Various antihypertensive drugs are in a wide use for the treatment of hypertension. It is important to investigate the influences of chronic administration of these drugs on genomic DNA. So the objective of the present study was to elucidate the effects of chronic administration of some antihypertensive drugs e.g. amlodipine, atenolol and captopril on alkaline phosphatase(ALP) and genomic DNA in liver, spleen and kidney of Swiss albino mice. A total of 150 Swiss albino mice were divided into 10 groups (15 mice each): a control group and 3 groups to be treated by various doses of each of the three drugs. ALP was assayed in liver, spleen and kidney after drugs administration for 1; 3 and 6 months. The genotoxic effects of the three antihypertensive drugs were evaluated by RAPD-PCR technique. All studied drugs caused elevations in the activities of ALP in liver, spleen and kidney homogenates. Amlodipine induced DNA damage in the homogenates of liver, spleen and kidney. On the other hand, atenolol and captopril did not affect the genomic DNA. From our findings we can conclude that the chronic administration of the above antihypertensive drugs induce inflammation and amlodipine had toxic effect on the genomic DNA while atenolol and captopril had no apparent effects on DNA.

Starch hydrolyzing α-amylase was purified from germinating soybean seeds. Amino acid sequence of soybean α-amylase (Accession No. Gm0237X0071) was taken from protein databases (http://soybeangenome.siu.edu/; http://soybase.org/; http://soybeangenome.org/) and used for identification of full length gene with available clone data at NCBI (http://www.ncbi.nlm.nih.gov/). Glycine max strain Williams 82 clone GM_WBb0115J10 (AC235387.1) was used for similarity search and annotation of full-length gene. The present in-silico investigation deals with full length gene (TPA BK007878) identification; and cis-acting elements study; identified the important promoter’s i.e. TATA, CAAT, GATABOX, DOFCOREZM, -300ELEMENT, WBOX, MYBST1, and EBOX for multifarious uses. A template structure (3AMK chain a) from Oryza sativa branching enzyme was selected for comparative modeling using an automated approach. Homology model was constructed using software DS Modeler and the quality of refined model was investigated using PDBSum, ERRAT and other bioinformatics softwares. The modeled structure showed acceptable Ramachandran statistics and remarkable active site residues. Structural analysis of the predicted model of α-amylase from soybean also gives an idea about potential sites inferring the region of catalytic active site responsible for inhibitory action; and opens the new opportunities for further investigations.

The DevR response regulator in Mycobacterium tuberculosis is believed to play a key role in bacterial dormancy adaptation during hypoxia and also shares a homologous genetic system with Mycobacterium smegmatis. Thus DevR is proposed to be an attractive target for the development of inhibitors against tuberculosis. Currently available first line anti-tuberculosis drugs have been caused several side effects in the body as well as resistance development by mycobacterium against these drugs, necessitates the considerable need for finding new drugs. Therefore, we propose a structure based computational method to find a new potential inhibitor for DevR protein. Natural sources provide numerous examples of interesting secondary metabolites with antimycobacterial activity, indicating that natural products could be a rewarding field for the discovery of new anti-TB leads. The present study is to deduce the structure of the DevR (UniprotID: A0R2V2) protein using prime module (Schrodinger) and to validate the same with Ramachandran plot. The proposed model structure is further explored for insilico docking studies with natural inhibitors obtained from published literatures which describe the effectiveness of natural anti-tuberculosis compounds. 143natural compounds were computationally analyzed using glide module for their bioactivity against DevR protein using virtual screening approach. The best ligand that exhibited high docking score with DevR was finally reported. Further, structure optimization and in vitro validation of above inhibitors will prove its efficacy as a better candidate in the drug designing pipeline.

Intrinsically disordered proteins are those that fail to self-fold into fixed 3D geometries, and are found to be associated with innumerable abnormalities like cancer, diabetes, cardiovascular, neurodegenerative disorders etc. Based on the predictions that, about 79% of cancer proteins are disordered, an investigation was carried out to elucidate the importance of these sequences and their roles in drug binding and disease control. A search through Drug bank database revealed 210 ligand molecules associated with 253 cancer proteins. These amino acid sequences were examined with tools such as DisEMBL and SEG, to delineate the composition of their disordered regions. 127 of these 253 sequences were having 30 or more consecutive residues predicted to be “Disordered Regions”. Structural homologues for 52 of these 127 protein sequences revealed quality global alignments, and 25 of these had their active site / ligand binding site in the “disordered regions”, as deciphered by Accelrys Discovery Studio 2.5. Further, PDB analysis revealed that these sequences were co-crystallized with drug molecules, and these ligands were bound to the respective disordered regions in the active site. Using this as basis, docking studies were performed for 11 cancer proteins involved in key pathways, with respective drug molecules to ascertain the nature of drug-receptor interactions. The results indicated that molecules mentioned in drug bank towards treating cancer, bound to their respective receptors through the disordered regions in them, highlighting that these regions could play potentially important roles in ligand Pharmacophore interactions.

Although mobile phones among daily indispensable wireless accessories a big concern about their emitted electromagnetic radiation (EMR) hazard. The present study investigated the possible damage induced by their EMR strength and duration on mammalian genome, using male Albino rats as an animal model. Animals were exposed to mobile phone emitted radiation of 1800 MHz frequency for a period of 2 hours. Exposure was performed either continuously or intermittent manners for 3 different exposure periods. The possible mutation in BRCAI and TP53 tumor suppressor genes were studied, and the degree of genomic DNA fragmentation was followed. The obtained results revealed that longer period (six weeks) of continuous EMR exposure induced mutation in both studied genes with relative increase in DNA fragmentation when compared with intermittent exposure. The study warrants the public against excessive exposure to mobile phone-induced EMR. Minimization of such exposure has to safeguard against genetic DNA fragmentation with possible consequent mutation and cancer formation.