Adenosine Deaminase Activity Research Articles

Hypouricemic and nephroprotective effects of palmatine from Cortex Phellodendri Amurensis: A uric acid modulator targeting Keap1-Nrf2/NLRP3 axis

Ethnopharmacological relevancePalmatine (Pal) is a major bioactive alkaloid originated from ancient Chinese herbal medicine Cortex Phellodendri Amurensis (CPA), which has long been applied to treat hyperuricemia (HUA)-related diseases. Pal possesses potent anti-inflammatory and anti-oxidant effects against metabolic diseases. However, its potential beneficial effect against PO (potassium oxonate)/HX (hypoxanthine)-induced HUA remains elusive. Aim of the studyThis study aimed to investigate the potential pharmacological effect and mechanism of Pal on PO/HX-induced HUA in mice. Material and methodsA mouse model of HUA was established by co-administration of PO/HX once daily for 7 consecutive days. The HUA mice were orally given three doses (25, 50 and 100 mg/kg) of Pal daily for a week. Febuxostat (Feb, 5 mg/kg) was given as a positive control. At the scheduled termination of the experiment, the whole blood, liver and kidney were collected for subsequent analyses. The concentrations of uric acid (UA), creatinine (CRE) and blood urea nitrogen (BUN), and activities of adenosine deaminase (ADA) and xanthine oxidase (XOD) were evaluated. Histopathological alterations of the kidney were detected by H&E staining. The inflammatory and oxidative stress status was detected by assay kits. Additionally, key proteins involved in the urate transporter, Keap1-Nrf2 and TXNIP/NLRP3 signaling pathways were evaluated by immunohistochemistry and Western blotting. Finally, molecular docking was employed to probe the binding characteristics of Pal and target proteins Keap1, NLRP3, URAT1 and HO-1. ResultsAdministration of Pal substantially decreased the elevated kidney weight, lowered UA, CRE and BUN levels, and attenuated abnormal histopathological alterations. Meanwhile, treatment with Pal also dramatically lowered hepatic XOD and ADA activities. Besides, Pal treatment effectively mitigated the renal inflammatory and oxidative stress markers. Further mechanistic investigation indicated Pal distinctly downregulated the protein levels of GLUT9 and URAT1, while up-regulated the expression levels of OAT1 and ABCG2. Pal also restored Nrf2 activation, promoted subsequent expression of anti-oxidative enzymes, and downregulated the expressions of TXNIP, NLRP3, apoptosis-associated speck-like (ASC), caspase-1, IL-1β and IL-18. Molecular docking analysis also indicated Pal firmly bound with Keap1, NLRP3, URAT1 and HO-1. ConclusionsThese findings indicated that Pal exhibited favorable anti-HUA effect via modulating the expressions of transporter-related proteins and suppressing XOD activity. Furthermore, Pal also alleviated HUA-induced kidney injury, which was at least partially related to restoring Keap1-Nrf2 pathway and inhibiting TXNIP/NLRP3 inflammasome. Our investigation was envisaged to provide experimental support for the traditional application of CPA and CPA-containing classical herbal formulas in the management of HUA-related diseases and might provide novel dimension to the clinical application of Pal.

Measurement of Activities of Adenosine Deaminase and Superoxide Dismutase in Bladder Cancer Patients

The biochemical study investigated the specific activity of two enzymes; adenosine deaminase (ADA) and superoxide dismutase (SOD) in the sera of eighty three blader cancer (BC) patients and twenty controls. A significant reduced specific activity of ADA was observed in the patients (0.136 U/gm vs. 0.206 U/gm ), while SOD contrasted the picture, and instead, a significant elevation of the activity was observed (11.430 U/ml vs. 8 585 U/ml )., especially in the advanced stages of disease

Relationship between Adenosine Deaminase Activity in the Cerebral Cortex and the Stimulating Effect of Caffeine in Adult Wistar Rats of Different Ages.

The aim of this study was to test the hypothesis that the higher the activity of adenosinedeaminase (ADA) in the brain, the greater should be the motor activity of animals, and possibly the stronger the psychostimulant effect of caffeine. We studied the effect of caffeine (10 and 20 mg/kg) on the motor activity and ADA activity in the frontal cortex of the brain in 2- and 5-month-old rats with different levels of spontaneous motor activity. Total motor activity significantly decreased with age, which was accompanied by a decrease in ADA activity. Administration of caffeine in a dose of 10 mg/kg stimulated motor activity in both 2- and 5-month-old animals, while ADA activity decreased in 2-month-old rats and increased in 5-month-old animals. Administration of caffeine in a dose of 20 mg/kg did not change the motor activity, however, in 5-month-old animals it led to an even greater increase in ADA activity. Thus, the age-related decrease in motor activity can be due to a decrease in ADA activity. However, the effect of caffeine on motor activity is not directly related to ADA activity in the cerebral cortex.

Roasted cashew (Anacardium occidentale L.) nut-enhanced diet forestalls cisplatin-initiated brain harm in rats

The incessant dose constraining symptom of the chemotherapeutic agent, cisplatin is neurotoxicity. This examination tried to explore the neuroprotective impact of roasted cashew nut-enhanced diet against brain deficits related with treatment with cisplatin. Rats were separated in to six groups: Control, CIS (cisplatin [7 mg/kg body weight, i.p]), CIS +10% CN (cisplatin plus 10% roasted cashew nut), CIS +20% CN (cisplatin plus 20% roasted cashew nut), 10% CN (10% roasted cashew nut) and 20% CN (20% roasted cashew nut) for 28 days. Key enzymes associated with brain function, including cholinesterases (AChE and BChE), monoaminergic enzyme (MAO), arginase, and adenosine deaminase (ADA), were investigated after the treatment. The following oxidative stress indicators were also measured in the rat brain: glutathione-S-transferase (GST), glutathione peroxidase (GPx), total antioxidant capacity (TAC), total thiol (T-SH), non-protein thiol (NPSH), thiobarbituric acid reactive substances (TBARS), reactive oxygen species (ROS), nitric oxide (NO), superoxide dismutase (SOD). Our outcomes demonstrated that roasted cashew nut enhanced diet showed inhibitory impact on activities of AChE, BChE, ADA, MAO and arginase in cisplatin-induced rats. The roasted cashew nut supplemented diet also boosted redox equilibrium and displayed protection against cispaltin-induced oxidative damage to rats' brains by an increase in SOD, CAT, GST and GPx activities, TAC, T-SH, NPSH and NO levels as well as a considerable drop in ROS and RBARS levels. Roasted cashew nut enhanced diet additionally forestalled neuronal degeneration in rat brain. Thus, roasted cashew nuts could be used as a nutraceutical or functional food to treat cisplatin-induced neurotoxicity. Practical applicationsThe results show that increasing roasted cashew nut consumption can significantly improve antioxidant status, reduce lipid peroxidation, and suppress cholinesterase, adenosine deaminase, monoamine oxidase, and arginase activities in the brain under cisplatin-induced circumstances.

Correlations Of Adenosine Deaminase Activity In The Plasma Of Diabetic Patients With Arterial Hypertension

This work presents the preliminary data of one center study of the total activity of adenosine deaminase (tADA) and its isoforms (ADA1 and ADA2) in the blood plasma of patients with type 2 diabetes mellitus (T2DM), including cases with complication with arterial hypertension. As a nonspecific indicator of cellular immunity, altered serum tADA activity is used to evaluate diseases related to cell-mediated immune responses, it is considered a useful tool in the monitoring of clinical status of various diseases.

Inhibition of adenosine deaminase activity reverses resistance to the cytotoxic effect of high adenosine levels in cervical cancer cells

Adenosine (ADO) generation in the tumor microenvironment (TME) plays important roles in the promotion of tumor growth, invasion, and metastasis and in suppression of the antitumor immune response. Recently, adenosine deaminase (ADA) activity in the TME has been proposed to be a compensatory mechanism against toxic accumulation of ADO in cancerous tissues. In the present study, the expression and functional activity of ADA in cervical cancer (CeCa) tumor cells were analyzed: C33A (HPV-), CaSki (HPV + ), and HeLa (HPV + ) cells. CeCa tumor cells, as well as activated T lymphocytes (ATLs), which were used as a positive control, showed different ADA contents in the membrane and intracellularly and a strong ability to convert ADO into inosine (INO). Treatment of tumor cells with EHNA, a specific ADA inhibitor, decreased the viability of CeCa tumor cells in a dose-dependent manner. In C33A (EHNA half maximal inhibitory concentration (IC50) = 374 μM), CaSki (EHNA IC50 = 273.6 μM), and HeLa (EHNA IC50 = 252.2 μM) cells, EHNA strongly reversed the resistance of tumor cells to the cytotoxic effect of high concentrations of ADO; 38.82 ± 3.1%, 47.18 ± 4.7%, and 71.63 ± 6.9% of the cells were apoptotic, and 40 ± 4.8%, 52 ± 5.3% and 70 ± 6.8% of the cells had mitochondrial membrane damage, respectively. In ATLs (EHNA IC50 = 391.8 μM) treated with EHNA, 32.4 ± 4.4% were apoptotic, and 32 ± 4.3% had mitochondrial membrane damage. These results suggest that the presence and activity of ADA in CeCa tumor cells can provide protection against the cytotoxic effect of high ADO contents in the TME. Therefore, the inhibition of ADA could be a strategy for the treatment of CeCa.

Folic acid and zinc improve hyperuricemia by altering the gut microbiota of rats with high-purine diet-induced hyperuricemia.

A high-purine diet can cause hyperuricemia and destroy the microbial composition of the gut microbiota. Both folic acid and zinc significantly reduce uric acid levels and alleviate hyperuricemia. However, whether the underlying mechanisms are associated with the regulation of the gut microbiota remain unknown. To explore alterations of the gut microbiota related to folic acid and zinc treatment in rats with hyperuricemia in our study. A hyperuricemic rat model was established with a high-purine diet. The effects of folic acid and zinc on uric acid levels were evaluated. Alterations of the gut microbiota related to hyperuricemia and the treatments were evaluated by sequencing using the Illumina MiSeq system. The results demonstrated that uric acid levels dropped observably, and the activities of adenosine deaminase (ADA) and xanthine oxidase (XOD) were downregulated after folic acid or zinc intervention. 16S rRNA gene sequencing-based gut microbiota analysis revealed that folic acid and zinc enhanced the abundance of probiotic bacteria and reduced that of pathogenic bacteria, thus improving intestinal barrier function. PICRUST analysis indicated that folic acid and zinc restored gut microbiota metabolism. These findings indicate that folic acid and zinc ameliorate hyperuricemia by inhibiting uric acid biosynthesis and stimulating uric acid excretion by modulating the gut microbiota. Thus, folic acid and zinc may be new and safe therapeutic agents to improve hyperuricemia.

The features of enzymes activity to nucleoside and antioxidant systems in solid tumors

Background. Solid tumors can create their aggressive properties. There are characterized by the invasion and metastatic activity, the resistance of the tumor clone to apoptosis. These pathways triggering may be realized both by 2-deoxy-D-ribose and its phosphorylated form (2-d-D-Rib-1-P), and by hydrogen peroxide.Aim. To investigate the peculiarities of enzymes activity to nucleoside metabolism and antioxidant system in epithelial tumors of different localization.Materials and methods. The features of the thymidine phosphorylase, adenosine deaminase, superoxide dismutase (SOD) and glutathione peroxidase (GPO) activity were studied in tumor homogenates. The visually no transformed tissues of the surgical resection edges were used as a control. Enzymes activity was determined by spectrophotometrical and morphological features were examined by the immunohistochemical methods in tissues of non-small cell lung cancer (NSCLC), samples of gastric and colon carcinomas (GCC).Results. Thymidine phosphorylase activity and adenosine deaminase activity in various malignant tumors were increased in comparison to the control. Respectively, thymidine phosphorylase activity was higher than by 1.8 times (p= 0.002 for NSCLC,p= 0.001 for GCC). An increase of adenosine deaminase activity was revealed both in tissues of NSCLC (more than 1.7 times) and in GCC (by 1.9 times,p= 0.001). No significant changes in SOD activity were detected in the tumors. GPO activity tended to decrease by an average of 1.3 times (p= 0.01 for NSCLC,p= 0.02 for GCC). A cluster analysis of the enzymatic activity features of the studied NSCLC tumors, as well as GCC, revealed their metabolic heterogeneity. According to its results, tumors of different localization were distinguished into 2 clusters. Common feature to their second clusters was an increase the SOD activity. It was accompanied by increase of thymidine phosphorylase activity (p= 0.045 for NSCLC,p= 0.049 for GCC). Therefore, both hydrogen peroxide and 2-d-D-Rib-1-P could be formed in them more intensively. It is important to note that morphological indicators of tumor aggression (decreased or lost expression of cell-cell adhesion marker, expression of mesenchymal markers, active angiogenesis) were detected more frequently in these subgroups.Conclusion. The obtained results reveal that individual features of the enzymes activity in epithelial tumors may be available source of 2-d-D-Rib-1-P and hydrogen peroxide generation in human cancer cells. In the case of individual higher tumor activity of thymidine phosphorylase and SOD and low GPO activity the metabolic stimulation of tumor progression may be occur.

Concurrent training is able to increase the activity of adenosine deaminase in platelets in young women

Concurrent training is able to increase the activity of adenosine deaminase in platelets in young women

The immuneoreaction and antioxidant status of Chinese mitten crab (Eriocheir sinensis) involve protein metabolism and the response of mTOR signaling pathway to dietary methionine levels

To study the effects of dietary methionine on growth performance, immunity, antioxidant capacity, protein metabolism, inflammatory response and apoptosis factors in Chinese mitten crabs (Eriocheir sinensis). Five diets with different methionine levels (0.63%, 0.85%, 1.06%, 1.25% and 1.47%) were fed to E. sinensis for 8 weeks. Results showed that in the 1.25% Met group, both growth performance and feed utilization were significantly increased. The crude protein content of crab muscle in the 1.06% and 1.25% Met groups was significantly higher than that in the control group. The immune and antioxidant enzyme activities, as well as gene expression levels of anti-lipopolysaccharide factor 1 (ALF1), Crustin-1, prophenoloxidase (proPO), cap ‘n’ collar isoform C (CncC) in 1.25% Met group were significantly higher than other groups. The activities of adenosine deaminase (ADA) and glutamate transaminase (GPT) in serum decreased first and then increased with the increase of methionine content, while the changes of ADA and GPT in hepatopancreas increased first and then decreased. 1.25% Met group exhibited significantly increased levels of GOT, GPT, and ADA compared to the control group. 1.25% Met diet group significantly up-regulated protein synthesis and anti-apoptotic factors, and significantly down-regulated inflammatory and pro-apoptotic factors in hepatopancreas. At 1.25% in the diet, methionine was found to boost E. sinensis growth, muscle protein deposition and immunity, as well as its antioxidant capacity. Combined with the above results, based on the expression of factors involved in the mammalian target of rapamycin (mTOR) signaling pathway and the mitogen-activated protein kinase (MAPK) signaling pathway, it is proved that methionine can not only promote protein metabolism, improve feed utilization, but also alleviate the inflammatory response and apoptosis caused by oxidative stress in the body.

Missense mutation in RPS7 causes Diamond-Blackfan anemia via alteration of erythrocyte metabolism, protein translation and induction of ribosomal stress

Diamond-Blackfan anemia (DBA) is predominantly underlined by mutations in genes encoding ribosomal proteins (RP); however, its etiology remains unexplained in approximately 25 % of patients.We previously reported a novel heterozygous RPS7 mutation hg38 chr2:g.3,580,153G > T p.V134F in one female patient and two asymptomatic family members, in whom mild anemia and increased erythrocyte adenosine deaminase (eADA) activity were detected. We observed that altered erythrocyte metabolism and oxidative stress which may negatively affect the lifespan of erythrocytes distinguishes the patient from her asymptomatic family members. Pathogenicity of the RPS7 p.V134F mutation was extensively validated including molecular defects in protein translational activity and ribosomal stress activation in the cellular model of this variant.

Cordycepin (3'-Deoxyadenosine) Suppresses Heat Shock Protein 90 Function and Targets Tumor Growth in an Adenosine Deaminase-Dependent Manner.

Simple SummaryOur study contributes to understanding the therapeutic effects of cordycepin in cancer. First, we find that the anticancer effects of cordycepin alone are only seen in tumor cell lines with low ADA expression or activity. This was true in multiple tumor types and may be applied as a predictive biomarker for the future treatment of patients. Second, we show that inhibition of ADA enhances cordycepin’s anticancer effects by blocking its conversion to 3′-deoxyinosine in uveal melanoma and several other tumors. This raises the possibility of clinical combination treatments with cordycepin and ADA inhibitors, and our data suggest that much lower doses of cordycepin are possible in this context. Third, we identified a new mechanism of action for cordycepin: inhibiting the function of a protein known as Hsp90.Alterations in metabolism and energy production are increasingly being recognized as important drivers of neoplasia, raising the possibility that metabolic analogs could disrupt oncogenic pathways. 3′-deoxyadenosine, also known as cordycepin, is an adenosine analog that inhibits the growth of several types of cancer. However, the effects of cordycepin have only been examined in a limited number of tumor types, and its mechanism of action is poorly understood. We found that cordycepin slows the growth and promotes apoptosis in uveal melanoma, as well as a range of other hard-to-treat malignancies, including retinoblastoma, atypical teratoid rhabdoid tumors, and diffuse midline gliomas. Interestingly, these effects were dependent on low adenosine deaminase (ADA) expression or activity. Inhibition of ADA using either siRNA or pharmacologic approaches sensitized tumors with higher ADA to cordycepin in vitro and in vivo, with increased apoptosis, reduced clonogenic capacity, and slower migration of neoplastic cells. Our studies suggest that ADA is both a biomarker predicting response to cordycepin and a target for combination therapy. We also describe a novel mechanism of action for cordycepin: competition with adenosine triphosphate (ATP) in binding to Hsp90, resulting in impaired processing of oncogenic Hsp90 client proteins.

Abstract 1868: Targeting adenosine deaminase enhances anticancer effects of 3'-deoxyadenosine in uveal melanoma

Abstract Uveal melanoma, which arises from melanocytes located in the uveal tract, is one of the most common primary intraocular cancers. GNAQ and GNA11 mutations, which are detected most of primary uveal melanoma, activate MAPK signaling pathway, increasing cancer cell proliferation, tumor progression and growth. BAP1 mutation is highly associated with liver metastasis and death. However, there are no good therapeutic compounds for uveal melanoma treatment in clinic. 3’-deoxyadenosine (cordycepin) is an adenosine analog which inhibits growth of several types of cancer. However, its anticancer effects have been showed in limited cancer cell lines. In addition, action mechanism of 3’deoxyadenosin is poorly understood. In this study, we found different adenosine deaminase (ADA) expression or activity affects different anticancer results in uveal melanoma. Inhibition of ADA using either siRNA or pharmacologic approaches sensitized tumors to 3’-deoxyadenosine in vitro and in vivo, resulting in increased apoptosis, reduced clonogenic capacity and slower migration of uveal melanoma cells in vitro. These potent ADA-dependent anti-tumor effects were also seen in various cancer cell lines. Therefore, we suggest the potential of adenosine deaminase (ADA) as both a biomarker predicting response to 3’-deoxyadenosine, and a target for combination therapy. Citation Format: Su-Chan Lee, Lujain Alaali, HyukJean Kwon, Mohammed Rigi, Charles G. Eberhart. Targeting adenosine deaminase enhances anticancer effects of 3'-deoxyadenosine in uveal melanoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1868.

The possibility of predicting effectiveness oftherapy in patients with new infiltrative pulmonary tuberculosis by baseline activity of adenosine deaminase and inflammatory response parameters

The objective: to evaluate the possibility of using the baseline activity of adenosine deaminase (ADA) to predict effectiveness of therapy in patients with new infiltrative pulmonary tuberculosis (IPTB).Subjects and Methods. Data of 121 patients with new infiltrative pulmonary tuberculosis were analyzed; patients were divided into groups according to therapy effectiveness.Results., The discriminant analysis of data of new infiltrative pulmonary tuberculosis patients made it possible to obtain adiscriminant function which included the activity of ADA, the concentration of haptoglobin (HP) and ceruloplasmin (CP) – parameters reflecting that severity of the disease and protective potential of the host.Conclusion. Analysis of ADA activity in combination with level of HP and CP allows the following: predicting effectiveness of the intensive phase of therapy before it begins in patients with new infiltrative pulmonary tuberculosis (with the accuracy of 77.0%); assuming that the reduction of ADA activity and inhibition of the inflammatory response may be useful for treatment of patients with new infiltrative pulmonary tuberculosis.

The effects of ginger and its constituents in the prevention of metabolic syndrome: A review.

Metabolic syndrome is a multifactorial disorder characterized by hyperglycemia, hyperlipidemia, obesity, and hypertension risk factors. Moreover, metabolic syndrome is the most ordinary risk factor for cardiovascular disease (CVD). Numerous chemical drugs are being synthesized to heal metabolic risk factors. Still, due to their abundant side effects, herbal medicines have a vital role in the treatment of these abnormalities. Ginger (Zingiber officinale Roscoe, Zingiberaceae) plant has been traditionally used in medicine to treat disorders, including CVD. The unique ginger properties are attributed to the presence of [6]-gingerol, [8]-gingerol, [10]-gingerol, and [6]-shogaol, which through different mechanisms can be beneficial in metabolic syndrome. Ginger has a beneficial role in metabolic syndrome treatment due to its hypotensive, anti‐obesity, hypoglycemic, and hypolipidemic effects. It can significantly reduce atherosclerotic lesion areas, VLDL and LDL cholesterol levels, and elevate adenosine deaminase activity in platelet and lymphocytes. Also, it promotes ATP/ADP hydrolysis. In the current article review, the critical properties of ginger and its constituents’ effects on the metabolic syndrome with a special focus on different molecular and cellular mechanisms have been discussed. This article also suggests that ginger may be introduced as a therapeutic or preventive agent against metabolic syndrome after randomized clinical trials.

Deregulation of purinergic ectoenzyme activity in head and neck cancer promotes immunosuppression.

BackgroundHead and neck cancer (HNC) comprises a spectrum of neoplasms that affect the upper aerodigestive tract and are the sixth most common cancers worldwide. Individuals with HNC exhibit various symptoms and metabolic changes, including immune alterations and alterations of the purinergic pathway, which may signal worse outcomes. Therefore, the purpose of this research was to measure the activity of purinergic ectoenzymes and interleukins in patients with HNC, oral cavity cancer, and larynx cancer.Methods and ResultsWe recruited 32 patients and 33 healthy control subjects and performed the laboratory analyses. We identified dysregulation in the purinergic signaling pathway characterized by an increase in adenosine triphosphate (ATP) and adenosine monophosphate (AMP) hydrolysis and a decrease in the deamination of adenosine to inosine in these cancers (p < 0.05). These alterations were likely caused by increased activity of the ectoenzymes E-NTPDase and ecto-5’-nucleotidase and reduced adenosine deaminase activity. This dysregulation was associated with immune alterations, increased levels of IL-10, and decreased myeloperoxidase activity (p < 0.05), suggesting immunosuppression in these patients and suggesting possible accumulation of adenosine in the extracellular environment.ConclusionsAdenosine is a potent immunosuppressive molecule associated with tumor progression and immune evasion. Our findings suggest a relationship between extracellular purines and the development and progression of the tumor microenvironment and poor outcomes. These findings increase the understanding of biological mechanisms related to HNC and demonstrate that these components are potential diagnostic markers and therapeutic targets for future management strategies and improvement in the quality of life.

Pleural tuberculosis: experiences from two centers in Brazil

ObjectiveThis study aimed to describe the clinical and laboratory findings of patients diagnosed with pleural tuberculosis at two hospitals in southern Brazil. MethodsPatients aged < 18 years were evaluated retrospectively. The patients’ medical and epidemiological history, tuberculin skin test results, radiological and pathological findings, and pleural fluid analysis results were retrieved. ResultsNinety-two patients with pleural tuberculosis were identified. The mean age was 10.9 years old. Twenty-one percent were children aged six years or less. The most common symptoms were fever (88%), cough (72%), and chest pain (70%). Unilateral pleural effusion was observed in 96% of the cases. Lymphocyte predominance was found in 90% of the pleural fluid samples. The adenosine deaminase activity of the pleural fluid was greater than 40 U/L in 85% of patients. A diagnosis of community-acquired pneumonia with antibiotic prescriptions was observed in 76% of the study population. ConclusionsTuberculosis etiology must be considered in unilateral pleural effusion in a child with contact with a case of tuberculosis. Pleural fluid biomarkers contribute to the diagnosis of pleural tuberculosis in children and adolescents.

Evaluation of serum adenosine deaminase activity with reference to dyslipidemia in ischemic heart disease

Ischemic health disease is a major health and a modern epidemic which is increasing in India. Dyslipidemia is a major risk factor for atherosclerosis. Serum adenosine deaminase activity is associated with coronary artery disease.The present work was done to understand the relation of serum adenosine deaminase activity with dyslipidemia in ischaemic heart disease.This cross-sectional study comprised 200 subjects; healthy and myocardial infarction. Serum ADA and lipids were estimated. Obtained data was statistically analysed.Increase in serum ADA activity correlating with dyslipidemia was found in Myocardial infarction subjects.Increased ADA has role in LDL oxidation, dyslipidemia, foam cell transformation etc. leading to atherosclerosis and ischemic heart disease. Adenosine deaminase has a crucial role in the evolution of ischemic heart disease through dyslipidemia and coronary artery disease.

Comparison of Adenosine Deaminase Activity in COPD with Healthy Subjects

Background: Chronic obstructive pulmonary disease (COPD) is a disease condition characterised by non-reversible airflow restriction. Emphysema, which is the damage and inflammation of the lung alveoli, is a component of COPD. It has been demonstrated that adenosine levels rise in COPD leading to reduction in adenosine deaminase (ADA) activity. Aim: We determined the activity of ADA in COPD patients. Methods: Sixty subjects were included in this case-control study who had an acute exacerbation of COPD. The activity of the ADA was measured in 20 COPD, 20 non-smokers, and 20 smokers who served as controls. Results: Total ADA activity was significantly lower in the COPD and smoking control groups (17.87±6.73, 18.09±8.9, and 21.90±6.4 U/L, respectively) than in the non-smoker group. Conclusion: Reduction in ADA activity may play an important role in the development of lung damage in COPD patients. Keywords: Adenosine deaminase (ADA); Chronic Obstructive Pulmonary Disease (COPD), Lung.

Evaluation of Inflammatory markers in different stages of Chronic Renal Disease

Background: Chronic kidney disease (CKD) refers to a long-term loss of kidney function. The progression of CKD leads to the damage of other organs including cardiovascular disease which increased the risk of mortality. Early detection of kidney failure can slow down the end-stage renal disease. Aims and Objectives: To estimate the inflammatory marker Adenosine deaminase (ADA) activity in different stages of CKD. To correlate the level of ADA activity with Serum Creatinine with different stages of CKD on the basis of estimated glomerular filtration rate (eGFR). Materials and Methods: The participants having age more than 18 and &lt;60 years having CKD have been enrolled as a study group. CKD was confirmed by calculating eGFR using Cockcroft-Gault equation, plasma creatinine estimation done in all the patients. This study was approved by the Ethical Committee of TMMC and RC. Results: It is observed that the incidence of CKD reaches its maximum strength during middle age. 28% of the young patients, i.e., 45 years of age or younger at the time of CKD, had increased level of ADA. Serum levels of ADA, Creatinine were higher among participants with lower level of eGFR. Inflammation was higher among those with lower eGFR. All biochemical parameter (ADA, CRP, ESR) shows the negative correlation with eGFR. eGFR shows a negative highly significant correlation withESR with a correlation coefficient of r=−4.702 (P&lt;0.001). Conclusion: With the progression of Kidney disease (CKD stages 1–5) it comes to significantly increase of inflammatory markers as decrease in the eGFR with statistical significance. Inflammatory Biomarkers were inversely associated with the measure of kidney function. It is clear that a single indicator of renal function is not sufficient in evaluating the kidney disease stage.