosis group than in control group (11.5 ± 3.8 vs. 8.8 ± 3.7, respectively; p < 0.001). Correlation analysis in all the groups indicated that TAC was negatively correlated with urine fluoride (r = -0.25, p = 0.003), TOS was positively correlated with urine fluoride (r = 0.34, p < 0.001) and OSI was positively correlated with urine fluoride (r = 0.36, p < 0.001). The results of our study demonstrate that oxidative stress plays an important role in the pathogenesis of the endemic fluorosis.

Effects of lisinopril on NMDA receptor subunits 2A and 2B levels in the hippocampus of rats with L-NAME-induced hypertension.

Hypertension is major risk factor leading to cerebrovascular pathologies. N-methyl D-aspartate receptors (NMDARs) and renin-angiotensin system are involved in neuronal plasticity, as well as cognitive functions in the hippocampus. In this study, we examined the effects of lisinopril, an ACE inhibitor, on the levels of hippocampal NMDAR subunits; NR2A and NR2B in L-NAME (N(ε)-nitro-L-arginine Methyl Ester)-induced hypertensive rats. In addition, malondialdehyde (MDA) levels were measured as a marker for lipid peroxidation. Compared with the control group, the MDA level was significantly increased after 8 weeks in the L-NAME-treated group. Rats treated with lisinopril and L-NAME plus lisinopril were found to have significantly decreased hippocampal MDA levels. Regarding the hippocampal concentrations of NR2A and NR2B, there were no statistically significant differences between groups. We demonstrated that lisinopril treatment has no direct regulatory effect on the levels of NR2A and NR2B in the rat hippocampus. Our results showed that Lisinopril could act as an antioxidant agent against hypertension-induced oxidative stress in rat hippocampus. The findings support that the use of lisinopril may offer a good alternative in the treatment of hypertension by reducing not only blood pressure but also prevent hypertensive complications in the brain.

Aspirin increases NMDA receptor subunit 2A concentrations in rat hippocampus.

The N-methyl-d-aspartate receptor (NMDAR), a heteromeric protein, is a glutamate receptor that has three classes of subunits: NR1, NR2, and NR3. It has been reported that these receptors are involved in synaptogenesis, synaptic plasticity, and many other processes in the central nervous system. The aim of this study is to investigate the efficacy of aspirin on hippocampal NMDARs. Sixteen rats were studied in two groups, with eight animals in each group. The first group was the control group, and the second one was the aspirin-given group. Aspirin (acetylsalicylic acid) was administered orally to the rats (200 mg/kg). Tissue samples were obtained after 3 h. The brain was removed, and both hippocampi were dissected out for evaluation. It was found that acute doses of aspirin caused increases on the levels of NMDAR 2A (NR2A) receptors and malondialdehyde (MDA), the end product of lipid peroxidation. Production was significantly increased in the aspirin-given group. We know that MDA is a marker for free radical-mediated tissue damage. In conclusion, lipid peroxidation, caused by acute doses of aspirin may lead to excitotoxicity effects by a hippocampal NR2A-mediated mechanism.

Effects of chronic scopolamine administration on spatial working memory and hippocampal receptors related to learning.

Scopolamine has been used in neuropsychopharmacology as a standard drug that leads to symptoms mimicking cognitive deficits seen during the aging process in healthy humans and animals. Scopolamine is known to be a nonselective muscarinic receptor blocker, but its chronic effect on the expression of certain hippocampal receptors is not clear. The aim of the present study was to determine the effect of chronic scopolamine administration on hippocampal receptor expression and spatial working memory in two different learning tasks, the water maze and the eight-arm radial maze. Male rats (8-12 months) were trained in both tasks. Subsequently, different groups received physiological saline or 0.1, 0.8, or 2 mg/kg scopolamine hydrobromide, respectively, for 15 days. After drug administration, the rats were retested for both tasks, and hippocampal expressions of NR2A, NR2B, nAChRα7, and mAChRM1 receptors were assessed by western blotting analysis. In both tasks, the spatial working memory was decreased dose dependently in all groups compared with the control group. In terms of receptor expressions, 0.8 and 2 mg/kg scopolamine administration significantly decreased NR2A protein expression, which corroborates suggestions of an interaction between cholinergic and glutamatergic receptors in the hippocampus.

Plasma concentrations of asymmetric dimethylarginine, nitric oxide and homocysteine in patients with slow coronary flow.

OBJECTIVES: Slow coronary flow (SCF) is slow progression of contrast agent in the coronary arteries in the absence of stenosis in epicardial coronary vessels. Endothelial dysfunction and diffuse atherosclerosis have been proposed for the etiology of SCF. Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthesis, levels are associated with an increased risk of endothelial dysfunction and atherosclerosis. ADMA levels may be increased by homocysteine. The aim of this study was to evaluate the relationship between ADMA, nitric oxide and homocysteine in patients with SCF. METHODS: The study group consisted of 50 patients with SCF. An age- and gender-matched control group was composed of 30 patients with normal coronary arteries and normal coronary flow on coronary angiography. We measured ADMA, nitric oxide and homocysteine plasma concentrations in all patients. RESULTS: Plasma nitric oxide concentrations were significantly lower in the SCF group than in the control group (11.4 ± 6, 16.1 ± 9, p = 0.02). Plasma ADMA concentrations (0.9 ± 0.3, 0.7 ± 0.3, p = 0.01) and plasma homocysteine concentrations (12.4 ± 5, 9.8 ± 2, p = 0.03) were significantly higher in the SCF group than control group. The mean TIMI frame count (TFC) was significantly correlated with plasma ADMA (r = 0.26, p = 0.02) and homocysteine (r = 0.28, p = 0.02) concentrations, but not with nitric oxide concentrations (r = - 0.18, p = 0.13). In linear regression analysis, plasma ADMA concentrations (ß = 4.6, p = 0.005) and homocysteine concentrations (ß = 0.2, p = 0.03) were independently and positively associated with mean TFC. CONCLUSION: Our results suggest that plasma concentrations of ADMA and homocysteine are increased in SCF and also that these are independent predictors of SCF.

The effect of cadmium toxicity on renal nitric oxide synthase isoenzymes.

The aim of this study was to assess the cadmium (Cd) toxicity on renal nitric oxide synthase (NOS) isoenzymes. The study was carried out on 18 inbred male (Cd group: 10 and control group: 8) Wistar rats. Cd group received drinking water containing 15 mg/L Cd for 30 days; and at the end of the 30 days, plasma Cd was analysed. One kidney was snap frozen to assess the endothelial NOS (eNOS), inducible NOS (iNOS) and neuronal NOS (nNOS) expressions by Western blot analyses, and the other kidney was preserved for histopathological examination. Plasma Cd levels were significantly elevated in the Cd group. The Western blot analyses found higher levels of eNOS, iNOS and nNOS in the Cd group but only eNOS and nNOS levels were statistically significant. There was no difference in pathological assessment of the renal tissues. Cd toxicity increases NOS isoenzyme levels and may affect renal physiology.

The gingiva contains leptin and leptin receptor in health and disease.

The presence of leptin (OB) and soluble OB receptor (s-OB-R) in gingival tissue extract and gingival crevicular fluid has led the studies investigating the relationship between OB and periodontal diseases. This study aims to investigate the levels of OB and s-OB-R in serum and their presence in gingiva of healthy controls (HC), gingivitis (G), aggressive periodontitis (AP), and chronic periodontitis (CP) patients; and whether correlations exist between clinical and serum parameters, OB and s-OB-R. Seventy-seven subjects [HC (n = 20), G (n = 20), CP (n = 21), and AP (n = 16)] were included in this study. After the clinical periodontal parameter recordings and venous blood sampling, gingival tissues obtained. Serum parameters' levels determined with enzyme linked immune sorbent assay; and OB and OB-R in gingiva immunohistochemically. No significant differences were observed regarding the serum parameters [high sensitivity C-reactive protein (hs-CRP), lipids, OB, and s-OB-R] when the groups were compared (P > 0.0125). The serum OB has positive correlations with hs-CRP in the G group (P < 0.05), and s-OB-R has presented significant negative correlations with BOP in HC group (P < 0.05), with hs-CRP in G (P < 0.05) and AP groups (P < 0.05). The positive correlations were observed between the serum OB and HDL and body mass index in the CP group (P < 0.05). In all of the tissue samples of all groups, there was positive OB and OB-R immunoreactivity in the gingival epithelium. The gingival tissues contain both OB and OB-R. The serum levels of OB and s-OB-R do not vary between patients and with different periodontal conditions.

Effects of venlafaxine and escitalopram treatments on NMDA receptors in the rat depression model.

Depression may relate to neurocognitive impairment that results from alteration of N-methyl-D: -aspartate receptor (NMDAR) levels. Venlafaxine and escitalopram are two drugs commonly used to treat depression. The drugs may affect expression of NMDARs, which mediate learning and memory formation. The aim of the study was to examine whether the effects of venlafaxine and escitalopram treatments are associated with NMDARs in a rat model of depression. Forty male Wistar albino rats were randomly divided into four groups (n = 10) as follows: control group, chronic mild stress group (CMS), venlafaxine (20 mg/kg body weight per day) + CMS, and escitalopram (10 mg/kg body weight per day) + CMS. After induction of depression, a decrease in the concentration of NR2B was observed; venlafaxine treatment prevented the reduction of NR2B expression. Escitalopram treatment did not effect the reduced levels of NR2B resulting from depression. There was no significant difference in NR2A concentration among groups. The present data support the notion that venlafaxine plays a role in maintaining NR2B receptor in experimental depression. It may be possible that treatment with escitalopram has no effect on NMDARs in experimental depression.

Calorie restriction modulates hippocampal NMDA receptors in diet-induced obese rats.

Calorie restriction (CR) has attracted increased interest since CR enhances lifespan and alters age-related decline in hippocampal-dependent cognitive functions. Obesity is associated with poor neurocognitive outcome including impaired hippocampal synaptic plasticity and cognitive abilities such as learning and memory. N-Methyl-D-aspartate receptors (NMDARs) are linked to hippocampal-dependent learning and memory, which may be stabilized by CR. In the present study, we aimed to establish the effects of CR on NMDARs in CA1 region of hippocampus in obese and non-obese rats. In addition, malondialdehyde (MDA) levels were determined as a marker for lipid peroxidation (LPO) in hippocampus. Four groups were constituted as control group (C, n = 9), obese group (OB, n = 10), obese calorie-restricted group (OCR, n = 9), and non-obese calorie-restricted group (NCR, n = 10). OCR and NCR were fed with a 60% CR diet for 10 weeks. After 10 weeks of CR, the MDA levels significantly decreased in the calorie-restricted groups. Obesity caused significant decreases in NR2A and NR2B subunit expressions in the hippocampus. The hippocampal NR2A and NR2B levels significantly increased in the OCR group compared with the OB group (P < 0.05). In contrast, the hippocampal NR2A and NR2B levels significantly decreased in the NCR group compared with the C group (P < 0.05). Oxidative stress can be prevented by CR, and these data may provide a molecular and cellular mechanism by which CR may regulate NMDAR-mediated response against obesity-induced changes in the hippocampus.

Activated protein C and normal saline infusion might prevent deleterious effects of remote acute lung injury caused by intestinal ischemia-reperfusion: an experimental study in the rat model.

BACKGROUND: Intestinal ischemia-reperfusion is a common medical event associated with both clinical and experimental distant organ injury. In particular, the lung tissue appears to be susceptible to injury resulting from systemic inflammatory mediator activation. Drotrecogin α (activated) or recombinant human activated protein C has antithrombotic, anti-inflammatory, and profibrinolytic properties. We hypothesized that APC infusion would decrease lung inflammation and ameliorate lung injury resulting from intestinal ischemia-reperfusion (IIR). A rat model of intestinal ischemia-reperfusion was used to test this hypothesis, and several parameters of lung injury were measured in lung samples. MATERIAL AND METHODS: Forty Wistar albino rats were divided into four groups: a sham-operated group (Sham), an ischemic control group (IIR), an APC-infusion group (IIR'APC), and a normal saline-infusion group (IIR'NS) (n = 10, each). A marker for lipid peroxidation, malondialdehyde (MDA), free radical scavenger glutathione peroxidase (GSH-Px), an index of polymorphonuclear neutrophils, myeloperoxidase (MPO) activity, and lung polymorphonuclear leukocytes (PMNL) were investigated in the lung tissue samples. RESULTS: MDA and MPO levels, and lung PMNL sequestration were decreased, but GSH-Px levels were increased in APC treated group versus IIR group. MDA levels were decreased and GSH-Px levels were increased in NS treated group versus IIR group. MPO levels and lung PMNL counts were similar across the IIR and IIR'NS groups. CONCLUSIONS: This study documents that APC attenuates acute lung injury in intestinal ischemia-reperfusion. NS infusion had also some favorable effects regarding MDA and MPO.

Pro-inflammatory cytokine levels in association between periodontal disease and hyperlipidaemia.

AIM: The aim of this study was to evaluate serum and gingival crevicular fluid (GCF) pro-inflammatory cytokine levels in association between periodontal disease and hyperlipidaemia. MATERIAL AND METHODS: One hundred and twenty-three subjects with hyperlipidaemia and 68 systemically healthy controls (C) were included in the study. Hyperlipidaemic groups were divided into two groups as suggested diet (HD) and prescribed statin (HS). Both groups were divided into three subgroups as healthy (h), gingivitis (g) and periodontitis (p). The clinical periodontal parameters, fasting venous blood and GCF samples were obtained, and serum tumour necrosis factor-alpha (TNF-α), interleukin (IL)-1ß (IL-1ß) and IL-6 levels were evaluated. RESULTS: The ratio of total cholesterol to high-density lipoprotein (TC/HDL) was associated with gingival index and percentage of bleeding on probing (BOP%) in both hyperlipidaemic groups. In HS group, GCF and serum IL-6 were positively correlated with BOP% and TC/HDL. GCF TNF-α was positively associated with probing pocket depth and clinical attachment level, whereas serum TNF-α was associated with BOP% in the HD group. Serum and GCF TNF-α and IL-1ß were significantly associated with TC/HDL in the HD group. CONCLUSIONS: Serum pro-inflammatory cytokines may play an important role in the association between periodontal disease and hyperlipidaemia.

The role of carnitine in preventing renal damage developed as a result of infrarenal aortic ischemia-reperfusion.

BACKGROUND: This study was designed to use carnitine for preventing deposition of end products of lipid peroxidation in rat models in the prevention of ischemia-reperfusion (IR) damage frequently seen following operations of infrarenal abdominal aorta (AA). METHODS: Forty male rats of Sprague-Dawley type were evenly (n = 8) randomized to five groups: sham laparotomy (SHAM), carnitine control (CC), aortic IR (AIR), AIR + low-dose carnitine (AIR+LDC), and AIR + high-dose carnitine (AIR+HDC). RESULTS: Compared to other groups, serum creatinine levels of AIR group were significantly higher. Also tissue malondialdehyde (MDA) levels of AIR group were significantly higher compared to SHAM, CC, and AIR+HDC groups. In histopathological examination, although tubular necrosis atrophy and tubular degeneration observed in AIR group showed regression with low-dose carnitine, tubular necrosis atrophy, tubular degeneration, glomerular damage, and vascular congestion thrombosis decreased with high-dose carnitine. Total score of histological damage was significantly higher in AIR, AIR+LDC, and AIR+HDC groups compared to SHAM and CC groups. Moreover, total score of histological damage was significantly lower in AIR+HDC group than AIR+LDC group. CONCLUSIONS: In this study, we showed carnitine can partially prevent renal damage in infrarenal AIR models of rats. This result may open new prospects to us in the prevention of renal IR damage during surgery of aorta.

Melatonin modulates hippocampus NMDA receptors, blood and brain oxidative stress levels in ovariectomized rats.

We investigated the effects of melatonin administration on ovariectomy-induced oxidative toxicity and N-methyl-D: -aspartate receptor (NMDAR) subunits in the blood of rats. Thirty-two rats were studied in three groups. The first and second groups were control and ovariectomized rats. Melatonin was daily administrated to the ovariectomized rats in the third group for 30 days. Blood, brain cortical and hippocampal samples were taken from the three groups after 30 days. Brain cortical, erythrocyte and plasma lipid peroxidation (LP) levels were higher in the ovariectomized group than in controls, although the LP level was decreased in the ovariectomized group with melatonin treatment. Brain cortical and plasma concentrations of vitamins A, C and E as well as the NMDAR 2B subunit were lower in the ovariectomized group than in controls, although, except for plasma vitamin C, they were increased by the treatment. Brain cortical and erythrocyte reduced glutathione (GSH) levels were lower in the ovariectomized group than in controls, although erythrocyte GSH levels were higher in the melatonin group than in the ovariectomized group. Brain cortical and erythrocyte glutathione peroxidase activity and NMDAR 2A subunit concentrations were not found to be different in all groups statistically. Oxidative stress has been proposed to explain the biological side effect of experimental menopause. Melatonin prevents experimental menopause-induced oxidative stress to strengthen antioxidant vitamin and NMDAR 2A subunit concentrations in ovariectomized rats.