Dustri Online Services

Abstract

C.B. Tsiamis

Medicine Department, School of Medicine, Athens, Greece
Hypokinesia (diminished movement) is a factor of catabolism induction which may be developed, whenever there is a significant reduction of physical load on skeletal muscle system. Hypokinesia (HK) may occur due to age, disease, disability and sedentary living and working conditions. Among the effects of HK, the changes in fluid and electrolytes (sodium, chloride, potassium, phosphorus, calcium and magnesium) homeostasis and in particular in fluid and electrolyte deposition (ability of the body to use electrolytes and fluid after all fluid and electrolyte loss have been established) have been of the greatest interest. This is due to the higher fluid and electrolyte loss with higher than lower fluid and electrolyte depletion and the recent interest on fluid and electrolyte homeostasis and fluid and electrolyte deposition under sedentary living and working conditions. Stable volume, osmotic concentration and electrolyte composition of internal fluid is one of the mandatory prerequisites for humans to maintain adequate physiological and biochemical condition and a highly efficient physical state. However, physiological and biochemical systems that regulate the concentration of each electrolyte in blood and other endogenous fluids, and the balance between the consumption and elimination of electrolytes from the body and thus total electrolyte content of the body are drastically affected. At present some information has been accumulated about the effect of prolonged HK on fluid and electrolyte homeostasis and fluid and electrolyte loss with fluid and electrolyte depletion. To this end, the aim of this review was to report the findings on the fluid and electrolyte homeostasis and fluid-electrolyte loss with whole body fluid and electrolyte depletion.Correspondence to:
Dr. C.B. Tsiamis
Odos Kerasundos 2-4, 162 32 Athens, Greece
Email: cbtsiamis@in.gr

Abstract

G. Forte¹, A. Alimonti¹, N. Violante¹, G. Sancesario², L. Brusa² and B. Bocca¹

¹Department of Environment and Primary Prevention, Istituto Superiore di Sanità, Rome and ²Department of Neuroscience, University of Tor Vergata, Rome, Italy
The etiology of Parkinson’s disease (PD) is still not fully clear, but several studies have implicated metals as cofactors of risk. To assess a potential imbalance in the trace elements concentration of hair of subjects affected by PD, the content of Al, Ba, Cd, Co, Cr, Hg, Mn, Mo, Pb, Sn, Sr and Zr in 81 patients affected by PD and 17 age-matched controls was determined. Quantification of the elements was performed by inductively coupled plasma mass spectrometry. Results indicated significantly lower levels of Pb in the hair of patients (p £ 0.05) compared with controls. Manganese was slightly higher while Ba, Sn and Sr levels were lower in patients, although these differences were not significant, no variations in Al, Cd, Co, Cr, Mo and Zr levels were observed in PD. Barium and Sr in hair were higher in women than in men in both controls and patients. In addition, again Ba and Sr of patients decreased with age with a p < 0.01 for both elements. Finally, a decreased value of Pb with the duration and the severity of the disease and Hg with the severity duration of the pathology were observed.Correspondence to:
A. Alimonti, MD
Department of Environment and Primary
Prevention, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy
Email: alessandro.alimonti@iss.it

Abstract

T. Nasu and R. Urakawa

Department of Veterinary Pharmacology, Faculty of Agriculture, Yamaguchi University, Yamaguchi, Japan
At concentrations higher than 0.01 mM, Cu²⁺ induced dose-dependent contraction without the participation of neural elements in guinea pig taenia coli. Cu²⁺, at 0.1 mM, induced maximal tension of about 80% of hypertonic 60 mM K⁺-induced tonic tension 25 min after the application. The contraction in response to Cu²⁺ was dependent on extracellular Ca²⁺ and persisted for more than several h. After the application of Cu²⁺ at above 5 mM in Ca²⁺-free medium, the contractile response following the addition of Ca²⁺ in the presence of Cu²⁺ decreased rapidly, as the duration of pretreatment with Cu²⁺ in Ca²⁺-free medium increased. This suggests that under the condition of the failure of the contractile response by Cu²⁺ application in Ca²⁺-free medium, Cu²⁺ inhibits some sites involved in the contractile process, while Cu²⁺ itself above 2 mM induced small contractions even in Ca²⁺-free medium. The small contraction in response to 5 mM Cu²⁺ itself in Ca²⁺-free medium was barely affected by pretreatment with caffeine, a Ca²⁺ induced Ca²⁺ release activator of the sarcoplasmic reticulum or verapamil, an L-type Ca²⁺ channel blocker. In conclusion, Cu²⁺ induced direct contractile responses that involved the inhibitory action in guinea pig taenia coli. High concentrations of Cu²⁺ itself, above 2 mM, induced small contractions independent of Ca²⁺ and could affect the contractile system.Correspondence to:
Prof. T. Nasu
Department of Veterinary Pharmacology, Faculty of Agriculture, Yamaguchi University,
Yamaguchi 753, Japan
Email: nasu@yamaguchiu.ac.jp

Abstract

T. Nasu and J. Nobuhara

Department of Veterinary Pharmacology, Faculty of Agriculture, Yamaguchi University, Yamaguchi, Japan
Mn²⁺, at 5 mM, induced a large tension development in isotonic 126 mM K⁺ medium in taenia coli of guinea pig, although Na⁺ was not contained in the external medium. The contraction by 5 mM Mn²⁺ in isotonic 126 mM K⁺, Na⁺-deficient medium was more sensitive to inhibition by monoiodoacetic acid (glyceraldehyde-3-phosphate dehydrogenase inhibitor in glycolysis), but was more resistant to inhibition by 2,4-dinitrophenol (uncoupler of mitochondrial ATP production) than was the contraction by Mn²⁺ in hypertonic 60 mM K⁺, Na⁺-sufficient medium. Presumably, this indicates that the contraction by Mn²⁺ in isotonic 126 mM K⁺, Na⁺-deficient medium is dependent on energy supplied via glycolysis rather than that via aerobic metabolism in mitochondria.Correspondence to:
Prof. T. Nasu
Department of Veterinary Pharmacology, Faculty of Agriculture, Yamaguchi university, Yamaguchi 753, Japan
Email: nasu@yamaguchi-u.ac.jp

Abstract

J. Brandão-Neto, A. Conceição Ribeiro Dantas Saturnino, L. Dantas Leite, É. Dantas de Medeiros Rocha, C. Maria Passos Marcos, C.A. Bruno da Silva, J. Sérgio Marchini, A.A. de Rezende, M. das Graças Almeida and A. da Cunha Medeiros

Multidisciplinary Laboratory, Chronic Degenerative Diseases, Centro de Ciências da Saúde, Universidade Federal do Rio Grande do Norte, Natal-RN, Brazil
There is an interrelationship between zinc and thyroid hormones, but the mechanisms surrounding this topic are unclear. The aim of this study was to investigate the effect of a single venous dose of zinc on plasma thyroid-stimulating hormone (TSH), free triiodothyronine (FT₃), and free tetraiodothyronine (FT₄) in 10 healthy individuals, 5 of each sex. All of these individuals were studied after 25 mg zinc was administered intravenously for 1 min, at 8:00 a.m., after a 12-h fast. Blood samples were collected at –30, 0, 3, 30, 60, 90 and 120 min. There were no changes in the plasma levels of TSH, FT₃ and FT₄ in both groups studied after zinc administration. This study suggests that zinc in pharmacological doses does not significantly affect the hypothalamic pituitary thyroid axis in healthy individuals. The aim of the present study was to study the plasma profile of TSH, FT₃ and FT₄ following a single venous dose of zinc in healthy individuals, since zinc is a metal that affects thyroid hormone functions at several levels.Correspondence to:
J. Brandão-Neto, MD, PhD
Laboratório Multidisciplinar, Centro de Ciências da Saúde, UFRN, Natal-RN, CEP 59 010-180, Brazil
Email: jbn@ppgcsa.com.br

Abstract

A. Meißner¹, B. Nebe², R. Beck³, R. Guthoff³ and T. Noack¹

¹Institute of Physiology, Medical Faculty, ²Department of Internal Medicine, Clinical Research, ³Department of Ophthalmology, University of Rostock, Germany
Background: To prevent posterior capsule opacification (PCO), we followed the hypothesis that calcium channel blockers (antagonists) interfere with integrin signaling and block cell adhesion in lens epithelial cells (LEC). In primary human LEC we found that the T channel antagonist mibefradil induces apoptosis which was accompanied with cell shape changes and loss of cell adhesion. Although T-type calcium channels are substantially present in membranes of freshly dispersed primary cultured hLEC and calcium currents are inhibited by mibefradil at concentrations of 10^–8 M, the antiproliferative site of action of this drug remains unclear, since this feature is observed at concentrations 200-fold higher than that for calcium channel blockade. Methods: Epithelial cells of the human lens were dispersed by enzymatic treatment, recordings of membrane currents were performed using patch clamp technique in the whole cell configuration. Westernblot analysis was used for protein detection. Results: Total current elicited on depolarizing voltage steps from a holding potential of –80 mV was composed of inward (calcium) and outward (potassium) current. Outward current could be inhibited mostly by intracellular application of cesium ions. Currents in inward direction were activated fast (< 2 ms) and inactivated during the following 20 ms. They were characterized as calcium currents since the known calcium channel inhibitor nifedipine blocked these currents in a concentration-dependent manner. Using potassium in the pipette (145 mM) as main charge carrier, additionally a noninactivating potassium current and a voltage- and time-dependent potassium current which slowly inactivated (Kv) were observed (control). Adding mibefradil in concentrations from 10^–6 M – 10^–5 M to the bath solution, the inwardly directed and the non-inactivating current component were inhibited concentration-dependent. The Kv component was affected in a similar way, however, this component showed an increased inactivation behavior after application of mibefradil in the named concentrations. Conclusion: The total effects of mibefradil are significant for the calcium homeostasis since calcium current itself is inhibited but, moreover, the membrane is permanently depolarized up to 20 mV by the drug. Both effects may contribute to the observed reduced cell adhesion during mibefradil treatment.Correspondence to:
Prof. Dr. T. Noack
Department of Physiology, Gertrudenstraße 9,
University of Rostock, 18055 Rostock, Germany

Email: thomas.noack@uni-rostock.de

Abstract

G. Slapsyte¹,², J. Mierauskiene¹, V. Morkunas¹, G. Prasmickiene² and J. Didziapetriene²

¹Vilnius University, Ciurlionio ²¹/²⁷,
²Institute of Oncology, Vilnius University, Vilnius, Lithuania
Objective: The present study was carried out to evaluate the modifying effects of sodium selenite on adriamycin- and cyclophosphamide-induced chromosome damage and changes of antioxidant status in rats. Materials and methods: Wistar rats were treated with a single dose of adriamycin (5 mg/kg b.w.) or cyclophosphamide (30 mg/kg b.w.) by the intraperitoneal route. Sodium selenite was administered via gavage at a dose of 0.5 mg/kg b.w. once a day for 3 consecutive days before or after drug treatment. The cytogenetic endpoints screened were chromosome aberrations and micronuclei in rat bone marrow cells. Parameters of the oxidant/antioxidant status in rats included the activities of catalase and superoxide dismutase and the level of lipid peroxidation product malondialdehyde. Results: No significant increase of chromosome damage was determined in animals treated with sodium selenite alone. The protective effect of sodium selenite was dependent on the treatment schedule and the drug used. Chromosome aberration analysis revealed significant antimutagenic effect of sodium selenite against cyclophosphamide-induced chromosome damage in animals pretreated with sodium selenite, and against adriamycin-induced clastogenicity in animals posttreated with sodium selenite (p < 0.05). We determined significant correlation between chromosome damage and malondialdehyde level on an individual animal basis. In conclusion, our results revealed the antimutagenic potential of sodium selenite against adriamycin- and cyclophosphamide-induced chromosome damage in rat bone marrow cells, and the importance to tailor antimutagenicity treatment schedule to the individual class of drugs, or even drugs.Correspondence to:
Dr. G. Slapsyte
Vilnius University, Ciurlionio 21/27, LT-03101 Vilnius,
Lithuania
Email: grazina.slapsyte@gf.vu.lt

Abstract

K. Kisters¹, V. Rempel¹, I. Kabar¹, M. Cziborra¹, C. Funke¹, F. Wessels¹, F. Tokmak², B. Gremmler³, J. Büntzel⁴, H. Liebscher⁴ and M. Hausberg⁴

¹Medizinische Klinik I, St. Anna Hospital Herne,
²Nephrologie, Marienhospital Herne, Ruhr Universität Bochum, ³Kardiologie, Marienhospital Bottrop and ⁴AKTE, Bielefeld, Germany
Lowered Mg⁺⁺ stores in humans seem to be involved in the pathogenesis of essential hypertension. However, some antihypertensive drugs (e.g. in particular diuretics) can additionally decrease plasma or intracellular Mg⁺⁺ stores. In this context, the role of the new antihypertensive angiotensin II antagonists has not been studied in detail as yet, as long-term studies have not already been performed yet. In the study presented here, 20 essential hypertensive patients were monotreated with various angiotensin II antagonists (eprosartan, irbesartan, lorsatan, valsartan, candesartan). In each patient, plasma Mg⁺⁺ concentrations were studied before, under, and after therapy (36 ± 3 months). The results showed no significant difference in plasma Mg⁺⁺ and K⁺ concentrations in essential hypertensives before, under, and after a long-term treatment with various sartans. In conclusion, a monotherapy with various angiotensin II antagonists concerning Mg⁺⁺ and K⁺ handling is safe and reduces blood pressure significantly.Correspondence to:
Prof. Dr. K. Kisters
Medizinische Klinik I, St. Anna-Hospital, Hospitalstraße 19, 44649 Herne, Germany
Email: kisters@annahospital.de

Abstract

Kongressleitung: Prof. em. Dr. P. Eckermann (Rostock),
Prof. Dr. K. Kisters (Herne/Münster),
Prof. Dr. G. Kraatz (Greifswald),
Prof. Dr. T. Noack (Rostock),
PD Dr. R. Schubert (Rostock),
Prof. Dr. W. Zidek (Berlin)

Abstract

K. Kisters, M. Czibowa, C. Funke, A. Liebscher and D. H. Liebscher

Shopping Overview
Type	Qtty	Price
Your basket is empty

Username:
Password:

Volume 24, No. 4/2007(4th Quarter)