Caution may be required in using l-theanine in diabetes mellitus: A study on the rats.

BACKGROUND: The study aimed to identify the effects of l-theanine on kidney and heart tissues in diabetic rats. 24 male rats included in the study were divided into 4 groups (n = 6/group): SHAM, LTEA, DM and DM + LTEA. For 28 days, drinking water was given to SHAM and DM, and LTEA (200 mg/kg/day) to LTEA and DM + LTEA groups, intragastrically. DM was induced by 120 mg/kg nicotinamide (NA) + 60 mg/kg streptozotocin (STZ). The levels of cystatin C (CysC) and angiotensin-converting enzyme 2 (ACE2) were determined by ELISA kits, homocysteine, electrolytes and iron by an autoanalyzer, the ratio of oxidized/total reduced glutathione (GSSG/TGSH) by assay kits. The tissues were histopathologically analyzed. RESULTS: LTEA alleviated histopathological degenerations. However, it decreased significantly serum iron and homocysteine levels (p < 0.05). CONCLUSION: LTEA did not exhibit significant protective effects on kidney and heart tissues; it may have affected the homocysteine and iron metabolisms in diabetics.

How does l-theanine treatment affect the levels of serum and hippocampal BDNF, insulin and adipocytokines in diabetic rats?

BACKGROUND: Diabetes Mellitus (DM), a metabolic disease characterized by the increased blood glucose level, insulin deficiency or ineffectiveness, may cause structural and functional disorders in the brain. l-Theanine (LTN) has the relaxing, psychoactive, antidepressant, anti-inflammatory and antinecrotic properties, and regulates the functions of hippocampus (HP) in brain. In the present study, the aim was to identify the effects LTN on the levels of BDNF, insulin and adipocytokines (TNF-α, leptin, adiponectin and resistin) in both HP and serum of diabetic rats. METHODS: 32 male Wistar rats were divided into four groups (n = 8/group): Control, LTN, DM and DM + LTN. Diabetes was induced by by nicotinamide/streptozotocin. 200 mg/kg/day LTN treatment was applied for 28 days. The serum and hippocampal levels of the parameters were determined by using commercial ELISA kits. Additionally, HP tissues examined histopathologically. RESULTS: LTN treatment significantly decreased leptin and adiponectin levels in HP tissues in diabetic rats (p < 0.05). Although it decreased the insulin level in both serum and HP, this was not statistically significant. No significant effect on other parameters was observed (p > 0.05). In histopathological analysis, although the damage was reduced by LTN in all sections of HP, this change was significant mainly in CA3 region (p < 0.05). CONCLUSION: It was concluded that LTN has the ability to reduce hippocampal degeneration and modulates adipocytokines in diabetic rats.

Elevated Circulating Endocan Levels Are Associated with Increased Levels of Endothelial and Inflammation Factors in Postprandial Lipemia.

BACKGROUND: Postprandial lipemia (PPL) causes endothelial dysfunction by causing endothelial damage to lipoproteins that remain rich in triglycerides. Endocan is a proteoglycan with increased tissue expression, endothelial activation, and neovascularization. The aim of the study was to examine circulating endocan levels in PPL subjects by considering the degree of PPL response according to a high-fat test meal. The other aim was to determine the association between endocan levels and endothelial and inflammatory factors. METHOD: Fifty-four hyperlipidemic subjects and 28 normolipidemic subjects consumed the high-fat meal. Endocan, sICAM-1, sVCAM-1, and VEGFA as endothelial factors and IL-6 and LFA-1α as inflammatory factors were evaluated. RESULTS: Fasting serum endocan, VEGFA, sICAM-1, sVCAM-1 IL-6, and LFA-1α levels were increased in the PPL group compared to the control group. The PPL group was divided into tertiles based on mean AUC levels. Endocan levels in tertile 3 were at the highest and were increased significantly compared to tertiles 1 and 2. AUC and endocan levels were positively correlated with other endothelial and inflammation factors. ROC analysis showed endocan levels to be one of the highest values. CONCLUSIONS: Circulating endocan is seen at significantly higher levels and independently associated with endothelial and inflammatory factors in postprandial lipemia and dyslipidemia.

Effects of L-Theanine on Hepatic Ischemia-Reperfusion Injury in Rats.

OBJECTIVES: The effects of L-theanine on hepatic microcirculation during hepatic ischemia-reperfusion injury have not yet been investigated. The aim of this study was to investigate the influence of L-theanine on hepatic ischemia-reperfusion injury in rats. MATERIALS AND METHODS: Thirty-two male Sprague Dawley rats weighing 250 to 300 g were used. Rats were divided into 4 groups: sham + saline, sham + L-theanine, hepatic ischemia-reperfusion injury + saline, and hepatic ischemia-reperfusion injury + L-theanine. Hepatic ischemia-reperfusion injury in rats was induced by 60 minutes of 70% ischemia and 4 hours of reperfusion. The extent of hepatic cell injury, functional capillary density, hepatic functions, and changes in some enzyme markers in hepatic tissue were investigated in the 4 groups. RESULTS: The induction of hepatic ischemia-reperfusion injury resulted in significant increases in hepatic necrosis; serum activity of alanine aminotransferase, lactate dehydrogenase, gamma-glutamyltransferase, and tumor necrosis factor alpha; tissue activity of inducible nitric oxide synthase, myeloperoxidase, and malondialdehyde, and oxide glutathione; and H score for hypoxia-inducible factor 1-alpha in the liver. In the liver, there were significant reductions in reduced glutathione, ratio of reduced glutathione-to-oxide glutathione, and functional capillary density. The use of L-theanine improved these changes. CONCLUSIONS: L-theanine demonstrated protective effects on hepatic injury after ischemia-reperfusion injury in rats. However, new studies are needed to confirm the preventive or reducing effects of L-theanine on hepatic ischemia-reperfusion injury.

Effects of hazelnut supplemented diet on doxorubicin-induced damage of reproductive system in male rats.

The present study was objected to investigate the effect of hazelnut supplemented diet on the levels of oxidative stress and fertility parameters against doxorubicin-induced testicular and epididymal tissue damage of male rats. Rats were randomly divided into four groups (each n = 8), namely control group (CG), doxorubicin group (DG), doxorubicin + hazelnut group (DHG), and doxorubicin + vitamin E group (DEG). This is the first study designed using DHG. Doxorubicin was intraperitoneally injected into all diet groups except CG at a dose of 3 mg/kg body weight on days 1, 7, 14, 21, and 28. In addition, DHG was supplemented with a hazelnut diet at a dose of 3 g/kg body weight/day and vitamin E was added to the drinking water of DEG at a dose of 50 mg/kg body weight/day. DHG reversed the side effects of doxorubicin and positively improved the epididymis sperm quality, testicular and epididymal tissue injury, testosterone level, epididymis oxidative stress index, and lipid peroxidation in male rats. These findings suggest that hazelnut has positive effects against doxorubicin dependent damage on male rats and it may be a promising supplement for amelioration of testicular toxicity. PRACTICAL APPLICATIONS: Hazelnut has numerous positive health effects due to its macronutrients, micronutrients, lipid-soluble compounds and bioactive phenolics. Studies have shown that regular consumption of hazelnut may have a positive effect on lipid parameters, oxidative stress, inflammation markers, and endothelial dysfunction in both healthy people and patients with chronic diseases. Although doxorubicin (Adriamycin, DOX) is an antibiotic that has been widely used in cancer treatment for nearly 30 years, it causes organ toxicity including testicular tissue. Hazelnut may have positive effects on the damage caused by DOX in the reproductive system. However, studies on the effect of hazelnut on male reproductive health are scarce. Therefore, this study provided a basis for the clinical evaluation of the effects of hazelnut on the reproductive system.

Dexmedetomidine acts as an oxidative damage prophylactic in rats exposed to ionizing radiation.

STUDY OBJECTIVE: To investigate the effects of dexmedetomidine on oxidative injury caused by ionizing radiation. DESIGN: Randomized controlled experimental study. SETTING: Department of radiation oncology and research laboratory of an academic hospital. INTERVENTIONS: Twenty-eight rats were randomized to 4 groups (n=7 per group). Group S rats were administered physiologic serum; group SR rats were administered physiologic serum and 10 Gy external ionizing radiation. Groups D100 and D200 were administered 100 and 200 µg/kg dexmedetomidine intraperitoneally, respectively, 45 minutes before ionizing radiation. MEASUREMENTS: Liver, kidney, lung, and thyroid tissue and serum levels of antioxidant enzymes (glutathione peroxidase [GPX], superoxide dismutase, and catalase) and oxidative metabolites (advanced oxidation protein products, malondialdehyde, and nitrate/nitrite, and serum ischemia-modified albumin) were measured 6 hours postprocedure. MAIN RESULTS: In group SR, IR decreased antioxidant enzyme levels and increased oxidative metabolite levels (P<.05). In plasma, antioxidant enzyme levels were higher and oxidative metabolite levels were lower in groups D100 and D200 than in group SR (P<.01). In tissues, hepatic and lung GPX levels were higher in groups D100 and D200 than in group SR (P<.001). Renal and thyroid GPX levels were higher in D200 than in group SR (P<.01). Thyroid superoxide dismutase levels were higher in groups D100 and D200 than in group SR (P<.01). Renal, lung, and thyroid catalase levels were higher in group D200 than in group SR (P<.01). Hepatic, renal, and lung advanced oxidation protein products and malondialdehyde levels were lower in groups D100 and D200 than in group SR (P<.01). Hepatic, renal, and lung nitrate/nitrite levels were lower in group D200 than in group SR (P<.05). CONCLUSIONS: Dexmedetomidine preserves the antioxidant enzyme levels and reduces toxic oxidant metabolites. Therefore, it can provide protection from oxidative injury caused by ionizing radiation.

Exogenous L-arginine and HDL can alter LDL and ox-LDL-mediated platelet activation: using platelet P-selectin receptor numbers.

The aim of this study is to investigate the effects of exogenous L-arginine and HDL on LDL and oxidized LDL (ox-LDL)-mediated platelet activation. Adenosine diphosphate (ADP)-activated platelets have been incubated with lipoproteins with or without L-arginine. P-selectin receptor numbers per platelet have been measured by flow cytometry. After incubation with only L-arginine (without lipoproteins), platelet nitric oxide (NO) levels and P-selectin receptor numbers significantly increased compared to the controls (P < .05). After incubation with LDL or ox-LDL, receptor numbers of P-selectin significantly increased (P < .001). However, P-selectin receptor numbers in platelets treated with L-arginine + LDL or L-arginine + ox-LDL decreased compared to the levels in platelets treated with only LDL or ox-LDL (P < .01, P < .001, respectively). Addition of HDL to L-arginine + ox-LDL caused significant reduction in P-selectin receptor numbers as in the control values (P < .001).We have concluded that L-arginine causes enhanced platelet NO levels and blocks the effects of LDL or ox-LDL on platelet P-selectin receptor numbers and HDL also strengthens this effect of L-arginine.

Plasma homocysteine and its relationships with atherothrombotic markers in psoriatic patients.

BACKGROUND: Hyperhomocysteinemia may constitute an independent risk factor for cardiovascular disease and may promote atherothrombosis. Psoriasis is one of the diseases associated with increased atherothrombosis. The aim of the present study was to examine serum total homocysteine (tHcy) level and its relationships with atherothrombotic markers. METHODS: The study group included 30 patients with psoriasis (17 females and 13 males) with a mean age of 34.2 (age range: 27-40) and 30 sex and age matched healthy volunteers (15 females and 15 males) with a mean age of 36.7 (age range: 26-48). The concentrations of lipids, lipoproteins, acute phase reactants, tHcy and atherothrombotic markers [fibronectin, soluble vascular adhesion molecules-1 (sVCAM-1), soluble intercellular adhesion molecules-1 (sICAM-1), tissue plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1), autoantibodies against oxidized LDL (AuAb-oxLDL)] were determined. RESULTS: The mean levels of serum tHcy, fibrinogen, fibronectin, sICAM, PAI-1 and AuAb-oxLDL were increased in patients whereas tPA, vitamin B(12) and folate levels were decreased significantly. Increased levels of sVCAM were not statistically significant. tHcy levels were negatively correlated with vitamin B(12) (r=-0.40, P=0.027) and positively correlated with PAI-1 and AuAb-oxLDL levels (r=0.46, P=0.011; r=0.39, P=0.035, respectively). CONCLUSIONS: It was concluded that the increased homocysteine concentration and altered endothelial cell-mediated proteins associated with increased lipids and LDL oxidation may play an important role for the development of atherothrombotic complications with psoriasis.

Evaluation of the atherogenic tendency of lipids and lipoprotein content and their relationships with oxidant-antioxidant system in patients with psoriasis.

BACKGROUND: Psoriasis is a common chronic and recurrent inflammatory skin disease that can occur due to abnormalities in essential fatty acid metabolism, lymphokine secretion, free radical generation, lipid peroxidation and eicosanoid metabolism, and has been associated with increased frequency of cardiovascular events. The current study was designed to evaluate plasma lipids, susceptibility of LDL to oxidation and oxidant-antioxidant status and their relationships in patients with psoriasis. METHODS: The study group included 35 patients with psoriasis (18 females and 17 males), and 35 sex- and age-matched healthy volunteers (16 females and 19 males). From blood samples, their lipids, lipoproteins, acute phase reactants, lipid peroxidation products [lipid hydroperoxide (LHP) and malondialdehyde (MDA)], antioxidant enzymes [glutathione peroxidase (GSH-Px), glutathione reductase (GR), superoxide dismutase (SOD), catalase (CAT)], total antioxidant status (TAS) and autoantibodies against oxidized low-density lipoprotein (AuAb-oxLDL) levels were determined. Moreover, the susceptibility of copper-induced in vitro oxidation of LDL was examined. RESULTS: The mean levels of atherogenic lipids (total cholesterol [TC], triacylglycerol [TG] and LDL cholesterol [LDL-C]), acute-phase reactants (CRP, ESR, PMNLs, ceruloplasmin and fibrinogen) and lipid peroxidation products, AuAb-oxLDL levels in patients with psoriasis were found to be significantly higher than those of healthy subjects. On the other hand, TAS and antioxidant enzyme activities (CAT, SOD and GSH-Px in erythrocyte and SOD in plasma) were significantly lower when compared to healthy subjects. The lag times [t(lag)], a measure of resistance to oxidation of LDL, were also lower. The levels of AuAb-oxLDL in patients were correlated with TC, LDL-C, plasma LHP, erythrocyte MDA, oxidized LDL-MDA (oxLDL-MDA), fibrinogen, CRP, PMNL levels and plasma SOD activities (r = 0.69, P < 0.01; r = 0.64, P < 0.01; r = 0.38, P < 0.05; r = 0.65, P < 0.01; r = 0.34, P < 0.05; r = 0.34, P < 0.05; r = 0.53, P < 0.01, r = 0.34, P < 0.05; r = -0.67, P < 0.01, respectively). On the other hand, t(lag) was correlated negatively with the levels of VLDL-TG, VLDL-TC and LDL-TG but positively correlated with the levels of TAS in psoriatics (r = -0.49, P < 0.01; r = -0.49, P < 0.01, r = -0.65, P < 0.05; r = 0.37, P < 0.05). CONCLUSIONS: It was concluded that the psoriatic patients could be considered as a group with an increased atherosclerotic risk because of increased oxidant stress, decreased antioxidant capacity and susceptibility in lipid profile and lipoprotein content to atherogenicity.