Highly potent antioxidant Olea europaea L. leaf extract affects carotid and renal haemodynamics in experimental hypertension

Haemodynamic alterations in carotid and renal arteries are associated with the severity of target organ damage in patients with hypertension. Dietary habits, such as the Mediterranean diet, regulate blood pressure and oxidative stress, thus reduce the mortality rate due to cardiovascular diseases. In this study, our aim was to evaluate the reducing activity, antioxidant capacity and metal chelating ability of standardized Olea europaea L. leaf extract (OLE), and to test its (5, 25, 50 mg/kg) acute in vivo effects, as well as oleuropein’s (OP, 10 mg/kg) on oxidative stress, carotid, renal and systemic haemodynamic parameters (blood pressure, heart rate, cardiac output, peripheral resistance) in spontaneously hypertensive rats (SHR). OLE has a higher antioxidative capacity than BHT, higher reducing ability than vitamin C, and 23 times lower capacity for metal ion chelation than EDTA. All three doses of OLE, and OP, improved oxidative stress in SHR. OLE5 improved carotid and renal haemodynamics, without significant effects on systemic haemodynamics. Two different mechanisms of antihypertensive responses to OLE were observed, OLE25 was most effective in reducing cardiovascular risks by improving systemic and regional (carotid and renal) haemodynamics, peripheral and regional vascular resistance. OLE50 causes the improvement of blood pressure and cardiac performances, but tends to retain elevated vascular resistance, therefore, reducing the inflow of blood into the brain and kidneys of the SHR. The OP did not alter systemic or regional haemodynamics, suggesting others constituents responsible for changes of cardiac function, as well as carotid and renal haemodynamics in response to OLE50

Effects of losartan, tempol, and their combination on renal nitric oxide synthases in the animal model of chronic kidney disease

Down-regulation of nitric oxide synthase (NOS) and NO defi ciency in the kidneys have been implicated in the pathogenesis of chronic kidney disease (CKD). In this study we examined the effects of losartan, tempol, and combined treatment on three NOS isoforms expressions, kidney NO content and NOS correlation with renal function and structure in the early stage of adriamycin (ADR)-induced CKD in spontaneously hypertensive rats (SHR). Rats were divided into control group, and four other groups which were treated with ADR and received vehicle, losartan (L, angiotensin II type 1 receptor blocker), tempol (T, redox-cycling nitroxide) or T + L treatment (by gavage) in a six-week study. Reduction of all NOS isoforms expressions were signifi cantly improved by losartan or tempol, and correlated with proteinuria amelioration. Combined treatment induced down-regulation of constitutive NOS isoforms, whilst inducible NOS was up-regulated and followed by increased nitrite content and a signifi cant decline in the glomerular fi ltration rate. Losartan or tempol prevented ADR-induced neoexpression of vimentin in the glomeruli and tubulointerstital areas, whereas de novo vimentin expression was still observed in the atrophic tubules and in the interstitial fi broblasts and myofi broblasts in combined treatment. It can be concluded that single treatments, contrary to combined, were effective in improving NO bioavailability and slowing down the progression of CKD

Losartan Improved Antioxidant Defense, Renal Function and Structure of Postischemic Hypertensive Kidney

Ischemic acute renal failure (ARF) is a highly complex disorder involving renal vasoconstriction, filtration failure, tubular obstruction, tubular backleak and generation of reactive oxygen species. Due to this complexity, the aim of our study was to explore effects of Angiotensin II type 1 receptor (AT1R) blockade on kidney structure and function, as well as oxidative stress in spontaneously hypertensive rats (SHR) after renal ischemia reperfusion injury. Experiments were performed on anaesthetized adult male SHR in the model of ARF with 40 minutes clamping the left renal artery. The right kidney was removed and 40 minutes renal ischemia was performed. Experimental groups received AT1R antagonist (Losartan) or vehicle (saline) in the femoral vein 5 minutes before, during and 175 minutes after the period of ischemia. Biochemical parameters were measured and kidney specimens were collected 24h after reperfusion. ARF significantly decreased creatinine and urea clearance, increased LDL and lipid peroxidation in plasma. Treatment with losartan induced a significant increase of creatinine and urea clearance, as well as HDL. Lipid peroxidation in plasma was decreased and catalase enzyme activity in erythrocytes was increased after losartan treatment. Losartan reduced cortico-medullary necrosis and tubular dilatation in the kidney. High expression of pro-apoptotic Bax protein in the injured kidney was downregulated after losartan treatment. Our results reveal that angiotensin II (via AT1R) mediates the most postischemic injuries in hypertensive kidney through oxidative stress enhancement. Therefore, blockade of AT1R may have beneficial effects in hypertensive patients who have developed ARF

Cell wall invertase immobilisation within gelatin gel

Yeast cell wall invertase (CWI) was immobilised within 10% gelatin hydrogel. The result of entrapment was the complete immobilisation of all the added CWI. The activity of immobilised biocatalyst was 93 +/- 3 U/g, with activity yield of 30%. The optimum pH was in range of 4.5-5.0 for free and immobilised biocatalyst. The optimum temperature was 60 degrees C for both free and gelatin immobilised CWI. Immobilised CWI was more stable than free CWI above optimum activity temperatures. The K-m of free and immobilised CWI was 35.10 +/- 2.99 mM and 71.45 +/- 3.23 mM, respectively. The V-max, values were estimated as 8.23 +/- 0.24 mM/min and 0.121 +/- 0.002 mM/min, respectively. Immobilised CWI was tested in a batch reactor using 50% sucrose (w/v). After 70 consecutive cycles gelatin immobilised CWI retained 75% of its original activity. (C) 2010 Elsevier Ltd. All rights reserved

Improving the confectionery industry supply chain through second party audits

Purpose - The purpose of this paper is to evaluate benefits and constraints of improving suppliers' quality and food safety systems through second party audits. Design/methodology/approach - A quantitative quality and food safety audit tool was developed to perform second party audits within the confectionery industry supply chain. Nine flourmills and four food packaging producers were included in the audit program. Initial audits were performed at the beginning of the program, with follow-up audits performed after one year. Findings - Level of implementation of food safety and quality requirements were presented as scores. Flourmills improved their scores from 38.6 to 64.4 percent during the period of two years. In contrast, at the end of the second year, food packaging producers showed a lower level of improvement from 34.0 to 45.6 percent. This research confirmed that certification status does not imply high performance of a quality/food safety system. Companies experienced problems in identifying processes, setting performance indicators and objectives and implementing problem solving tools. Quality control has been identified as a dimension where most companies do not document their control methods and have no method in place to verify consistency in their results. Control of risks in terms of Hazard Analysis Critical Control Point implementation was identified as the main food safety constraint. Research limitations/implications - Limitations of the research stein from the use of results from one part of the confectionery supply chain, from auditing a limited number of companies and from excluding the technological level of the audited companies, Practical implications This study provides a valuable insight for quality and/or food safety assurance managers on benefits of using second party audits as a supply chain developing tool. Originality/value - The, findings of this study are worthy, as second party audits are identified as slow but effective tools in directing suppliers toward improvements

Immunohistochemical Pattern of Histone H2A Variant Expression in an Experimental Model of Ischemia–Reperfusion-Induced Acute Kidney Injury

Ischemia–reperfusion injury (IRI) is a frequent cause of AKI, resulting in vasoconstriction, cellular dysfunction, inflammation and the induction of oxidative stress. DNA damage, including physical DNA strand breaks, is also a potential consequence of renal IRI. The histone H2A variants, primary H2AX and H2AZ participate in DNA damage response pathways to promote genome stability. The aim of this study was to evaluate the immunohistochemical pattern of histone H2A variants’ (H2AX, γH2AX(S139), H2AXY142ph and H2AZ) expression in an experimental model of ischemia–reperfusion-induced acute kidney injury in spontaneously hypertensive rats. Comparing the immunohistochemical nuclear expression of γH2AX(S139) and H2AXY142ph in AKI, we observed that there is an inverse ratio of these two histone H2AX variants. If we follow different regions from the subcapsular structures to the medulla, there is an increasing extent gradient in the nuclear expression of H2AXY142ph, accompanied by a decreasing nuclear expression of γH2AX. In addition, we observed that different structures dominated when γH2AX and H2AXY142ph expression levels were compared. γH2AX was expressed only in the proximal tubule, with the exception of when they were dilated. In the medulla, H2AXY142ph is predominantly expressed in the loop of Henle and the collecting ducts. Our results show moderate sporadic nuclear H2AZ expression mainly in the cells of the distal tubules and the collecting ducts that were surrounded by dilated tubules with PAS (periodic acid–Schiff stain)-positive casts. These findings may indicate the degree of DNA damage, followed by postischemic AKI, with potential clinical and prognostic implications regarding this condition

Antioxidant enzymes activities in kidney among the experimental groups.

<p>SOD—superoxide dismutase, CAT—catalase, and GSH-Px—glutathione peroxidase. *<i>p<0</i>.<i>05</i>, **<i>p<0</i>.<i>01</i>, ***<i>p<0</i>.<i>001</i> vs. SHC; ^#<i>p<0</i>.<i>05</i>, ^###<i>p<0</i>.<i>001</i> vs. SHADR; ^$<i>p<0</i>.<i>05</i>, ^$ $<i>p<0</i>.<i>01</i>, ^$ $$<i>p<0</i>.<i>001</i> vs. SHADR+L; ^&&<i>p<0</i>.<i>01</i> vs. SHADR+T; n = 8 animals per group. Data represent mean ± SEM. SHC—control group, SHADR–SHR treated with adriamycin, L—losartan, T—tempol.</p