Peripheral biomarkers as a predictor of poor prognosis in severe cases of COVID-19.

We evaluated glycemia and triglyceride, hepatic, muscular, and renal damage markers, redox profile, and leptin and ghrelin hormone levels of COVID-19 patients. We also realized statistical analysis to verify the potential of biomarkers to predict poor prognosis and the correlation between them in severe cases. We assessed glycemia and the levels of triglycerides, hepatic, muscular, and renal markers in automatized biochemical analyzer. The leptin and ghrelin hormones were assessed by the ELISA assay. Severe cases presented high glycemia and triglyceride levels. Hepatic, muscular, and renal biomarkers were altered in severe patients. An oxidative stress status was found in severe COVID-19 patients. Severe cases also had increased levels of leptin. The ROC curves indicated many biomarkers as poor prognosis predictors in severe cases. The Spearman analysis showed that biomarkers correlate between themselves. Patients with COVID-19 showed significant dysregulation in the levels of several peripheral biomarkers. We bring to light that a robust panel of peripheral biomarkers and hormones predict poor prognosis in severe cases of COVID-19, as well as correlates between them. Early monitoring of these biomarkers may conduct the correct clinical intervention associated with the clinical symptoms for treating patients infected by SARS-CoV-2.

COVID-19, Anxiety, and Body Mass Index Increase Leptin Levels: a Cross-sectional Multicentric Study.

Although many efforts have been made to understand the pathophysiological mechanisms of COVID-19, critical gaps remain to be explored. This study aimed to investigate potential alterations in adipokine levels (specifically adiponectin, leptin, and resistin) among individuals with COVID-19. Within this population, we further assessed the association between these markers with both, body mass index (BMI) and psychiatric symptoms. This cross-sectional study included an age- and sex-matched sample of adults with COVID-19 (cases) and without COVID-19 (controls). We evaluated the severity of psychiatric symptoms, BMI, and adipokines. Individuals with COVID-19 presented greater BMI, stress levels, and leptin levels when compared to controls. Leptin levels were greater in individuals with moderate/severe COVID-19 as compared to individuals with COVID-19 who were asymptomatic or having mild symptoms. Leptin levels were positively correlated with BMI, severity of depressive and anxiety symptoms, and stress levels in the total sample. Leptin levels were also positively correlated with BMI, severity of anxiety symptoms, and stress levels in controls. In cases, there was a positive correlation between adiponectin and the severity of depressive symptoms and stress levels and leptin/resistin with BMI. A linear regression model revealed that BMI, severity of anxiety symptoms, and the diagnosis of COVID-19 are independently associated with increased leptin levels. Thus, leptin levels seem to be impacted by the COVID-19 infection, anxiety, and BMI.

ABO Blood Type and Metabolic Markers in COVID-19 Susceptibility and Severity: A Cross-Sectional Study.

Background and Aims: To evaluate the effect of the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) virus on the function and metabolic changes, as well as the relationship of the virus with blood groups. Methods and Results: This cross-sectional study included a matched sample of adult individuals with coronavirus disease 2019 (COVID-19) (n = 114) or without (controls; n = 236). Blood samples were collected and processed for triglycerides (TGs), total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol, and blood typing analysis. The results showed that subjects with COVID-19 had higher TG and lower HDL-C levels compared with the control group. As for blood typing, the risk of COVID-19 was higher in subjects with blood group A than in those with blood group B and in those with other blood groups. In addition, an association of COVID-19 with blood type and Rh A- was observed. When related to the severity of COVID-19 symptoms, blood type A was more protective against moderate/severe symptoms compared with blood type O. In addition, individuals with blood type O were 2.90 times more likely to have symptoms moderate/severe symptoms of COVID-19 than those with other blood groups and individuals with type A blood were less likely to have severe/moderate symptoms of COVID-19 compared with individuals without type A blood. Conclusion: The results suggest that blood type may play a role in susceptibility to SARS-CoV-2 infection and add evidence that infection with the novel coronavirus may be associated with changes in lipid metabolism.

Stress levels, psychological symptoms, and C-reactive protein levels in COVID-19: A cross-sectional study.

BACKGROUND: Although many studies have pointed out a possible relationship between COVID-19 and the presence of psychiatric disorders, the majority of the studies have significant limitations. This study investigates the influence of COVID-19 infection on mental health. METHODS: This cross-sectional study included an age- and sex-matched sample of adult individuals positive (cases) or negative (controls) for COVID-19. We evaluated the presence of psychiatric conditions and C-reactive protein (CRP). RESULTS: Findings showed greater severity of depressive symptoms, higher levels of stress, and greater CRP in cases. The severity of depressive and insomnia symptoms, as well as the CRP were more remarkable in individuals with moderate/severe COVID-19. We found a positive correlation between stress and severity of anxiety, depression, and insomnia in individuals with or without COVID-19. There was a positive correlation between CRP levels and severity of depressive symptoms in cases and controls, and a positive correlation between CRP levels and the severity of anxiety symptoms and stress levels only in individuals with COVID-19. Individuals with COVID-19 and depression had greater CRP than those with COVID-19 without current major depressive disorder. LIMITATIONS: We cannot infer causality because this is a cross-sectional study, and the majority of COVID-19 sample was asymptomatic or had mild symptoms, which may limit the generalizability of our findings for moderate/severe cases. CONCLUSIONS: Individuals with COVID-19 showed greater severity of psychological symptoms, which may impact on the development of psychiatric disorders in the future. CPR seem to be a promising biomarker for earlier detection of post-COVID depression.

Action of the Purinergic and Cholinergic Anti-inflammatory Pathways on Oxidative Stress in Patients with Alzheimer's Disease in the Context of the COVID-19 Pandemic.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiologic agent of the 2019 coronavirus disease (COVID-19), has affected more than 20 million people in Brazil and caused a global health emergency. This virus has the potential to affect various parts of the body and compromise metabolic functions. The virus-mediated neural inflammation of the nervous system is due to a storm of cytokines and oxidative stress, which are the clinical features of Alzheimer's disease (AD). This neurodegenerative disease is aggravated in cases involving SARS-CoV-2 and its inflammatory biomarkers, accelerating accumulation of ß-amyloid peptide, hyperphosphorylation of tau protein, and production of reactive oxygen species, which lead to homeostasis imbalance. The cholinergic system, through neurons and the neurotransmitter acetylcholine (ACh), modulates various physiological pathways, such as the response to stress, sleep and wakefulness, sensory information, and the cognitive system. Patients with AD have low concentrations of ACh; hence, therapeutic methods are aimed at adjusting the ACh titers available to the body for maintaining functionality. Herein, we focused on acetylcholinesterase inhibitors, responsible for the degradation of ACh in the synaptic cleft, and muscarinic and nicotinic receptor agonists of the cholinergic system owing to the therapeutic potential of the cholinergic anti-inflammatory pathway in AD associated with SARS-CoV-2 infection.

Neuroprotective Effect of Taurine against Cell Death, Glial Changes, and Neuronal Loss in the Cerebellum of Rats Exposed to Chronic-Recurrent Neuroinflammation Induced by LPS.

The present study investigated the neuroprotective effect of taurine against the deleterious effects of chronic-recurrent neuroinflammation induced by LPS in the cerebellum of rats. Adult male Wistar rats were treated with taurine for 28 days. Taurine was administered at a dose of 30 or 100 mg/kg, by gavage. On days 7, 14, 21, and 28, the animals received LPS (250 µg/kg) intraperitoneally. The vehicle used was saline. The animals were divided into six groups: vehicle, taurine 30 mg/kg, taurine 100 mg/kg, LPS, LPS plus taurine 30 mg/kg, and LPS plus taurine 100 mg/kg. On day 29, the animals were euthanized, and the cerebellum was removed and prepared for immunofluorescence analysis using antibodies of GFAP, NeuN, CD11b, and cleaved caspase-3. LPS group showed a reduction in the immunoreactivity of GFAP in the arbor vitae and medullary center and of NeuN in the granular layer of the cerebellar cortex. LPS increased the immunoreactivity of CD11b in the arbor vitae and in the medullary center. Taurine protected against these effects induced by LPS in immunoreactivity of GFAP, NeuN, and CD11b, with the 100 mg/kg dose being the most effective. LPS induced an increase in the number of positive cleaved caspase-3 cells in the Purkinje cell layers, granular layer, arbor vitae, and medullary center. Taurine showed its antiapoptotic activity by reducing the cleaved caspase-3 cells in relation to the LPS group. Here, a potential neuroprotective role of taurine can be seen since this amino acid was effective in protecting the cerebellum of rats against cell death and changes in glial and neuronal cells in the face of chronic-recurrent neuroinflammation.

Stress and serum cortisol levels in major depressive disorder: a cross-sectional study.

Major depressive disorder (MDD) is one of the disorders that most causes disability and affects about 265 million people worldwide, according to the World Health Organization (WHO). Chronic stress is one of the most prevalent factors that trigger MDD. Among the most relevant biological mechanisms that mediate stress and MDD are changes in the hypothalamic-pituitary-adrenal (HPA) axis function. Hypercortisolism is one of the relevant mechanisms involved in response to stress and is present in many people with MDD and in animals subjected to stress in the laboratory. This study aimed to investigate the levels of stress and cortisol in individuals diagnosed with MDD from the Basic Health Unit (BHU) in a small city in the western region of Santa Catarina, Brazil. Depression scores were assessed using Beck's inventory. For the investigation of stress, an adaptation with twenty-four questions of the Checklist-90-R manual was performed. The analysis of the cortisol levels in the individuals' serum was by the chemiluminescence method. Depression and stress scores were significantly higher in individuals with MDD than in control subjects (p < 0.001). Cortisol levels were also significantly higher in individuals with MDD (p < 0.05). Besides, depression scores were positively correlated with stress scores in individuals with MDD (Pearson's "r" = 0.70). Conclusion: Individuals with MDD had higher stress levels and cortisol than control subjects. The positive correlation between the levels of stress and depression in MDD individuals suggests that these conditions are related to a dysregulation of the HPA axis function.

The anti-inflammatory effect of resistance training in hypertensive women: the role of purinergic signaling.

BACKGROUND AND METHODS: Essential arterial hypertension triggers a chronic inflammatory process that seems to be linked to purinergic signaling. Physical exercise exhibit anti-inflammatory properties and is able to modulates purinergic system. The aim of this study was to evaluate the effect of 6 months of resistance training on inflammatory markers, purinergic system components, hemodynamic and anthropometric parameters in hypertensive woman. METHODS: A total of 31 hypertensive group and 28 normotensive (control group) middle-aged sedentary women were submitted to 6 months of resistance training. All measurements and blood collection were carried out before (pretest), after 3 months and after 6 months (posttest) of training. Purinergic enzymes [nucleoside triphosphate diphosphohydrolase (NTPDase) and adenosine deaminase] were assessed in lymphocytes; IL-6, IL-10, ATP and C-reactive protein levels were measured in serum. RESULTS: Six months of resistance training was able to significantly reduce blood pressure (BP), IL-6, C-reactive protein, ATP levels as well as NTPDase and adenosine deaminase activities in hypertensive group. Physical training was also able to increase IL-10 levels in hypertensive group. A positive correlation was found between BP, enzyme activities and levels of ATP and IL-6. A negative correlation was found between BP and IL-10. Positive correlation was found between NTPDase and IL-6 levels (P < 0.05) as well as ATP levels and IL-6 levels. CONCLUSION: Our findings demonstrated the relationship between purinergic signaling and inflammation in hypertension and suggests that resistance training serve as tool to reduce inflammation in hypertensive woman by modulating purinergic system.

Exercise with blood flow restriction as a new tool for health improvement in hypertensive elderly women: the role of purinergic enzymes.

BACKGROUND: Purinergic signaling has been considered one of the mechanisms by which exercise exerts its antihypertensive effects; and research on the effects of blow flow restriction (BFR) exercise has increased as an alternative for elderly hypertensive patients. We analyzed the acute responses of NTPDase and adenosine deaminase (ADA) activities to low intensity aerobic exercise (LIAE) with BFR in lymphocytes of hypertensive elderly women. METHODS: Sixteen hypertensive elderly women performed three exercise protocols: LIAE; high intensity aerobic exercise (HIAE) and LIAE+BFR. Blood pressure, heart rate and blood collection were carried out before exercise, immediately after exercise and 30 min after exercise. NTPDase and ADA activities were measured in lymphocytes. RESULTS: Our results showed that LIAE+BFR triggered the same stimuli when compared to HIAE exercise regarding to NTPDases activities, suggesting that both protocols trigger an augment of these enzyme activities in response to: 1) increase in ATP release during exercise; and 2) need of adenosine generation to promotes anti-inflammatory responses in the recovery period. HIAE protocol was more effective than the others to trigger combined hypotensive and anti-inflammatory effects in the recovery period. CONCLUSIONS: This study showed that BFR is a good tool to promote anti-inflammatory effects similar (not equal) to HIAE. Moreover, LIAE+BFR promotes much more stimuli and adaptations related to immune functions than low intensity protocols, bringing more benefits for the hypertensive elderly population.

Ectonucleotide pyrophosphatase/phosphodiesterase (E-NPP) and adenosine deaminase (ADA) activities in prostate cancer patients: influence of Gleason score, treatment and bone metastasis.

The relation between adenine nucleotides and cancer has already been described in literature. Considering that the enzymes ectonucleotide pyrophosphatase/phosphodiesterase (E-NPP) and adenosine deaminase (ADA) act together to control nucleotide levels, we aimed to investigate the role of these enzymes in prostate cancer (PCa). E-NPP and ADA activities were determined in serum and platelets of PCa patients and controls. We also verified the influence of the Gleason score, bone metastasis and treatment in the enzyme activities. Platelets and serum E-NPP activity increased, whereas ADA activity in serum decreased in PCa patients. In addition, Gleason score, metastasis and treatment influenced E-NPP and ADA activities. We may propose that E-NPP and ADA are involved in the development of PCa. Moreover, E-NPP and ADA activities are modified in PCa patients with distinct Gleason score, with bone metastasis, as well as in patients under treatment.

NTPDase and 5'-nucleotidase activities from synaptosomes and platelets of rats exposed to cadmium and treated with N-acetylcysteine.

The purpose of the present investigation was to evaluate the hydrolysis of adenine nucleotides on synaptosomes and platelets obtained from rats exposed to cadmium (Cd) and treated with N-acetylcysteine (NAC). Rats received Cd (2 mg/kg) and NAC (150 mg/kg) by gavage every other day for 30 days. Animals were divided into four groups (n = 4-6): control/saline, NAC, Cd, and Cd/NAC. The results of this study demonstrated that NTPDase and 5'-nucleotidase activities were increased in the cerebral cortex synaptosomes of Cd-poisoned rats, and NAC co-treatment reversed these activities to the control levels. In relation to hippocampus synaptosomes, no differences on the NTPDase and 5'-nucleotidase activities of Cd-poisoned rats were observed and only the 5'-nucleotidase activity was increased by the administration of NAC per se. In platelets, Cd-intoxicated rats showed a decreased NTPDase activity and no difference in the 5'-nucleotidase activity; NAC co-treatment was inefficient in counteracting this undesirable effect. Our findings reveal that adenine nucleotide hydrolysis in synaptosomes and platelets of rats were altered after Cd exposure leading to a compensatory response in the central nervous system and acting as a modulator of the platelet activity. NAC was able to modulate the purinergic system which is interesting since the regulation of these enzymes could have potential therapeutic importance. Thus, our results reinforce the importance of the study of the ecto-nucleotidases pathway in poisoning conditions and highlight the possibility of using antioxidants such as NAC as adjuvant against toxicological conditions.

Hematological indices and activity of NTPDase and cholinesterase enzymes in rats exposed to cadmium and treated with N-acetylcysteine.

The present study aimed to investigate the influence of N-acetylcysteine (NAC) on cadmium (Cd) poisoning by evaluating Cd concentration in tissues, hematological indices as well as the activity of NTPDase, acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) enzymes of rats exposed to Cd and co-treated with NAC. For this purpose, the rats received Cd (2 mg/kg) and NAC (150 mg/kg) by gavage every other day for 30 days. Animals were divided into four groups (n = 6-8): control/saline, NAC, Cd, and Cd/NAC. Cd exposure increased Cd concentration in plasma, spleen and thymus, and NAC co-treatment modulated this augment in both lymphoid organs. Cd exposure reduced red blood cell count, hemoglobin content and hematocrit value. Cd intoxication caused a decrease in total white blood cell count. NAC treatment per se caused an increase in lymphocyte and a decrease in neutrophil counts. On contrary, Cd exposure caused a decrease in lymphocyte and an increase in neutrophil and monocyte counts. NAC reversed or ameliorated the hematological impairments caused by Cd poisoning. There were no significant alterations in the NTPDase activity in lymphocytes of rats treated with Cd and/or NAC. Cd caused a decrease in the activities of lymphocyte AChE, whole blood AChE and serum BChE. However, NAC co-treatment was inefficient in counteracting the negative effect of Cd in the cholinesterase activities. The present investigation provides ex vivo evidence supporting the hypothesis that Cd induces immunotoxicity by interacting with the lymphoid organs, altering hematological parameters and inhibiting peripheral cholinesterase activity. Also, it highlights the possibility to use NAC as adjuvant against toxicological conditions.

Purinergic system ecto-enzymes participate in the thromboregulation of patients with indeterminate form of Chagas disease.

Chagas disease (CD) is a chronic and endemic illness caused by the parasite Trypanosoma cruzi. Microvascular disturbances play an important role in the progress of the disease. The purinergic signaling system participates in regulatory functions, such as immunomodulation, neuroprotection, and thromboregulation. This study aimed to investigate the activities of purinergic system ecto-enzymes present on the platelet surface and the platelet aggregation profile from patients with indeterminate form of Chagas disease (IFCD). Thirty patients diagnosed with IFCD and 30 healthy subjects were selected. Ecto-nucleoside triphosphate diphosphohydrolase (E-NTPDase), ecto-nucleotide pyrophosphatase/phosphodiesterase (E-NPP), ecto-5'-nucleotidase (E-5'-NT) and ecto-adenosine deaminase (E-ADA) activities were measured in platelets isolated from these individuals as well as the platelet aggregation. Results demonstrated an increase of 21 % in the E-NPP activity and 30 % in the E-5'-NT activity in IFCD group (P < 0.05); however, a decrease of 34 % in the E-ADA activity was determined in the same group (P < 0.001). A significant decrease of 12.7 % and 12.8 % in the platelet aggregation of IFCD group in two different concentrations of ADP (5 and 10 µM) was observed, respectively (P < 0.05). Increased E-NPP and E-5-NT activities as well as decreased E-ADA activity in platelets of patients with IFCD contributed to decrease platelet aggregation, suggesting that the purinergic system is involved in the thromboregulation process in these patients, since adenosine (the final product of ATP hydrolysis) has cardioprotective and vasodilator effects that prevent the clinical progress of the disease.

Cholinesterase activities and biochemical determinations in patients with prostate cancer: influence of Gleason score, treatment and bone metastasis.

Prostate cancer (PCa) is the sixth most common type of cancer worldwide. Cholinesterase is well known as having non-cholinergic functions such as cellular proliferation and differentiation, suggesting a possible influence of cholinesterase in tumorogenesis. Thus, the aim of this study was to investigate the whole blood acetylcholinesterase (AChE) and plasma butyrylcholinesterase (BChE) activities and some biochemical parameters in PCa patients. This study was performed in 66 PCa patients and 40 control subjects. AChE and BChE activities were determined in PCa patients and the influence of the Gleason score; bone metastasis and treatment in the enzyme activities were also verified. Furthermore, we also analyzed possible biochemical alterations in these patients. AChE and BChE activities decreased in PCa patients in relation to the control group and various biochemical changes were observed in these patients. Moreover, Gleason score, metastasis and treatment influenced cholinesterase activities and biochemical determinations. Our results suggest that cholinesterases activities and biochemical parameters are altered in PCa. These facts support the idea that the drop in the cholinesterase activity and the consequent increased amount of acetylcholine could lead to a cholinergic overstimulation and increase the cell proliferation in PCa.

Oxidative stress and antioxidant status in prostate cancer patients: relation to Gleason score, treatment and bone metastasis.

Over the last decade, epidemiological, experimental and clinical studies have implicated oxidative stress in the development and progression of prostate cancer. In the present study, we evaluated the oxidative status and antioxidant defense in patients with prostate cancer (PCa) taking into consideration: treatment, Gleason score and bone metastasis. For this, we measured concentrations of plasmatic thiobarbituric acid reactive substances (TBARS), serum protein carbonylation, whole blood catalase (CAT) and superoxide dismutase (SOD) activities, as well as the plasma and erythrocyte thiol levels and serum vitamin C and E concentration. This study was performed on 55 patients with PCa and 55 healthy men. TBARS levels and serum protein carbonylation were higher in PCa patients than in controls and altered levels of antioxidants were found in these patients. CAT activity was decreased and SOD activity was higher in PCa patients when compared with controls. Non-protein thiol levels were increased, however, serum vitamin C and vitamin E content were reduced in PCa patients when compared with controls. In addition, different parameters analyzed in PCa patients based on metastasis, treatment and Gleason score showed changes in oxidative stress biomarkers and antioxidant defenses. These findings may indicate an imbalance in the oxidant/antioxidant status, supporting the idea that oxidative stress plays a role in PCa, moreover, the oxidative profile appear to be modified by bone metastasis, treatment and Gleason score.

Enzymes that hydrolyze adenine nucleotides in patients with ischemic heart disease.

BACKGROUND: The extracellular nucleotides, ATP and ADP, as well as the nucleoside adenosine have been implicated in a great number of pathologic and physiological functions. However, extracellular adenine nucleotide levels are controlled by a complex cell surface-located group of enzymes called ectonucleotidases. We evaluated activities of enzymes that hydrolyze adenine nucleotides and nucleosides in platelets from patients with ischemic heart disease (IHD). METHODS: Sixty IHD patients were selected for the study. The activities of ectonucleoside triphosphate diphosphohydrolase (NTPDase, CD39), ectonucleotide pyrophosphatase/phosphodiesterase (E-NPP), ecto-5'-nucleotidase and adenosine deaminase (ADA) were studied in isolated platelets of these patients, as well as the platelet aggregation and NTPDase expression. RESULTS: The results show that NTPDase, ecto-5'-nucleotidase, E-NPP activities and NTPDase expression were increased in platelets of IHD patients when compared with the control group (p < 0.05). On the other hand, ADA activity and platelet aggregation were decreased in IHD patients, when compared with the control group (p < 0.05). CONCLUSIONS: The pathological condition in IHD generates alterations in ectonucleotidase activities as a compensatory organic response to thrombotic events that occur in IHD.

Activities of enzymes that hydrolyze adenine nucleotides in platelets from patients with rheumatoid arthritis.

OBJECTIVES: To investigate whether there are changes in the activity of the enzymes NTPDase, 5'-nucleotidase, E-NPP and ADA in platelets from patients with rheumatoid arthritis (RA). DESIGN AND METHODS: Thirty-five RA patients diagnosed with RA through American College of Rheumatology criteria, as well as 35 healthy patients were selected. NTPDase, 5'-nucleotidase, E-NPP and ADA activities were verified in platelets isolated from these patients. RESULTS: The results demonstrate that an increase in NTPDase (approximately 100%), 5'-nucleotidase (170%), E-NPP (approximately 100%) and ADA (approximately 45%) activities occurred in RA patients when compared to the control group. CONCLUSIONS: Ours results suggest an increase in the NTPDase, 5'-nucleotidase and E-NPP activities, which could be related to a compensatory organic response to excessive platelet aggregation which occurs during the inflammation. The increased ADA activity found in this work could lead to a decrease in the adenosine concentration in the circulation, which could explain the accelerated atherosclerosis found in patients with RA.

Oxidative stress in hypercholesterolemia and its association with Ala16Val superoxide dismutase gene polymorphism.

OBJECTIVES: To investigate the role of the oxidative stress and the antioxidant system as well as the influence of the manganese superoxide dismutase (Ala16Val) polymorphism on hypercholesterolemia. DESIGN AND METHODS: Levels of glucose, lipid, high-sensitivity C reactive protein (hs-CRP), thiobarbituric acid reactive substances (TBARS), carbonyl protein, thiols, reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), and vitamin C, vitamin E, as well as the presence of the manganese superoxide dismutase (Ala16Val) polymorphism were determined in 40 subjects with hypercholesterolemia and 40 controls. RESULTS: Lipid profile, hs-CRP, glucose, TBARS, carbonyl protein, CAT, and vitamin E were significantly higher in subjects with hypercholesterolemia. In contrast, GSH and SOD were lower. TBARS, carbonyl protein, thiols, CAT, and vitamin E were significantly higher in hypercholesterolemic subjects with VV genotype for MnSOD, while GSH, SOD, and vitamin C were lower in these subjects. CONCLUSIONS: We suggest an association between the genotypes of MnSOD, hypercholesterolemia, and oxidative stress biomarkers.

Changes in acetylcholinesterase (AchE) activity in lymphocytes and whole blood in acute lymphoblastic leukemia patients.

BACKGROUND: Acute lymphoblastic leukemia (ALL) is a type of cancer that affects lymphocytes and it is the most common form of cancer in children. Acetylcholinesterase (AChE) is well known as having non-cholinergic functions and has been detected in the blood and plasma of humans including in lymphocytes. Thus, we investigated whole blood and lymphocyte AChE activity in patients with ALL. METHODS: This study was performed on 72 children with ALL divided into 4 groups: newly diagnosed, remission induction, remission maintenance and out-of-treatment and one control group of 50 healthy subjects. We determined AChE activity in whole blood and lymphocytes of these patients. RESULTS: Results demonstrated that whole blood AChE activity was enhanced in the newly diagnosed group and reduced in the remission induction and remission maintenance groups in relation to the control group. For lymphocyte AChE activity we found an increase in the newly diagnosed group and a decrease in the remission induction group in relation to the control. CONCLUSIONS: These results suggest that AChE activity was altered in ALL patients. This fact may be related with the essential role played by AChE in the development of hematological disease and its contribution to the regulation of immune function.

Hydrolysis of adenine nucleotides in platelets from patients with acute myocardial infarction.

OBJECTIVES: To investigate the rate of ATP, ADP and AMP hydrolysis on the surface of platelets from acute myocardial infarction (AMI) patients. DESIGN AND METHODS: Twenty-five patients diagnosed with AMI, through clinical criteria, electrocardiographic changes and increase of cardiac biomarkers, as well as 25 healthy patients were selected. The hydrolysis of ATP, ADP and AMP was verified in isolated platelets of these patients. RESULTS: The results demonstrated that an increase in ATP (54%) and ADP (45%) hydrolysis occurred in AMI patients when compared to the control group. The hydrolysis of AMP also increased by 46% in AMI patients probably leading to an enhancement in the adenosine level. CONCLUSIONS: Our results suggest an increase in nucleotide hydrolysis in platelets from AMI patients, which could be related to a compensatory organic response to thrombotic events that occur in AMI.