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The increment of eryptosis in lead-exposed workers has been associated with oxidative stress, having as the main mediator [Ca 2+ ] 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., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Arterial hypertension is a disease that often coexists with dyslipidemia. Both disorders can produce oxidative stress. Studies in vivo and in vitro have proven that oxidative stress can induce an increment of the erythrocyte apoptosis (eryptosis), through the rise of free intracellular calcium concentration ([Ca 2+ ] i ). Higher levels of eryptosis have not been described in patients with hypertension, dyslipidemia, or both combined. This study involved 81 men between 26 and 50 years old, assorted into four groups: normotensive with and without dyslipidemia, and hypertensive with and without dyslipidemia. Hypertensive and/or dyslipidemic patients had double mean lipid peroxidation and 30% less mean GSH concentration than the normotensive non-dyslipidemic patients. Mean [Ca 2+ ] i in hypertensive patients was 100 and 200% higher, in patients without and with dyslipidemia, respectively, compared to normotensive patients. Dyslipidemic normotensive patients had three times higher mean PS externalization than the normotensive non-dyslipidemic patients, and the hypertension condition doubled this difference. Hypertensive patients had higher eryptosis associated with higher levels of [Ca 2+ ] i and oxidative stress, suggesting that eryptosis participates in the pathophysiological mechanisms of hypertension. The quantitative analysis, when the dyslipidemic factor is included, shows that oxidative stress-[Ca 2+ ] i -eryptosis do not follow a unique pattern in the different groups and suggests the existence of mechanisms of induction and molecular pathways alternative or additional to oxidative stress and [Ca 2+ ] i , respectively.

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]

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]