Semi-industrial production of a minimally processed infant formula powder using membrane filtration.

Infant formula (IF) is submitted to several heat treatments during production, which can lead to denaturation or aggregation of proteins and promote Maillard reaction. The objective of this study was to investigate innovative minimal processing routes for the production of first-age IF powder, thus ensuring microbial safety with minimal level of protein denaturation. Three nutritionally complete IF powders were produced at a semi-industrial scale based on ingredients obtained by fresh bovine milk microfiltration (0.8 and 0.1-µm pore size membranes). Low-temperature vacuum evaporation (50°C) and spray-drying (inlet and outlet temperatures of 160 and 70°C, respectively) were conducted to produce the T- formula with no additional heat treatment. The T+ formula was produced with a moderate heat treatment (75°C for 2 min) applied before spray-drying, whereas the T+++ formula received successive heat treatments (72°C for 30 s on the milk; 90°C for 2-3 s before evaporation; 85°C for 2 min before spray-drying), thus mimicking commercial powdered IF. Protein denaturation and Maillard reaction products were followed throughout the production steps and the physicochemical properties of the powders were characterized. The 3 IF powders presented satisfactory physical properties in terms of aw, free fat content, glass transition temperature, and solubility index, as well as satisfactory bacteriological quality with a total flora <103 cfu/g and an absence of pathogens when a high level of bacteriological quality of the ingredients was ensured. Protein denaturation occurred mostly during the heat treatments of T+ and T+++ and was limited during the spray-drying process. The IF powder produced without heat treatment (T-) presented a protein denaturation extent (6 ± 4%) significantly lower than that in T+++ (58 ± 0%), but not significantly different from that in T+ (10 ± 4%). Although T- tended to contain less Maillard reaction products than T+ and T+++, the Maillard reaction products did not significantly discriminate the infant formulas in the frame of this work. The present study demonstrated the feasibility of producing at a semi-industrial scale an infant formula being bacteriologically safe and containing a high content of native proteins. Application of a moderate heat treatment before spray-drying could further guarantee the microbiological quality of the IF powders while maintaining a low protein denaturation extent. This study opens up new avenues for the production of minimally processed IF powders.

[Advanced glycation end products: A risk factor for human health]. / Les produits de glycation avancée : un risque pour la santé humaine.

Advanced glycation end products (AGE) result from a chemical reaction between the carbonyl group of reducing sugar and the nucleophilic NH2 of a free amino acid or a protein; lysine and arginine being the main reactive amino acids on proteins. Following this first step, a molecular rearrangement occurs, rearrangement of Amadori resulting to the formation of Maillard products. Glycation can cause the clouding of the lens by inducing reactions crosslinking proteins. Specialized receptors (RAGE, Galectin 3…) bind AGE. The binding to the receptor causes the formation of free radicals, which have a deleterious effect because they are powerful oxidizing agents, but also play the role of intracellular messenger, altering the cell functions. This is especially true at the level of endothelial cells: the attachment of AGE to RAGE receptor causes an increase in vascular permeability. AGE binding to endothelium RAGE and to monocytes-macrophages, led to the production of cytokines, growth factors, to the expression of adhesion molecules, and the production of procoagulant activity. Diabetic retinopathy is related to excessive secretion of vascular growth factor (vascular endothelial growth factor [VEGF]). AGE-RAGE receptor binding causes the synthesis and secretion of VEGF. Increased permeability, facilitation of leukocyte migration, the production of reactive oxygen species, cytokines and VEGF suggest that the AGE could be an element of a cascade of reactions responsible for the diabetic angiopathy and vascular damages observed during aging and chronic renal failure. Balanced diet or some drugs can limit the deleterious effect of AGE.

Early- and life-long intake of dietary advanced glycation end-products (dAGEs) leads to transient tissue accumulation, increased gut sensitivity to inflammation, and slight changes in gut microbial diversity, without causing overt disease.

Dietary advanced glycation end-products (dAGEs) accumulate in organs and are thought to initiate chronic low-grade inflammation (CLGI), induce glycoxidative stress, drive immunosenescence, and influence gut microbiota. Part of the toxicological interest in glycation products such as dietary carboxymethyl-lysine (dCML) relies on their interaction with receptor for advanced glycation end-products (RAGE). It remains uncertain whether early or lifelong exposure to dAGEs contributes physiological changes and whether such effects are reversible or permanent. Our objective was to examine the physiological changes in Wild-Type (WT) and RAGE KO mice that were fed either a standard diet (STD - 20.8 ± 5.1 µg dCML/g) or a diet enriched with dCML (255.2 ± 44.5 µg dCML/g) from the perinatal period for up to 70 weeks. Additionally, an early age (6 weeks) diet switch (dCML→STD) was explored to determine whether potential harmful effects of dCML could be reversed. Previous dCML accumulation patterns described by our group were confirmed here, with significant RAGE-independent accumulation of dCML in kidneys, ileum and colon over the 70-week dietary intervention (respectively 3-fold, 17-fold and 20-fold increases compared with controls). Diet switching returned tissue dCML concentrations to their baseline levels. The dCML-enriched diet had no significative effect on endogenous glycation, inflammation, oxidative stress or senescence parameters. The relative expression of TNFα, VCAM1, IL6, and P16 genes were all upregulated (∼2-fold) in an age-dependent manner, most notably in the kidneys of WT animals. RAGE knockout seemed protective in this regard, diminishing age-related renal expression of TNFα. Significant increases in TNFα expression were detectable in the intestinal tract of the Switch group (∼2-fold), suggesting a higher sensitivity to inflammation perhaps related to the timing of the diet change. Minor fluctuations were observed at family level within the caecal microbiota, including Eggerthellaceae, Anaerovoracaceae and Marinifilaceae communities, indicating slight changes in composition. Despite chronic dCML consumption resulting in higher free CML levels in tissues, there were no substantial increases in parameters related to inflammageing. Age was a more important factor in inflammation status, notably in the kidneys, while the early-life dietary switch may have influenced intestinal susceptibility to inflammation. This study affirms the therapeutic potential of RAGE modulation and corroborates evidence for the disruptive effect of dietary changes occurring too early in life. Future research should prioritize the potential influence of dAGEs on disease aetiology and development, notably any exacerbating effects they may have upon existing health conditions.

Glycated bovine serum albumin for use in feeding trials with animal models - In vitro methodology and characterization of a glycated substrate for modifying feed pellets.

This study investigated different methods to produce Nε-carboxymethyl-lysine (CML)-enriched bovine serum albumin (BSA) as alternatives to the classical approach using glyoxylic acid (GA) and sodium cyanoborohydride (NaBH3CN) which results in toxic hydrogen cyanide (HCN). The reaction of GA (6 mmol/L) and NaBH3CN (21 mmol/L) to produce CML remained the most effective with CML yields of 24-35%, followed by 13-24% using 300 mmol/L glyoxal (GO). GA promoted specific modification of lysine to CML, and fewer structural modifications of the BSA molecule compared with GO, as evidenced by fluorescence and proteomic analyses. GO promoted greater arginine modification compared with GA (76 vs 23%). Despite structural changes to BSA with GO, murine fecal clearance of CML was similar to literature values. Hence, BSA glycation with 300 mmol/L glyoxal is a suitable alternative to GA and NaBH3CN for generating CML-enriched protein free of HCN, but a CML-only fortification model remains to be described.

Radiation shielding materials and radiation scatter effects for interventional radiology (IR) physicians.

PURPOSE: To measure the attenuation effectiveness and minimize the weight of new non-Pb radiation shielding materials used for radiation protection by interventional radiology (IR) physicians, to compare the accuracy of the different standard measurement geometries of these materials, and to determine x-ray qualities that correspond to the scattered radiation that IR physicians typically encounter. METHODS: Radiation attenuation capabilities of non-Pb materials were investigated. Typically, most studies of non-Pb materials have focused on the attenuating properties of metal powders. In this study, layers of materials incorporating non-Pb powdered compounds such as Bi(2)O(3), Gd(2)O(3), and BaSO(4) were measured individually, as bilayers, and as a Bi(2)O(3)-loaded hand cream. Attenuation measurements were performed in narrow-beam (fluorescence excluded) and broad beam (fluorescence included) geometries, demonstrating that these different geometries provided significantly different results. The Monte Carlo (MC) program EGSnrc was used to calculate the resulting spectra after attenuation by radiation shielding materials, and scattered x-ray spectra after 90° scattering of eight ASTM Standard primary x-ray beams. Surrogate x-ray qualities that corresponded to these scattered spectra were tabulated. RESULTS: Radiation shielding materials incorporating Bi(2)O(3) were found to provide equivalent or superior attenuation compared with commercial Pb-based and non-Pb materials across the 60-130 kVp energy range. Measurements were made for single layers of the Bi(2)O(3) compound and for bilayers where the ordering was low atomic number (Z) layer closest to x-ray source∕high Z (Bi(2)O(3)) layer farthest from the x-ray source. Narrow-beam Standard test methods which do not include the contribution from fluorescence overestimated the attenuating capabilities of Pb and non-Pb materials. Measurements of a newly developed, quick-drying, and easily removable Bi(2)O(3)-loaded hand cream demonstrated better attenuation capabilities than commercial Bi(2)O(3)-loaded gloves. Scattered radiation measurements and MC simulations illustrated that the spectra resulting from 90° scattering of primary x-ray beam qualities can be approximated by surrogate x-ray qualities which are more representative of the radiation actually encountered by IR physicians. A table of surrogate qualities of the eight ASTM F2547-06 Standard qualities was compiled. CONCLUSIONS: New non-Pb compound materials, particularly single layers or bilayers incorporating Bi(2)O(3), can reduce the weight of radiation protection materials while providing equivalent or better protection compared to Pb-based materials. Attenuation measurements in geometries that exclude the contribution from fluorescence substantially underestimate the quantity of transmitted radiation. A new Bi(2)O(3)-loaded hand cream demonstrated a novel and effective approach for hand protection. Standard testing protocols for radiation protection materials used by IR physicians specify a wider kVp range than is necessary. A more realistic range would acknowledge the lower kVp resulting from scatter and allow IR physicians to confidently utilize lighter-weight materials while still receiving adequate protection. Standards protocols incorporating the adjustments described in this work would maintain the safety of IR personnel and lessen the physical repercussions of long hours wearing unnecessarily heavy radiation protection garments.

The Maillard reaction in the human body. The main discoveries and factors that affect glycation.

Ever since the discovery of the Maillard reaction in 1912 and the discovery of the interaction between advanced glycation end-products and cellular receptors, impressive progress has been made in the knowledge of nonenzymatic browning of proteins in vivo. This reaction which leads to the accumulation of random damage in extracellular proteins is known to have deleterious effects on biological function, and is associated with aging and complication in chronic diseases. Despite a controlled membrane permeability and a protective regulation of the cells, intracellular proteins are also altered by the Maillard reaction. Two main factors, protein turnover and the concentration of carbonyls, are involved in the rate of formation of the Maillard products. This paper reviews the key milestones of the discovery of the Maillard reaction in vivo, better known as glycation, and the factors which are likely to affect it.

EGSnrc calculation of activity calibration factors for the Vinten ionization chamber.

The National Physical Laboratory Vinten 671 chamber was selected as a proving ground for a new radionuclide source model in the EGSnrc software. The computational Vinten model is validated against measurements of radionuclide artifacts whose activities were determined by absolute methods. The response of the Vinten chamber is first calculated as a function of gamma energy, but more strikingly, an explicit simulation of radionuclide decay was implemented and now permits the direct determination of a calibration factor, including additional effects due to all decay paths of the radionuclide. The Monte Carlo and experimental calibration factors are found to agree at the percent level, in absolute terms.

Carbamylation is a competitor of glycation for protein modification in vivo.

AIM: Chronic kidney disease (CKD) and diabetes mellitus are two diseases that accelerate protein molecular ageing through carbamylation and glycation reactions, characterized by the binding of urea-derived isocyanic acid and of sugars on proteins, respectively. These two reactions target the same protein amino groups and, thus, compete with each other. Such competition may arise especially in diabetic patients with nephropathy. This study aimed to evaluate their potential competitive effects in vitro and under conditions reproducing CKD and/or diabetes in vivo. METHODS: Albumin was incubated in vitro with glucose, urea or cyanate. Carbamylation in vivo was enhanced in normal and diabetic (db/db) mice by either subtotal nephrectomy or cyanate consumption. Homocitrulline, carbamylated haemoglobin and furosine were measured by LC-MS/MS, fructosamine by colorimetric assay and HbA1c by immunological assay. RESULTS: Reciprocal inhibition between carbamylation and glycation was observed during albumin incubations in vitro. Besides, 5 weeks after induction of CKD in vivo, plasma homocitrulline concentrations were similar in both diabetic and non-diabetic mice, whereas fructosamine and HbA1c were decreased (-23% and -42%, respectively) in diabetic mice with CKD compared with only diabetic ones. Fructosamine and HbA1c were also decreased in cyanate-spiked water-drinking mice compared with plain water-drinking diabetic mice. CONCLUSION: Carbamylation competes with glycation in vivo, especially under conditions of high glycation. Thus, the classic markers of glycaemic control should be interpreted with caution in diabetic patients with CKD because of this competitive effect.

Free glutamine as a major precursor of brown products and fluorophores in Maillard reaction systems.

Glutamine is one of the most abundant free amino acid found in raw food. In this study, the contribution of free glutamine to nonenzymatic browning and fluorescence was investigated using an aqueous model system with methylglyoxal. The results indicated that glutamine contributed to the Maillard reaction via two pathways. First, the hydrolysis of the amide bond of glutamine led to the release of ammonia which was implicated in the formation of brown color and fluorescence. Among other nitrogen donors tested (asparagine, glutamic acid and urea) our results demonstrated that free glutamine was a major source of ammonia during heating. When heated at 120 and 180 degrees C, 100% of ammonia was released from glutamine after 60 and 10 min, respectively. The second pathway involved a direct Maillard reaction with the alpha-amino group of glutamine. Both pathways led to a rapid and complete destruction of glutamine when heated in the model systems. With reference to the Maillard browning (absorbance at 420 nm) glutamine turned out to be the most reactive amine, followed by asparagine, glutamate, ammonia and urea. Maximum fluorescence (excitation and emission wavelengths at 330 and 450 nm, respectively) was also observed with glutamine followed by urea and ammonia. Overall this study suggested that free glutamine predominantly contributes to the color and fluorescence formations of foodstuffs.

Fecal excretion of Maillard reaction products and the gut microbiota composition of rats fed with bread crust or bread crumb.

A comparison between the impacts of advanced (Nε-carboxymethyllysine - CML) and terminal (melanoidins) Maillard reaction products from bread on gut microbiota was carried out in this study. Gut microbiota composition as well as fecal excretion of CML from both bread crust and bread crumb, and of melanoidins from bread crust were assessed on a rodent model. Rats were fed with pellets supplemented or not with 13% of bread crust, bread crumb, a fiber-free bread crust model (glucose, starch and gluten heated together) or a fiber-free-melanoidin-free bread model (glucose-starch and gluten heated separately) for four weeks. These model systems were developed to limit the presence of wheat-native dietary fibers such as cellulose, hemicelluloses and lignin. CML and melanoidins in pellets and feces were evaluated by LC/MS-MS and HPLC/fluorescence respectively, and gut microbiota composition was determined by cultivation and molecular approaches. Diets supplemented with crumb or the fiber-free-melanoidin-free model contained respectively 17% and 64% less melanoidins than their respective controls. A higher excretion of melanoidins was observed for rats fed with crust or bread crust model compared to their controls, confirming that melanoidins are in contact with gut microbiota. No impact of diets was observed on Firmicutes, Bacteroidetes and lactic flora. A decrease of enterobacteria was only observed for rats fed with the diet supplemented with the fiber-free bread crust model. Moreover, a significant increase of bifidobacteria numbers in the presence of crust, crumb and both bread models was observed, showing that this bifidogenic effect of bread is not due to the presence of melanoidins or wheat-native dietary fibers.

Factors Generating Glucose Degradation Products In Sterile Glucose Solutions For Infusion: Statistical Relevance Determination Of Their Impacts.

Sterilising glucose solutions by heat promotes the generation of a large number of glucose degradation products (GDPs). It has been shown that high levels of GDPs may result in Advanced Glycation End products that have an impact on cellular homeostasis and health in general. If data is available for peritoneal dialysis solutions, little has been published for glucose infusion fluids. It is essential to identify the parameters causing the formation of GDPs and so limit the risk of exposing patients to them. After quantifying both 5-hydroxymethyl-2-furfural, considered as an important indicator of degradation, and 2-furaldehyde, an ultimate GDP of one degradation pathway, in marketed solutions, the aim of this work is to build a model integrating all the parameters involved in the formation rates of these two GDPs: supplier, glucose amount, container material, oxygen permeability coefficient and time-lapse since manufacture. Our results show a good logarithmic relationship between GDP formation rates and time-lapse since manufacture for both GDPs. The amount of GDPs in the glucose solutions for infusion depends on the initial glucose amount, the polymer of the container, the time elapsed since manufacturing and the supplier.

[Spinal stereotactic body radiotherapy: French assessment in 2016]. / État des lieux de la radiothérapie en conditions stéréotaxiques vertébrale en France en 2016.

PURPOSE: Stereotactic body radiotherapy to vertebral column remains uncommon practice and only relevant in selected group of patients. The main objective of the study was to describe the current state of medical practices of stereotactic body radiotherapy to vertebral column in France in 2016 and to assess the diversity of practices to identify areas for improvement and establish a common database set for this technique. MATERIALS AND METHODS: A questionnaire was written with contribution of a medical physicist, a radiation oncologist, an information technologist and a radiotherapy resident. The questionnaire was distributed online to a radiation oncologists and a medical physicists partner of selected French radiotherapy specialized centres that provide stereotactic body radiotherapy to vertebral metastasis from April to June 2016. The questionnaire surveyed the following topics: patients' selection, simulation, targeted volume and organs at risk delineation, prescription, dosimetric implementation and image guidance. RESULTS: A total of 31 centres were surveyed. Seventy eight per cent of centres (n=21) completed the questionnaire. The "ideal" patient for spine stereotactic radiotherapy according to these institutions has a good performance status, a long life expectancy, controlled primary tumour with oligometastatic spread. The most prescribed protocol was 30Gy in three fractions. For clinical target volume delineation, about two thirds of centres used the International Spine Radiosurgery Consortium (ISRC) recommendations (Noël G et al.,2006). CONCLUSION: This study identified some consistency of practices in some aspects despite the lack of consensus guidelines. Nevertheless, further studies are needed to establish consensus of planning and treatment.

Age-related macular degeneration and antioxidant status in the POLA study. POLA Study Group. Pathologies Oculaires Liées à l'Age.

OBJECTIVE: To give the levels of antioxidant nutrients in relation to age-related macular degeneration (AMD). METHODS: Pathologies Oculaires Liees a l'Age is a population-based study on cataract and AMD and their risk factors, carried out on 2584 inhabitants of Sete, France. Age-related macular degeneration was defined by findings from fundus photographs according to an international classification. Biological measurements were taken from fasting blood samples. RESULTS: After multivariate adjustment, plasma alpha-to-copherol levels showed a weak negative association with late AMD (P = .07). Lipid-standardized plasma alpha-tocopherol levels showed a significant negative association with late AMD (P= .003): the risk of late AMD was reduced by 82% in the highest quintile compared with the lowest. Similarly, lipid-standardized plasma alpha-tocopherol levels were inversely associated with early signs of AMD (odds ratio, 0.72 [95% confidence interval, 0.53-0.98]; P=.04). No associations were found with plasma retinol and ascorbic acid levels or with red blood cell glutathione values. COMMENT: These results suggest that vitamin E may provide protection against AMD. Only randomized interventional studies could prove the protective effect of vitamin E on AMD.

Outcome of fetuses diagnosed with atrioventricular septal defect.

OBJECTIVE: To quantify the association of prenatally diagnosed atrioventricular septal defect with Down syndrome and to evaluate its impact on obstetric and neonatal outcomes. METHODS: Charts of 42 cases of atrioventricular septal defect diagnosed by fetal echocardiography from July 1985 to July 1997 were reviewed for prenatal history and outcome data (pregnancy outcome, pathologic confirmation, postnatal echocardiographic findings, and neonatal outcome). Statistical analysis was done using Fisher exact test and odds ratios. RESULTS: The mean gestational age at diagnosis was 26 weeks. Four cases could not be confirmed antenatally on repeat echocardiograms and were excluded. Reasons for referral of the remaining 38 fetuses included an abnormal four-chamber view in 76%. Twenty-two fetuses (58%) had abnormal karyotypes: 19 trisomy 21, one trisomy 18, one trisomy 13, and one mosaicism. The cardiac lesions were isolated in 20 fetuses (53%). After excluding cases of termination, ten of 12 fetuses (83%) with Down syndrome survived, compared with seven of 13 (54%) with normal karyotypes (P = .125). The odds of trisomy 21 were 16 times higher (95% confidence interval 3.0, 85.3) in fetuses with isolated cardiac lesions compared with those with associated cardiac anomalies. CONCLUSION: Prenatal diagnosis of atrioventricular septal defect was associated with a 58% risk of aneuploidy (mainly trisomy 21). Down syndrome fetuses with this cardiac anomaly appeared to have a better survival rate than fetuses with normal karyotypes. Our sample did not have enough power to show a statistically significant difference. When an isolated atrioventricular septal defect was diagnosed prenatally, the odds of trisomy 21 were significantly higher than when other associated cardiac lesions were diagnosed. This information should be considered in prenatal counseling for atrioventricular septal defect.

Lack of effect of copper on advanced Maillard reaction and glucose autoxidation at physiological concentrations of albumin.

This study examines the possible action of copper on advanced glycation. Copper has been shown to induce fluorescence due to advanced-glycated-end-products (AGEs) on albumin incubated with glucose, and this was interpreted as activation of the glucose or Amadori product (AP) autoxidation. We glycated albumin (60 g/L) to several levels with increasing concentrations of glucose. The dialysed glucose-free glycated albumin was then incubated with 1.5 µmol/L copper or 1 mmol/L diethylenetriaminepentaacetic acid (DTPA), plus or minus glucose. The production of AP, measured as furosine, was similar whether DTPA or copper was present in the incubation medium. It linearly increased as a function of time and glucose concentration in both cases up to a maximum (furosine around 20 mmol/g protein), indicating saturation of the free NH2 residues on the protein. The fluorescence due to AGEs increased linearly over time for glycated albumin incubated without glucose, and exponentially when glucose was added to the incubation medium. This fluorescence was also unaffected by DTPA or copper for a glucose concentration below 125 mmol/L and initial furosine below 10 mmol/g. However copper caused a slight activation in samples with very high glucose (1.25 mol/L) and furosine (30-40 mmol/g) concentrations. We therefore find no effect of copper in this experiment, because the copper concentration is lower and the albumin higher than that used in previous studies. In these conditions, albumin chelates copper and inhibits its oxidative activity. The protein concentrations used in most in vitro studies showing a copper effect were below 10 g/L with copper often above 10 µmol/L, so that copper may act oxidatively. As the lens and arterial wall have high protein concentrations, copper should have no action on protein glycation in vivo, unless altered protein structure impedes the inactivation of copper by chelation.

Selenium and training effects on the glutathione system and aerobic performance.

Changes in blood glutathione antioxidant system in response to exercise and training, and aerobic performance, were investigated. Selenium (Se) supplementation effects on these changes were evaluated. The study was double blind. Both groups selenium (Sel, N = 12) and placebo (Pla, N = 12), followed a 10-wk endurance training program, with a prolonged exhaustive exercise bout performed (Cap Max), before (Pre) and after (Post) training. Blood was sampled before (Bef) and after (Aft) Cap Max. The oxidation of blood glutathione after Cap Max exercise showed a reactive oxygen species production. Training developed maximal aerobic power and capacity, significantly increased (P < 0.001) plasma and erythrocyte glutathione peroxidase (GPx) activity, and decreased (P < 0.001) erythrocyte glutathione reductase activity. The Se supplementation caused an increase in the basal plasma GPx level (P < 0.05). There was also a correlation (r = 0.66, P < 0.05) between the variation in VO2max and that of erythrocyte GPx only in supplemented subjects. Our results confirm that blood glutathione remains a sensitive marker of oxidative stress induced by exhausting submaximal exercise and that the antioxidant potential of GPx can be developed by endurance training. Se supplementation at the dose used had no effect on physical performance.

Effects of endurance training on skeletal muscle oxidative capacities with and without selenium supplementation.

The purpose of this study was to examine the changes induced by endurance training, with or without selenium (Se) supplementation on: 1) mitochondrial activity of succinate dehydrogenase (SDH) and cytochrome c oxidase (Cyt Ox),2) the myosin heavy chain (MHC) expression in muscle fibers and 3) their association with aerobic performance. Twenty-four male students volunteered to participate in this double blind study: selenium (Sel, N = 12) vs placebo (Pla, N = 12). During a 10-wk endurance training program, the Sel group received a daily Se supplementation containing 180 micrograms of organic selenium (selenomethionine), while the Pla group received a placebo. Before (Pre) and after (Post) the program (3 sessions wk-1) an endurance exercise (Capmax) was performed in order to determine the aerobic endurance capacity assessed by the total oxygen uptake during the running test (VO2tot). All parameters of aerobic performance were increased in both groups, concomitantly to a rise in mitochondrial Cyt Ox activity. Two positive relationships were found: 1) between type I MHC and VO2tot increments (r = 0.65, P < 0.05), 2) between training volumes and VO2tot increments (r = 0.53, P < 0.05; N = 23). The training program produced an 8.2% significant increase in type I MHC (P < 0.05) while type II MHC decrease was not significant (-4.4%). Although they were almost non-existent before the program, muscle fibers which co-expressed type I and II MHC displayed a marked increase afterwards (4.9 +/- 5.7 vs 1.1 +/- 2.1%, P < 0.05). Muscle GSH-Px activity, at rest, did not respond to endurance training or Se supplementation. The results suggest that the neuromuscular system is still in an evolutive state after 10 weeks of endurance training, and that selenium supplementation has no effect on endurance training-induced adaptations.

Antioxidant vitamins and degenerative pathologies. A review of vitamin C.

In this review we describe how tissues are protected against free radicals and we detail the mechanisms by which the insufficient reduction of ascorbate is involved in glycation and oxidation processes on proteins.

Muscle GSH-Px activity after prolonged exercise, training, and selenium supplementation.

A double-blind study of the effects of supplementing with selenium vs. placebo on the physiological responses to acute and chronic exercise was conducted in 24 healthy, nonsmoking males, mean age 22.9 +/- 2.1 yr, randomly divided into two groups of 12 (Pla/Sel). After a controlled period in the absence of training, all subjects were put on an individualized endurance training program with the same rules of progression and overload (3 sessions/wk x 10 wk). Supplementation, either real (240 micrograms of organic selenium/d in Sel group) or imaginary (Pla group) was administered during the same period. In each of the conditions Pre- and Post- (training +/- sel supplementation), muscle, plasma, and systemic parameters were determined before (BF) and after (AF) acute exercise, involving the repetition of muscle work cycles separated by 5-min recovery periods, combining 20 min at 65% and a maximal duration of 100% VO2 max of running on a treadmill, leading the subjects to exhaustion between 2 h 40 min and 3 h 30 min. Changes in parameters as a function of three independent variables: 1. Acute exercise (E); 2. Chronic exercise (T); and 3. Selenium supplementing (S) were tested with ANOVA and the Student's t-test on paired series. Among the variables examined, muscle glutathione peroxidase (GPx) presented a remarkable behavior.(ABSTRACT TRUNCATED AT 250 WORDS)

Decrease in vitamin C concentration in human lenses during cataract progression.

Cataract formation is believed to result from an oxidative insult which decreases the antioxidant defense of the lens, particularly the vitamin C concentration. Upon oxidation, vitamin C contributes with glucose to protein glycation. It also favours tryptophan oxidation, resulting in fluorescent peptide cross-links and protein insolubilisation. The relationship between cataract and lenticular vitamin C was analysed in 48 cataractous lens nuclei classified into four severity grades, considering the sum of the colour and opacity. Ascorbic and dehydroascorbic acids were quantified by HPLC-fluorescence. The Amadori product was measured by means of furosine, advanced glycation end products by their fluorescence and tryptophan concentration by HPLC-UV. The lens vitamin C concentration significantly decreased with cataract severity, but mostly in severe brown cataracts (around 88 mumol/100 g lens in mild cataracts, and 50 mumol/100 g in dark brown lenses). The dehydroascorbic acid concentration was always low and stable (1.9 +/- 0.9 mumol/100 g), as was the furosine concentration (0.4 +/- 0.1 mumol/g). The fluorescence of insoluble advanced glycated end products was significantly higher in severe cataracts than in milder ones. The peptide tryptophan content was stable but the tryptophan to tyrosine ratio decreased and was highly correlated to the ascorbic acid concentration. Vitamin C content appears to be a good indicator of cataract severity, suggesting that oxidation could take part in cataract progression.