Member area login

You don't have or don't remember the password!
Click Here

Editor-in-chief
Maria Stella Graziani

Deputy Director
Martina Zaninotto

Associate Editors
Ferruccio Ceriotti
Davide Giavarina
Bruna Lo Sasso
Giampaolo Merlini
Martina Montagnana
Andrea Mosca
Paola Pezzati
Rossella Tomaiuolo
Matteo Vidali

EIC Assistant
Francesco Busardò

International Advisory Board Khosrow Adeli Canada
Sergio Bernardini Italy
Marcello Ciaccio Italy
Eleftherios Diamandis Canada
Philippe Gillery France
Kjell Grankvist Sweden
Hans Jacobs The Netherlands
Eric Kilpatrick UK
Magdalena Krintus Poland
Giuseppe Lippi Italy
Mario Plebani Italy
Sverre Sandberg Norway
Ana-Maria Simundic Croatia
Tommaso Trenti Italy
Cas Weykamp The Netherlands
Maria Willrich USA
Paul Yip Canada

Publisher
Biomedia srl
Via L. Temolo 4, 20126 Milano

Responsible Editor
Giuseppe Agosta

Editorial Secretary
Chiara Riva
Biomedia srl
Via L. Temolo 4, 20126 Milano
Tel. 0245498282
email: biochimica.clinica@sibioc.it

--------------------

ISSN print: 0393 – 0564
ISSN digital: 0392- 7091

BC: Articoli scritti da G. Nordera

Serial measurements of oxidative stress markers after ozone autohemotherapy

A. Bolner \| L. Chiamenti \| G. Nordera \| O. Bosello \|
<p>Background: the ozone autohemotherapy (O3-AHT) is an alternative medical practice where an aliquot of patient's blood is treated with an ozone-oxygen mixture (O3/O2), and reinfused to induce an hormetic effect, that is to obtain a mild oxidative stress that empowers the antioxidant response and improves the oxidative balance. The customization of the ratio O3/O2 and the amount of blood is a crucial aspect of this therapy. The measure of some biomarkers of oxidative balance may be useful to calibrate the treatment and avoid damages.<br />Methods: O3-AHT was performed on 9 volunteers healthy subjects, treating 150 g of blood with 30 μg/mL O3/mL O2/g. Aliquots of blood and urine were collected before therapy (t0), and 4, 8, 24 and 48 hours (t4-t48) after reinfusion to measure the derivates of reactive oxygen metabolites (dROMs), the biological antioxidant potential (BAP), the single components of antioxidant barrier coenzyme Q10, and glutathione in both total (GSH+GSSG) and reduced (GSH) forms, the oxidative biomarkers homocysteine (Hcy), 8-hydroxy-deoxyguanosine (8-OHdG) and 2-deoxyguanosine (2-dG) and the nitrative biomarker 3-nitrotyrosine (3-NT).<br />Results: within the first 4-8 hours after O3-AHT, as dROMs increased, the median of GSH had an initial considerable decrease (-20% at t8 versus t0) followed by a final net increase (+12% at t48). In a similar way, 3-NT had an initial decrease (-19% at t4) followed by a remarkable increase at t8 and t24 (+28% and +57% respectively) and a subsequent important decrease at t48 (-44%), which led to final nitration levels lower than the one observed at t0.<br />Conclusions: When used in correct concentrations, O3 induces a moderate oxidative stress which initially consumes antioxidant species and produces nitrative damages. Within 24-48 hours however, the beginning of a virtuous counter-regulatory response that increases the reducing power (particularly GSH levels) and decreases molecular damages, improving the redox balance, can be observed. Serial measurements of GSH and 3-NT, allow to monitor that the induced oxidative stress causes only moderate and transient damages, and help the physician to choose the more effective O3 therapeutic concentrations.</p>
Biochimica Clinica ; 44(4) 374-379 Contributi Scientifici - Scientific Papers

Effetti della restrizione calorica sullo stress ossidativo nell'obesità: sono miglioramenti transitori?
Effect of caloric restriction on oxidative stress in obesity: are these transient improvements?
A. Bolner \| A. Vanzo \| D. Giavarina \| G. Nordera \| O. Bosello \|
<p>Background: the effects of caloric restriction (CR) on oxidative stress in obesity has been previously studied using markers that not always were able to describe all the components of the oxidative-inflammatory picture.<br />Methods: in this study, the redox state of 20 obese was evaluated at baseline and after 30 and 60 days of CR using a complete panel of markers: the majority of them were determined using HPLC methods.<br />Results: before CR (V0), serum peroxides (dROMs) were very high, total antioxidant barrier (BAP) was at the lower limit of the reference interval and C-reactive protein (hsCRP) was increased; on the opposite, glutathione was well within the reference intervals in both total and reduced form. Despite the imbalance of the dROMs/BAP equilibrium, the markers of oxidative damage, such 3-nitrotyrosine (3NT) and 8-hydroxy-deoxyguanosine (8OHdG), index of a mild oxidative-inflammatory imbalance, were not particularly relevant.<br />After 30 days of CR (V30), in addition to the slight improvements of glucose, fructosamine and HOMA-IR, hsCRP was decreased, while BAP and total glutathione were increased, with consequent improvement of the oxidative stress-inflammatory balance (oxidative-inflammation). After 60 days of CR (V60) the improvements observed at V30 appeared to be slowing down for glucose and fructosamine, in slight inverse tendency for HOMA-IR and hsCRP, and decreasing for BAP and glutathione. The slight increase of inter-quartile range (IQR) of 3NT showed a lower counter-regulatory antioxidant response capacity, as if the ameliorative effects of CR in the first period had turned off.<br />Conclusion: the improvements of the oxidative-inflammatory equilibrium appear to be transient in the course of CR. The rearrangements of the gut microbiota during CR and the consequent epigenetic modulations could be responsible for this peculiar trend.</p>
Biochimica Clinica ; 44(3) 232-238 Contributi Scientifici - Scientific Papers

Obesità, microbiota e stress ossidativo
Obesity, microbiota and oxidative stress
A. Vanzo \| A. Bolner \| G. Nordera \| O. Bosello \|
<p>Only in recent years, scientific societies and governments of many countries have considered obesity and its precursors, namely overweight, such as a disease that causes other diseases and reduces life quality and expectancy. According to the latest researches, obesity is a complex disease, with multifactorial etiology, not exclusively linked to eating disorders and lifestyle, which contribute inflammatory, infectious, toxic and also mental phenomena. Among many pathogenetic and pathophysiological invoked mechanisms, the effects of oxidative stress have recently received special attention. The imbalance between the production of free oxygen and nitrogen radicals and the physiological contrast mechanisms could actually play a causal role in the development of obesity by stimulating the deposition of white adipose tissue and altering the assumption of food. Oxidative stress and systemic inflammation are also key factors in the pathogenesis of obesity-related diseases, including atherosclerosis, insulin resistance, type 2 diabetes and cancer. Despite the correlation between obesity and oxidative stress, none of the biochemical markers of oxidative damage can be considered predictive of obesity; on the contrary, some markers seem to predict the development and progression of cardiovascular and metabolic disease in overweight and obese subjects. Recent observations also demonstrate the existence of quantitative and qualitative differences in the intestinal microbiota between individuals at high and low risk of development of obesity and related complications. Therefore, the intestinal microbiota might play a key role in the pathogenesis of obesity.</p>
Biochimica Clinica ; 41(3) 199-207 Rassegne - Reviews

Armonizzazione in Medicina di Laboratorio
Harmonization in Laboratory Medicine
F. Ceriotti \| M. Panteghini \| A. Tosetto \| V. Valentini \| L. Politi \| R. Rolla \| T. Guastafierro \| T. Köken \| E. Capoluongo \| C. Mazzaccara \| V. D'Argenio \| V. D'Argenio \| G. Lippi \| M. Plebani \| D. Giavarina \| M. Berardi \| A survey on sample matrix and preanalytical management in clinical laboratories \| D. Bozzato \| G. Messeri \| M. Zaninotto \| M. Vidali \| A. Padoan \| G. Parigi \| A. Clerico \| L. Sciacovelli \| M. Ciaccio \| G.L. Salvagno \| G. Barberio \| G. Barberio \| G.L. Salvagno \| M. Pepe \| M. Panteghini \| F. Braga \| G. Gessoni \| M. Montagnana \| N. Doğan \| M. Barberis \| M. Barberis \| A. Marchetti \| F. Borrillo \| L. Bonfanti \| P.M. Ness \| G. Messeri \| S. Nannini \| J. Queraltò \| M. Zaninotto \| A. Mosca \| BM. Henry \| G. Santini \| A. Coglianese \| V. D'Argenio \| E. Fiorio \| L. Crinò \| M. A. V. Willrich \| A. Modenese \| M. Berardi \| G. Nordera \| M. Girelli \| R. Tomaiuolo \| D. Giavarina \| R. Dittadi \| L. Pighi \| V. Guaraldo \| G. Bambagiotti \| E. Franceschini \| R. Danesi \| M. Locatelli \| F. Balboni \| D. Cosseddu \| M. Savoia \| S. Bernardini \| C. Domenichini \| M. Lamonaca \| M. Perrone \| M. Perrone \| per il Gruppo di Studio Intersocietario SIBioC-SIPMeL Diabete Mellito \| P. Pradella \| A. Padoan \| M.T. Sandri \| L. Belloni \| A. D'Avolio \| T. Trenti \| A. Fortunato \| T. Trenti \|

Biochimica Clinica ; 39(6) 546-547 Editoriale - Editorial