Nanoparticle formulation increases Syzygium cumini antioxidant activity in Candida albicans-infected diabetic rats.

CONTEXT: Syzygium cumini (L.) Skeels (Myrtaceae) is a medicinal plant widely used in folk medicine for the treatment of diabetes mellitus (DM). However, studies on the use of this plant and of nanoparticle formulations against DM-related fungal infections are scarce. OBJECTIVE: To evaluate the effect of the treatments with aqueous seed extract of S. cumini (ASc) and ASc-loaded polymeric nanoparticles (NPASc) on biochemical parameters in Candida albicans-infected diabetic rats. MATERIALS AND METHODS: Male Wistar rats were divided into eight groups: Control, DM, C. albicans, C. albicans + ASc, C. albicans + NPASc, DM + C. albicans, DM + C. albicans + ASc and DM + C. albicans + NPASc. Rats were daily treated with ASc or NPASc (100 mg/kg) for 21 days. Biochemical parameters in serum and urine, advanced oxidation protein product (AOPP) and TBARS levels in the serum, kidney, liver and pancreas and N-acetyl-ß-d-glucosaminidase (NAG) activities in kidney and urine were evaluated. RESULTS: Biochemical and oxidative stress parameters increased in rats with DM and/or candidiasis. NPASc was more effective than ASc in decreasing glucose (56%), cholesterol (33%) and creatinine (51%) levels; serum (16%) and pancreatic (46%) AOPP and renal (48%) TBARS levels when compared with DM + C. albicans group. In C. albicans group, both treatments decreased NAG activity but did not decrease creatinine levels. CONCLUSIONS: These data suggest that the use of nanotechnology is able to improve plant extract properties such as antioxidant activity that may be useful in diabetes-related complications.

Protective effect of gallic acid and Syzygium cumini extract against oxidative stress-induced cellular injury in human lymphocytes.

CONTEXT: Syzygium cumini (Myrtaceae) presents antioxidant, anti-inflammatory, hypoglycemic and antibacterial effects; however, the cellular and molecular mechanisms of action in the immune system are not yet completely elucidated. OBJECTIVE: This study evaluates the in vitro effect of gallic acid and aqueous S. cumini leaf extract (ASc) on adenosine deaminase (ADA) and dipeptidyl peptidase IV (DPP-IV) activities, cell viability and oxidative stress parameters in lymphocytes exposed to 2, 2'-azobis-2-amidinopropane dihydrochloride (AAPH). MATERIALS AND METHODS: Lymphocytes were incubated with ASc (100 and 500 µg/ml) and gallic acid (50 and 200 µM) at 37 °C for 30 min followed by incubation with AAPH (1 mM) at 37 °C for 2 h. After the incubation time, the lymphocytes were used for determinations of ADA, DPP-IV and lactate dehydrogenase (LDH) activities, lipid peroxidation, protein thiol (P-SH) group levels and cellular viability by colorimetric methods. RESULTS: (i) HPLC fingerprinting of ASc revealed the presence of catechin, epicatechin, rutin, quercitrin, isoquercitrin, quercetin, kaempferol and chlorogenic, caffeic, gallic and ellagic acids; (ii) for the first time, ASc reduced the AAPH-induced increase in ADA activity, but no effect was observed on DPP-IV activity; (iii) ASc increased P-SH groups and cellular viability and decreased LDH activity, but was not able to reduce the AAPH-induced lipid peroxidation; (iv) gallic acid showed less protective effects than ASc. DISCUSSION AND CONCLUSION: ASc affects the purinergic system and may modulate adenosine levels, indicating that the extract of this plant exhibits immunomodulatory properties. ASc also may potentially prevent the cellular injury induced by oxidative stress, highlighting its cytoprotective effects.

Neuroinflammation after neonatal hypoxia-ischemia is associated with alterations in the purinergic system: adenosine deaminase 1 isoenzyme is the most predominant after insult.

Hypoxic-ischemic (HI) injury perinatal brain is a major contributor to morbidity and mortality to infants and children. Adenosine may play a role in the pathophysiology of HI, since it modulates the inflammatory process and the release of several neurotransmitters. Thus, the aim of this study was to identify the isoforms of adenosine deaminase (ADA) responsible for the enzymatic activity as well as the adenosine kinase (ADK) and A1 adenosine receptor (A1R) expression in the cerebral cortex eight days after HI. Myeloperoxidase (MPO) and N-acetyl-glucosaminidase (NAG) were assessed as inflammation markers. ADA activity was analyzed, in the presence or absence of a specific ADA1 inhibitor, erythro-9-(2-hydroxy-3-nonyl) adenine. The ADA1 activity (92.6%) was significantly higher than ADA2 (7.4%) activity in the cerebral cortex eight days after HI. A1Rs and ADK protein expression showed decreased 8 days after insult. Interestingly, the ADA1, MPO, and NAG activities were correlated positively. In view of this, we conclude that the inhibitor of ADA1, in in vitro conditions, was effective in decreasing the ADA activity, and that mainly ADA1 isoform is responsible for the increase in the ADA activity 8 days after HI insult. Therefore, HI neonatal was able to alter the ADK and A1R expression. Thus, due to the importance of adenosine signaling in the regulation of inflammatory and immune process and the crucial role of ADA in the postischemic homeostase of adenosine as well as during inflammatory process, we suggest that ADA1 inhibitors may play an important role in the regulation of events that follow the HI insult, favoring the increase in the adenosine in the sites of tissue injury. Together, these results highlight a role of the purinergic signaling cascade in the pathophysiology of HI neonatal.

Adenosine deaminase, dipeptidyl peptidase-IV activities and lipid peroxidation are increased in the saliva of obese young adult.

BACKGROUND: Obesity is the hallmark of the metabolic syndrome representing a major global health problem. It is considered a state of chronic inflammation with minimal exploration of salivary biomarkers. Thus, the intent of the present study was to assess the activities of salivary dipeptidyl peptidase IV (DPP-IV), adenosine deaminase (ADA) and lipid peroxidation in obese young and overweight young subjects. METHODS: ADA, DPP-IV activities and lipid peroxidation were investigated in saliva, as well as insulin, glucose, HbA1c, HOMA and anthropometric measurements in 149 young adults, including 54 with normal weight, 27 overweight and 68 obese subjects. RESULTS: Salivary ADA and DPP-IV activities as well as lipid peroxidation were higher in patients with obesity compared to the normal weight group. Correlations between ADA/DPP-IV activities, lipid peroxidation/ADA activity, ADA activity/hip circumference and BMI/weight were observed. CONCLUSIONS: Our results indicate that the increase in the salivary ADA and DPP-IV activities as well as in the lipid peroxidation could be related of the regulation to various aspects of adipose tissue function and inflammatory obesity. It is suggested that these salivary biomarkers may be used as biochemical test in clinical abnormalities present in obesity, in the absence of oral inflammatory diseases.

Extracellular Hydrolysis of Adenine Nucleotides and Nucleoside Adenosine is Higher in Patients with ST Elevation than Non-ST Elevation in Acute Myocardial Infarction.

BACKGROUND: The hydrolysis of adenine nucleotide linked to the membrane of the platelets is changed in acute myocardial infarction (AMI) probably due to a greater arterial blockage and cell damage in patients with ST elevation (STEMI) than in those without ST segment elevation (NSTEM). METHODS: This study aimed to compare the extracellular hydrolysis of adenine nucleotides on the platelet surface of STEMI and NSTEMI patients. This study was carried out with 50 patients with AMI (STEMI and NSTEMI). The extracellular hydrolysis of adenine nucleotides and nucleoside adenosine as well as the expression of NTPDase were verified in platelets. RESULTS: The results demonstrated that STEMI patients had significantly higher extracellular hydrolysis of adenine nucleotides (p < 0.001), ADA (adenosine deaminase) activity (p < 0.05), as well as troponin levels (p < 0.0001) when compared to NSTEMI patients. CONCLUSIONS: Findings suggest that the extracellular hydrolysis of adenine nucleotides and increase in the ADA activity are higher in patients with STEMI than in those with NSTEMI probably because there was a blockage in this major arterial with a large area of damaged tissue.

Ischemia-modified albumin and inflammatory biomarkers in patients with prostate cancer.

BACKGROUND: Prostate cancer has become a public health problem in many countries and there is evidence which indicates that inflammation and oxidative stress play a key role in the pathogenesis of this disease. Thus, the aim of this study was to evaluate the concentrations of new biomarkers of oxidative stress, ischemia-modified albumin (IMA) and ferric reducing ability of plasma (FRAP), as well as the inflammatory markers in patients with prostate cancer. METHODS: CRP, IMA, FRAP, fasting glucose, total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides, uric acid, creatinine, albumin, AST, ALT, ADA, total PSA (tPSA), free PSA, and proportion of free PSA (fPSA%) were measured in 25 patients with prostate cancer and in 30 healthy subjects. RESULTS: tPSA, CRP, and IMA were significantly higher in patients with prostate cancer. In contrast, fPSA% and FRAP were significantly lower in these patients. However, no significant differences were observed when IMA values were adjusted for serum albumin. Significant correlations were also observed for tPSA and CRP (r = 0.5104, p < 0.001) and for fPSA% and CRP (r = -0.5059, p < 0.001). CONCLUSIONS: We demonstrated that both inflammatory and oxidative processes are increased during prostate cancer and also that there is a reduction of antioxidant defenses in this pathology.

Hypoxia-ischemia alters nucleotide and nucleoside catabolism and Na+,K+-ATPase activity in the cerebral cortex of newborn rats.

It is well known that the levels of adenosine in the brain increase dramatically during cerebral hypoxic-ischemic (HI) insults. Its levels are tightly regulated by physiological and pathophysiological changes that occur during the injury acute phase. The aim of the present study was to examine the effects of the neonatal HI event on cytosolic and ecto-enzymes of purinergic system--NTPDase, 5'-nucleotidase (5'-NT) and adenosine deaminase (ADA)--in cerebral cortex of rats immediately post insult. Furthermore, the Na(+)/K(+)-ATPase activity, adenosine kinase (ADK) expression and thiobarbituric acid reactive species (TBARS) levels were assessed. Immediately after the HI event the cytosolic NTPDase and 5'-NT activities were increased in the cerebral cortex. In synaptosomes there was an increase in the ecto-ADA activity while the Na(+)/K(+) ATPase activity presented a decrease. The difference between ATP, ADP, AMP and adenosine degradation in synaptosomal and cytosolic fractions could indicate that NTPDase, 5'-NT and ADA were differently affected after insult. Interestingly, no alterations in the ADK expression were observed. Furthermore, the Na(+)/K(+)-ATPase activity was correlated negatively with the cytosolic NTPDase activity and TBARS content. The increased hydrolysis of nucleotides ATP, ADP and AMP in the cytosol could contribute to increased adenosine levels, which could be related to a possible innate neuroprotective mechanism aiming at potentiating the ambient levels of adenosine. Together, these results may help the understanding of the mechanism by which adenosine is produced following neonatal HI injury, therefore highlighting putative therapeutical targets to minimize ischemic injury and enhance recovery.

Evaluation of acetylcholinesterase and adenosine deaminase activities in brain and erythrocytes and proinflammatory cytokine levels in rats submitted to neonatal hypoxia-ischemia model.

Perinatal hypoxic-ischemic (HI) brain injury is a common problem with severe neurologic sequelae. The definitive brain injury is a consequence of pathophysiological mechanisms that begin at the moment of HI insult and may extend for days or weeks. In this context, the inflammatory response and the formation of reactive oxygen species seem to play a key role during evolution of brain damage after injury. Thus, the aim of this study was to describe the chronological sequence of acetylcholinesterase (AChE) activity and the lipid peroxidation changes in the cerebral cortex using the classic model of neonatal HI. Furthermore, the erythrocyte AChE and adenosine deaminase (ADA) activities as well as the serum levels of proinflammatory cytokines were assessed. We observed that neonatal HI caused an increase of lipid peroxidation immediately after HI insult, which remained for several days afterward. There was a time-related change in the AChE activity in the cerebral cortex and the same was observed in erythrocyte AChE and ADA activities. In addition, immediately after HI, ADA activity showed a strong positive correlation with all proinflammatory cytokines assessed. Together, these findings may help the understanding of some mechanism related to the pathophysiology of neonatal HI, therefore highlighting the putative therapeutic targets to minimize brain injury and enhance recovery.

Syzygium jambos and Solanum guaraniticum show similar antioxidant properties but induce different enzymatic activities in the brain of rats.

Syzygium jambos and Solanum guaraniticum are both employed in Brazil as medicinal plants, even though their potential toxicity is not well established and they are frequently misused. The aim of this study was investigate the effect of the aqueous leaf extracts of both plants on δ-aminolevulinate dehydratase (δ-ALA-D) and acetylcholinesterase (AChE) activities and the antioxidant action against oxidative damage induced by sodium nitroprusside in rats, using in vitro assays. In addition, the presence of gallic, caffeic and chlorogenic acids, as well as rutin, quercetin and kaempferol as bioactive compounds in the extracts was identified by HPLC and their levels quantified. The antioxidant activities of both extracts were assessed by their capabilities to scavenge nitric oxide and to inhibit lipid peroxidation. Only Syzygium jambos presented thiol-peroxidase-like activity. Although neither extract affected the AChE activity, the aqueous extract of Solanum guaraniticum inhibited brain δ-ALA-D activity, suggesting a possible impairment effect on the central nervous system. Our results showed that both extracts exhibited efficient free radical scavenger activity and are an interesting source of bioactive compounds, justifying their use in folk medicine, although Solanum guaraniticum extract could have neurotoxicity properties and we therefore suggest that its use should be restricted to ensure the health of the population.

Effects of curcumin on the activities of the enzymes that hydrolyse adenine nucleotides in platelets from cigarette smoke-exposed rats.

The aim of the present study was to investigate the effect of curcumin (Cur) on the activity of ectonucleoside triphosphate diphosphohydrolase (CD39), 5'-nucleotidase (CD73) and adenosine deaminase in platelets of cigarette smoke-exposed rats. For that purpose, we subjected male Wistar rats to a treatment with Cur and cigarette smoke, once a day, 5 days each week, for 30 days. The rats were treated by gavage with Cur or corn oil and then exposed to cigarette smoke. The experimental procedures were divided into two sets of experiments. In the first, the animals were divided into four groups: vehicle (corn oil) or Cur 12·5, 25 or 50 mg·kg(-1) . In the second, the animals were divided into five groups: vehicle (corn oil), smoke, or smoke and Cur 12·5, 25 or 50 mg·kg(-1) . The results showed that treatment with Cur significantly prevented the increased adenosine triphosphate (ATP) (121%) and adenosine monophosphate (AMP) (159%) and the decreased adenosine diphosphate (ADP) (51%) hydrolysis observed in the cigarette smoke-exposed rats Our results suggest that those purinergic enzyme alterations observed in the cigarette smoke-exposed rats could be related to an excessive platelet aggregation and point toward the potential of Cur to modulate purinergic signalling and, consequently, regulate the thrombus formation.

A single high dose of ascorbic acid and iron is not correlated with oxidative stress in healthy volunteers.

Fe (II) is a potential prooxidant in vivo and can induce cellular oxidative stress. Ascorbic acid (AA) is a powerful physiological antioxidant and, in the presence of free Fe (II), can exhibit prooxidant effects in vitro. However, in vivo prooxidant effects of Fe (II) and AA have not yet been indisputably demonstrated. Here we evaluate the potential toxic effect of supplementation of Fe (II) associated with AA. Nine healthy, nonsmoking male volunteers (20-31 years old) participated in the crossover study design. The volunteers were supplemented with either a dose of 2 g of AA, 150 mg of iron carbonyl or 2 g of AA plus 150 mg of iron carbonyl with a washout period of 15 days between each treatment. AA, iron, ferritin, thiobarbituric acid-reactive substances, catalase, delta-aminolevulinic dehydratase and SH thiol groups were measured in the blood of the volunteers. Plasma AA levels were increased at 2, 5 and 24 h after AA or AA plus iron ingestion. Plasma Fe levels were increased at 2 and 5 h in the AA plus iron group. Erythrocyte malondialdehyde levels decreased at 5 and 24 h after AA and 5 h after AA plus iron ingestion. Catalase activity from erythrocytes was increased 5 h after supplementation with AA plus iron. There was no significant difference between groups in the other biochemical parameters evaluated. Thus, the present study does not support the hypothesis that the combination of high plasma concentrations of AA and iron, or iron alone, could cause in vivo oxidative damage after a single supplementation dose.

Antioxidant effect of diphenyl diselenide against sodium nitroprusside (SNP) induced lipid peroxidation in human platelets and erythrocyte membranes: an in vitro evaluation.

An in vitro evaluation on the antioxidant effect of diphenyl diselenide (PhSe)(2), an organochalcogenide, against sodium nitroprusside (SNP)-induced lipid peroxidation (LPO) was conduced. Human platelets and erythrocyte membranes (ghosts), as well as rat brain homogenates (S(1)), were pre-incubated with different concentrations of SNP (0-10 microM). All SNP concentrations tested significantly increased LPO in human platelets and S(1). Platelets were more sensitive to SNP-induced peroxidative damage when compared to S(1). SNP 10 microM decreased glutathione peroxidase (GPx) activity and did not affect glutathione reductase (GR) and catalase (CAT) activities in human platelets. However, ghosts were insensitive to SNP-induced LPO and no changes on GPx, GR and CAT activities were observed. Diphenyl diselenide significantly protected human platelets against SNP-induced LPO and recovered GPx inactivation. This effect was more evident at (PhSe)(2) concentrations above 2 microM. The presented results indicate that (PhSe)(2) exerts protective effects on SNP-induced oxidative damage in human blood components and in rat brain. These phenomena seem to be related to its thiol peroxidase-like activity and to a possible direct interaction with SNP and derivatives. Based on our results and on literature, diphenyl diselenide can be pointed as a promising antioxidant molecule.

Adipocytokines, inflammatory and oxidative stress markers of clinical relevance altered in young overweight/obese subjects.

OBJECTIVE: The aim of the study was to assess the influence of overweight and obesity in youth on adipocytokines levels, inflammatory and oxidative markers. DESIGN AND METHODS: Cross-sectional study of 149 young adults (54 normal weight, 27 overweight, 68 obese).Clinical and biochemical parameters, including lipid profile, fasting glucose, insulin and HOMA were determined. The levels of adipocytokines(adiponectin, retinol-binding protein 4 (RBP4), and resistin), markers of inflammation (high-sensitivity C-reactive protein (hs-CRP) adenosine deaminase (ADA), dipeptidyl peptidase-IV (DPP-IV) activities, serum IL-6 levels and oxidative stress (malondialdehyde and ferric reducing antioxidant power - FRAP) were measured. RESULTS: Obese subjects presented significantly lower levels of Sulfhydryl groups (SH groups), adiponectin, HDL-C and the highest levels of RBP4, hs-CRP, resistin, IL-6, ADA, DPP-IV activities, and oxidative markers than compared to those who were of normal weight. There was a positive correlation between hs-CRP, IL-6, DDP-IV activity, anthropometric measurements and biochemical parameters. CONCLUSIONS: This analysis shows that resistin, RBP4, IL-6, ADA and DPP-IV activities and the reduction of adiponectin can promote inflammation, impairment of insulin sensitivity, and may contribute development of the pathways involved in obesity. These findings may hold promise in identifying new inflammatory markers, benchmarks that assist in the diagnosis and monitoring of patients with overweight and obese.

In Vitro Oxidation of Collagen Promotes the Formation of Advanced Oxidation Protein Products and the Activation of Human Neutrophils.

The accumulation of advanced oxidation protein products (AOPPs) has been linked to several pathological conditions. Here, we investigated collagen as a potential source for AOPP formation and determined the effects of hypochlorous acid (HOCl)-treated collagen (collagen-AOPPs) on human neutrophil activity. We also assessed whether alpha-tocopherol could counteract these effects. Exposure to HOCl increased the levels of collagen-AOPPs. Collagen-AOPPs also stimulated the production of AOPPs, nitric oxide (NO), superoxide radicals (O2(-)), and HOCl by neutrophils. Collagen-AOPPs induced apoptosis and decreased the number of viable cells. Alpha-tocopherol prevented the formation of collagen-AOPPs, strongly inhibited the collagen-AOPP-induced production of O2(-) and HOCl, and increased the viability of neutrophils. Our results suggest that collagen is an important protein that interacts with HOCl to form AOPPs, and consequently, collagen-AOPP formation is related to human neutrophil activation and cell death.

Evidence that intracellular Ca2+ mediates the effect of alpha-ketoisocaproic acid on the phosphorylating system of cytoskeletal proteins from cerebral cortex of immature rats.

In this study we investigated the involvement of Ca2+ on the effects of alpha-ketoisocaproic acid (KIC), the main metabolite accumulating in maple syrup urine disease (MSUD), on the phosphorylating system associated with the intermediate filament (IF) proteins in slices from cerebral cortex of 9-day-old rats. We first observed that KIC significantly decreased the in vitro phosphorylation of IF proteins in brain slices. KIC-induced dephosphorylation was mediated especially by the protein phosphatase PP2B, a Ca2+-dependent protein phosphatase, but also by PP2A. We also demonstrated the involvement of Ca2+-dependent mechanisms in the KIC effects using the specific L-voltage-dependent Ca2+ channels (L-VDCC) inhibitor nifedipine, the NMDA antagonist DL-AP5 and the intracellular Ca2+ chelator BAPTA-AM. Blockage of Ca2+ channels or chelating intracellular Ca2+ completely prevented the effects of KIC on the phosphorylating system associated to IF proteins. In addition, we verified that KIC increased 45Ca2+ uptake in brain slices after 3 and 30 min incubation. Taken together, our present data indicate that KIC increase intracellular Ca2+ levels, probably promoting the activation of calcineurin. These results might be associated with the increased dephosphorylation of the IF proteins in slices of cerebral cortex of immature rats exposed to KIC at similar concentrations from those found in blood and tissues of patients with MSUD.

Syzygium cumini seed extract ameliorates adenosine deaminase activity and biochemical parameters but does not alter insulin sensitivity and pancreas architecture in a short-term model of diabetes.

BACKGROUND: The effects of the aqueous seed extract of Syzygium cumini (ASc) in a short-term model of diabetes in rats are little explored. The present study was designed to evaluate the effect of the ASc on adenosine deaminase (ADA) activity and on biochemical and histopathological parameters in diabetic rats. METHODS: ASc (100 mg/kg) was administered for 21 days in control and streptozotocin (STZ)-induced (60 mg/kg) diabetic rats. ADA activity, lipoperoxidation (cerebral cortex, kidney, liver and pancreas) and biochemical (serum) and histopathological (pancreas) parameters were evaluated. RESULTS: The main findings in this short-term model of Diabetes mellitus (DM) were that the ASc (i) significantly reverted the increase of ADA activity in serum and kidney; (ii) ameliorated the lipoperoxidation in the cerebral cortex and pancreas of the diabetic group; (iii) demonstrated hypolipidemic and hypoglycemic properties and recovered the liver glycogen; and iv) prevented the HOMA-IR index increase in the diabetic group. Therefore, the ASc can be a positive factor for increasing the availability of substrates with significant protective actions, such as adenosine. Moreover, by maintaining glycogen and HOMA-IR levels, the extract could modulate the hyperglycemic state through the direct peripheral glucose uptake. CONCLUSIONS: Our data revealed that the short-term treatment with ASc has an important protective role under pathophysiological conditions caused by the early stage of DM. These results enhance our understanding of the effect of the ASc on the purinergic system in DM.

Effect of subchronic treatment with mercury chloride on NTPDase, 5'-nucleotidase and acetylcholinesterase from cerebral cortex of rats.

The aim of the present investigation was to evaluate the effect of a subchronic treatment (30 days/30 doses) with subcutaneous injections (0.1 mg/kg) of HgCl2 on NTPDase (E.C. 3.6.1.5), 5'-nucleotidase (E.C 3.1.3.5) and acetylcholinesterase (AChE, E.C. 3.1.1.7) activities in brain from adult rats. NTPDase and 5'-nucleotidase were measured in cortical synaptosomal fraction and AChE was measured in the homogenate of cerebral cortex and hippocampus. After the subchronic treatment (30 days), NTPDase activity was enhanced approximately 35% (p < 0.05) with ATP and ADP as substrates and no difference was observed in 5'-nucleotidase activity (AMP hydrolysis). In addition, AChE activity was enhanced in the cerebral cortex (22%, p < 0.05) and hippocampus (26%, p < 0.05) after the subchronic treatment. Mercury deposited in brain was measured by cold vapor (atomic absorption spectrometry) and no difference between the control and the subchronically treated group was observed. Here we showed for the first time that exposure to low levels of Hg2+, which resembles occupational exposure to low levels of mercury, caused a marked increase in NTPDase and AChE activities. The relationship of these alterations with the neurotoxicity of inorganic mercury deserves further studies.

Delta-ALA-D inhibitory potential and protective action of Syzygium jambos and Solanum guaraniticum leaf extracts on oxidatively stressed erythrocytes.

OBJECTIVE: This study aimed to investigate the effect of the leaf extracts of Syzygium jambos and Solanum guaraniticum on the δ-aminolevulinate dehydratase (δ-ALA-D) activity, their antioxidant activity and potential protective action on oxidatively stressed erythrocytes, in order to demonstrate the safety or toxicity of the plant. METHODS: In erythrocyte samples, the effect of both extracts on δ-ALA-D activity, H2O2-induced oxidative stress, and 2,2'azobis (2-amidinopropane) (AAPH)-induced hemolysis was evaluated, as well as some antioxidant mechanisms. RESULTS: Both extracts inhibited δ-ALA-D activity (S. guaraniticum > S. jambos), and an involvement of the zinc ion of the δ-ALA-D structure on the inhibition of enzyme activity was verified. S. jambos leaf extract showed marked efficiency in countering H2O2-induced lipid peroxidation and in maintaining cellular integrity against AAPH-induced hemolysis. Furthermore, S. jambos exhibited greater H2O2 scavenging activity and stronger reduction power than S. guaraniticum. DISCUSSION: Both extracts bear potent antioxidant property as an important beneficial effect. However, the inhibition of δ-ALA-D activity suggests a possible harmful effect of these vegetal preparations and indicates the need for further investigation regarding their toxicological properties. All together, these data represent a significant contribution to the knowledge of these plants, both to the scientific community and to the folk medicine.

Aqueous seed extract of Syzygium cumini inhibits the dipeptidyl peptidase IV and adenosine deaminase activities, but it does not change the CD26 expression in lymphocytes in vitro.

Syzygium cumini (Sc) have been intensively studied in the last years due its beneficial effects including anti-diabetic and anti-inflammatory potential. Thus, the aim of this study was to evaluate the effect of aqueous seed extract of Sc (ASc) in the activity of enzymes involved in lymphocyte functions. To perform this study, we isolated lymphocytes from healthy donors. Lymphocytes were exposed to 10, 30, and 100 mg/mL of ASc during 4 and 6 h and adenosine deaminase (ADA), dipeptidyl peptidase IV (DPP-IV), and acetylcholinesterase (AChE) activities as well as CD26 expression and cellular viability were evaluated. ASc inhibited the ADA and DPP-IV activities without alteration in the CD26 expression (DPP-IV protein). No alterations were observed in the AChE activity or in the cell viability. These results indicate that the inhibition of the DPP-IV and ADA activities was dependent on the time of exposition to ASc. We suggest that ASc exhibits immunomodulatory properties probably via the pathway of DPP-IV-ADA complex, contributing to the understanding of these proceedings in the purinergic signaling.

Assessment of inflammatory and oxidative biomarkers in obesity and their associations with body mass index.

The aim of this study was to evaluate the inflammatory and oxidative biomarkers' levels in obese subjects and their associations with body mass index (BMI), in order to investigate the role of these biomarkers in obesity. Fasting glucose, total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides, apolipoprotein A, apolipoprotein B, albumin, urinary albumin, creatinine, glomerular filtration rate, interleukin-6 (IL-6), nitrate/nitrite (NOx), and ischemia-modified albumin (IMA) were measured in 93 subjects divided according to different BMI. IL-6, urinary albumin, and IMA levels were significantly higher in obese subjects. However, the levels of NOx were significantly lower in this population. Significant correlations between BMI and IL-6 (r = 0.326, P = 0.002), NOx (r = -0.249, P = 0.021), urinary albumin (r = 0.270, P = 0.008), and IMA (r = 0.286, P = 0.005) were reported. We have shown an increase of IL-6, urinary albumin, and IMA combined with lower levels of NOx in obese patients and an association between of these biomarkers with BMI, suggesting a possible interplay of oxidative stress, inflammation, and endothelial dysfunction state in obesity.