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Background: The metabolic syndrome is characterized by abnormalities in the metabolism of lipids and glucose, and its major complications are cardiovascular disease and type 2 diabetes mellitus. It has been proposed that oxidative stress is related with metabolic syndrome. Objective: To relate the markers of oxidative stress in patients with clinical expression of metabolic syndrome. Material and method: An observational, cross-sectional and prospective study was done in 50 women of 30-50 years of age, with diagnosis of metabolic syndrome according to the criteria established by ATP-III. Results: The groups with three, four and five metabolic syndrome components showed significant differences in systolic blood pressure, glucose, triglycerides and high-density lipoprotein cholesterol blood levels, respectively, finding a statistically significant negative association with total plasma antioxidant capacity between groups. Conclusions: The finding that total plasma antioxidant system decreases as the number of components of the metabolic syndrome increases indicates that having a smaller provided antioxidant defense is associated with increased clinical expression of metabolic syndrome, highlighting the adaptation system of patients with metabolic syndrome who, despite the condition indicated, do not show oxidative damage. [ABSTRACT FROM AUTHOR]

This paper analyzes the patterns of health biotechnology publications in six Latin American countries from 2001 to 2015. The countries studied were Argentina, Brazil, Chile, Colombia, Cuba and Mexico. Before our study, there were no data available on HBT development in half of the Latin-American countries we studied, i.e., Argentina, Colombia and Chile. To include these countries in a scientometric analysis of HBT provides fuller coverage of HBT development in Latin America. The scientometric study used the Web of Science database to identify health biotechnology publications. The total amount of health biotechnology production in the world during the period studied was about 400,000 papers. A total of 1.2% of these papers, were authored by the six Latin American countries in this study. The results show a significant growth in health biotechnology publications in Latin America despite some of the countries having social and political instability, fluctuations in their gross domestic expenditure in research and development or a trade embargo that limits opportunities for scientific development. The growth in the field of some of the Latin American countries studied was larger than the growth of most industrialized nations. Still, the visibility of the Latin American research (measured in the number of citations) did not reach the world average, with the exception of Colombia. The main producers of health biotechnology papers in Latin America were universities, except in Cuba were governmental institutions were the most frequent producers. The countries studied were active in international research collaboration with Colombia being the most active (64% of papers co-authored internationally), whereas Brazil was the least active (35% of papers). Still, the domestic collaboration was even more prevalent, with Chile being the most active in such collaboration (85% of papers co-authored domestically) and Argentina the least active (49% of papers). We conclude that the Latin American countries studied are increasing their health biotechnology publishing. This strategy could contribute to the development of innovations that may solve local health problems in the region. [ABSTRACT FROM AUTHOR]

Abstract The increment of eryptosis in lead-exposed workers has been associated with oxidative stress, having as the main mediator [Ca2+] i. However, other molecules could participate as signals, such as PLA 2 and SMase, which have been proposed to increase PGE 2 and ceramides, both involved in the increment of PS externalization due to osmotic stress. To study the role of these enzymes in lead intoxication, we studied 30 lead exposed workers and 27 non-lead exposed individuals. We found, compared to non-exposed subjects, lead intoxication characterized by high blood lead concentration (median = 39.1 μg/dL), and low δ -ALAD activity (median = 348 nmol of porphobilinogen/h/mL); oxidative stress with high lipid peroxidation (median = 1.31 nmol of malondialdehyde/mL) and low TAC (median = 370 mM Trolox equivalents); a higher enzymatic activity of PLA 2 (median = 518 AFU/mg) and SMase (median = 706 AFU/mg) and higher eryptosis (median = 0.92% PS externalization). Correlation and conditional probability analyses permit to associate oxidative stress and eryptosis with high PLA 2 activity. However, high SMase activity was only associated with PLA 2 activity. The role of these enzymes in the signal path to eryptosis induced by oxidative stress in lead-exposed workers is discussed. Highlights • Lead exposition induces high blood lead concentration in workers • Lead intoxication in workers is characterized by low δ-ALAD activity • Lead exposed workers have cellular oxidative damage and low antioxidant state • Phosphatidylserine exposure is induced by oxidative stress in lead exposed workers • PLA 2 and SMase are mediators of eryptosis associated with oxidative stress [ABSTRACT FROM AUTHOR]

Chronic lead exposure can generate pro-oxidative and pro-inflammatory conditions in the blood, related to high platelet activation and aggregation, altering cell functions. We studied ADP-stimulated aggregation and the oxidant/antioxidant system of platelets from chronically lead-exposed workers and non-exposed workers. Platelet aggregation was low in lead-exposed workers (62 vs. 97%), who had normal platelet counts and showed no clinical manifestations of hemostatic failure. ADP-activated platelets from lead-exposed workers failed to increase superoxide release (3.3 vs. 6.6 µmol/g protein), had low NADPH concentration (60 vs. 92 nmol/mg protein), high concentration of hydrogen peroxide (224 vs. 129 nmol/mg protein) and high plasma PGE 2 concentration (287 vs. 79 pg/mL). Altogether, those conditions, on the one hand, could account for the low platelet aggregation and, on the other, indicate an adaptive mechanism for the oxidative status of platelets and anti-aggregating molecules to prevent thrombotic problems in the pro-oxidant and pro-inflammatory environment of chronic lead exposure. • Chronically lead-exposed workers have lower levels of platelet aggregation than non-exposed workers. • Platelets from lead-exposed workers failed to increase superoxide release in response to ADP-activation. • Platelets from lead-exposed workers showed an adaptive mechanism related to the oxidant/antioxidant system. • Lead-exposed workers have elevated plasma PGE 2 levels, which contribute to the platelet's adaptive response. [ABSTRACT FROM AUTHOR]

Eryptosis is a physiological phenomenon in which old and damaged erythrocytes are removed from circulation. Erythrocytes incubated with lead have exhibited major eryptosis. In the present work we found evidence of high levels of eryptosis in lead exposed workers possibly via oxidation. Blood samples were taken from 40 male workers exposed to lead (mean blood lead concentration 64.8 μg/dl) and non-exposed workers (4.2 μg/dl). The exposure to lead produced an intoxication characterized by 88.3% less δ-aminolevulinic acid dehydratase (δALAD) activity in lead exposed workers with respect to non-lead exposed workers. An increment of oxidation in lead exposed workers was characterized by 2.4 times higher thiobarbituric acid-reactive substance (TBARS) concentration and 32.8% lower reduced/oxidized glutathione (GSH/GSSG) ratio. Oxidative stress in erythrocytes of lead exposed workers is expressed in 192% higher free calcium concentration [Ca 2 + ] i and 1.6 times higher μ-calpain activity with respect to non-lead exposed workers. The adenosine triphosphate (ATP) concentration was not significantly different between the two worker groups. No externalization of phosphatidylserine (PS) was found in non-lead exposed workers (< 0.1%), but lead exposed workers showed 2.82% externalization. Lead intoxication induces eryptosis possibly through a molecular pathway that includes oxidation, depletion of reduced glutathione (GSH), increment of [Ca 2 + ], μ-calpain activation and externalization of PS in erythrocytes. Identifying molecular signals that induce eryptosis in lead intoxication is necessary to understand its physiopathology and chronic complications. [ABSTRACT FROM AUTHOR]

Highlights: [•] We founded beneficial effects of vitamin E/C supplementation in lead exposed workers. [•] Lead intoxication was accompanied by high oxidative damage and antioxidant response. [•] Vitamin supplementation (E 400IU+C 1g/daily, one year) decreases oxidative damage. [•] Antioxidant supplementations decreased the oxidative damage and antioxidant capacity. [ABSTRACT FROM AUTHOR]

Lead intoxication can generate pro-inflammatory conditions that have been proposed to be associated with cell injuries and oxidative stress. The pro-inflammatory state can participate in the pathophysiology of this toxicity to generate immune response dysfunctions, which could condition the presence of clinical manifestations and susceptibility to infections already described in lead-exposed patients. In the present work, we study workers of a battery recycler factory (n = 24) who are chronically exposed to lead and compared them with non‐lead exposed workers (n = 17). Lead-exposed workers had high lead concentrations in blood (med 69.8 vs. 1.7 μg/dL), low δ-ALAD activity (med 149 vs. 1100 nmol PBG/h/mL), high lipid peroxidation (med 0.86 vs. 0.69 nmol/mL) and high erythrocytes apoptosis (med 0.81 vs. 0.50% PS externalization) in relation to non‐lead exposed workers. Also, lead-exposed workers had a high incidence of signs and symptoms related to lead intoxication and a higher frequency of infections. The higher leukocyte apoptosis (med 18.3 vs. 8.2% PS externalization) and lower basal TNF-α concentration (med 0.38 vs. 0.94 pg/mL) in lead-exposed workers imply an immune response dysfunction; however, there was no difference in the TNF-α concentration when leukocytes were stimulated with lipopolysaccharide in whole blood (med 44 vs. 70 pg/mL), suggesting that lead-exposed workers might develop adaptation mechanisms to reduce basal TNF-α release through downregulation processes proposed for this cytokine. • Lead-intoxicated workers have oxidative damage and apoptosis in erythrocytes • Leukocyte apoptosis is high in lead-exposed workers • Intoxicated workers have low Tumor Necrosis Factor-alpha (TNF-α) concentrations • Lipopolysaccharide-stimulated TNF-α concentration is lead exposure independent • Lead-intoxicated workers suffer a high infection frequency [ABSTRACT FROM AUTHOR]