Phosphatases are known to play a crucial role in phosphate turnover in plants. However, the exact role of acid phosphatases in plants has been elusive because of insufficient knowledge of their in vivo substrate and subcellular localization. We investigated the biochemical properties of a purple acid phosphatase isolated from red kidney bean (Phaseolus vulgaris) (KBPAP) with respect to its substrate and inhibitor profiles. The kinetic parameters were estimated for five substrates. We used 31P nuclear magnetic resonance to investigate the in vivo substrate of KBPAP. Chemical and enzymological estimation of polyphosphates and ATP, respectively, indicated the absence of polyphosphates and the presence of ATP in trace amounts in the seed extracts. lmmunolocalization using antibodies raised against KBPAP was unsuccessful because of the nonspecificity of the antiserum toward glycoproteins. Using histoenzymological methods with ATP as a substrate, we could localize KBPAP exclusively in the cell walls of the peripheral two to three rows of cells in the cotyledons. KBPAP activity was not detected in the embryo. In vitro experiments indicated that pectin, a major component of the cell wall, significantly altered the kinetic properties of KBPAP. The substrate profile and localization suggest that KBPAP may have a role in mobilizing organic phosphates in the soil during germination.

No abstract

No abstract

Inhibiting Hsp90 chaperone roles using 17AAG induces cytostasis or apoptosis in tumor cells through destabilization of several mutated cancer promoting proteins. Although mitochondria are central in deciding the fate of cells, 17AAG induced effects on tumor cell mitochondria were largely unknown. Here, we show that Hsp90 inhibition with 17AAG first affects mitochondrial integrity in different human tumor cells, neuroblastoma, cervical cancer and glial cells. Using human neuroblastoma tumor cells, we found the early effects associated with a change in mitochondrial membrane potential, elongation and engorgement of mitochondria because of an increased matrix vacuolization. These effects are specific to Hsp90 inhibition as other chemotherapeutic drugs did not induce similar mitochondrial deformity. Further, the effects are independent of oxidative damage and cytoarchitecture destabilization since cytoskeletal disruptors and mitochondrial metabolic inhibitors also do not induce similar deformity induced by 17AAG. The 1D PAGE LC MS/MS mitochondrial proteome analysis of 17AAG treated human neuroblastoma cells showed a loss of 61% proteins from membrane, metabolic, chaperone and ribonucleoprotein families. About 31 unmapped protein IDs were identified from proteolytic processing map using Swiss-Prot accession number, and converted to the matching gene name searching the ExPASy proteomics server. Our studies display that Hsp90 inhibition effects at first embark on mitochondria of tumor cells and compromise mitochondrial integrity.

Context:Chronic Kidney Disease (CKD) is associated with a high risk of developing further severe complications such as, cardiovascular disease and eventually End Stage Renal Disease (ESRD) leading to death. Hypertension plays a key role in the progression of renal failure and is also a chief risk factor for the occurrence of End Stage Renal Disease (ESRD).Aim:This study investigates the possible association of insertion (I) and deletion (D) polymorphism of ACE gene in patients of Chronic Kidney Disease (CKD) with and without hypertension (HT).Settings and Design:Total 120 participants with 30 members in each group (Control, HT, CKD and CKD-HT) were chosen followed by informed consent.Materials and Methods:Blood samples were collected and subjected to biochemical analyses and nested PCR amplification was performed to genotype the DNA, for ACE I/D using specific primers.Statistical Analysis:Statistical analyses were performed using SPSS version 13. Allele and genotypic frequency was calculated by direct gene counting method. Comparison of the different genotypes was done by using Chi square test. Odd's ratios were calculated with a 95% confidence interval limit.Results:The ACE genotype were distributed as II, 27 (90%); DD, 2 (6.67%) and ID, 1 (3.33%) in control, II, 1 (3.33%); DD, 5 (16.67%) and ID, 24 (80%) in HT, II, 4 (13.33%); DD, 24 (80%) and ID, 2 (6.67%) in CKD and II, 0 (0%); DD, 2 (6.67%) and ID, 28 (93.33%) in CKD-HT group.Conclusions:D allele of ACE gene confers a greater role in genetic variations underlying CKD and hypertension. This result suggest that CKD patients should be offered analysis for defects in ACE I/D polymorphisms, especially if they are hypertensive.

No abstract

non disponibile

Introduction: Assessment of host response to inflammation will throw light on the critical role of antioxidants (AOs) and free radicle damage in the etiology of periodontal disease. The purpose of the study was to assess the level of plasma oxidative stress in those having aggressive periodontal disease before and after full-mouth disinfection. Objectives were to find the influence of full-mouth disinfection analyzing the level of thiobarbituric acid reactive substances (TBARSs), thereby quantifying the lipid peroxidation (LPO) and also the activities of reduced glutathione (GSH), glutathione peroxidase (GP X ), and catalase (CAT), valuing the AO defense systems in health and disease. Materials and methods: The valuation composed of 30 subjects with aggressive periodontal disease and 30 healthy controls. Clinical assessment included following periodontal parameters: plaque index (PI), papillary bleeding index (PBI), probing pocket depth (PPD), and clinical attachment level (CAL). Levels of bone loss were assessed by taking full-mouth periapical radiographs. Initial periodontal therapy comprises of full-mouth disinfection which includes subgingival scaling and root planing within 24 hours combined with adjunctive chlorhexidine chemotherapy for aggressive periodontitis subject's at sites indicated. The parameters (clinical) were evaluated at the baseline and 8 weeks after initial periodontal therapy at six sites of teeth indicated. Plasma samples were taken and evaluated by standard procedures as defined in the literature. All the values were weighed and related. Results: Strong positive associations were detected among periodontal parameters and TBARS, enzymatic/nonenzymatic AO levels (p < 0.05), and pre-and postperiodontal management. The plasma levels of patients with aggressive periodontitis had high levels of TBARS and displayed a substantial escalation in the activities of GSH and GP X levels in the plasma matched to the healthy individuals (p < 0.05). Conclusion:This paper evaluated ROS activity and AO defense before and after treatment to stimulate added periodontal investigation in this part which will give an insight into the therapeutic options with foreseeable results.