Novel targets for antibiotics discovery: riboswitches / 药学学报

Riboswitches are cis-acting domains located in mRNA sequences that could regulate gene expression by sensing small molecules without employing protein. Most known riboswitches in bacteria have naturally evolved to bind essential metabolite ligands and are involved in the regulation of critical genes that are responsible for the biosynthesis or transport of the cognate ligand. The riboswitch-mediated gene expression could be repressed by metabolite analogs, which caused bacterial growth inhibition or even death. A number of leading compounds targeting riboswitches have been discovered. A promising avenue for the development of new class of riboswitch-based antibiotics has been opened. Herein we reviewed the current findings of riboswitches that served as targets for antibacterial drug development and the underlying mechanisms. The development of high-throughput methods and rational drug design for riboswitch-specific drug discovery are relevant challenges are discussed. summarized.

histochemical changes on the activity of some enzymes in gamma-irradiated rat neurons

The effect of whole body gamma-irradiation at a single exposure dose of 600 and 1200 reds on the activity of acid phosphatase [ACP], adenosine triphosphatase [ATP], thiamine pyrophosphatase [TPP] and succinic dehy-drogenase [SDH] was studied. Neurons in the cerebellum, spinal cord and trigeminal ganglia of control and irradiated rats were investigated. Significant changes in [ACP] activity in irradiated nerve cells were observed. Marked increase in the number and size of lysosomes were detected in animals exposed to 600 rads. A high dose of 1200 rads induced lysis of the lysosomal membrane resulting in consequent diffusion of [ACP] and an increase in its activity indicating that the effect of radiation increases with increasing dose. Two hours post irradiation, an increase in TPP activity was observed. However, gradual decrease in the enzyme activity was recorded 24 and 48 hours following irradiation. A decrease in ATP and SDH activity was noticed between 2-48 hours post irradiation. The decrease in the enzyme activity is considerably higher by increasing the dose of irradiation and the time post exposure

Transition of Marker Enzymes of Rat Hepatocyte Organelles in Culture / 영남의대학술지

To investigate recovery, growth, and activity of hepatocyte in primary culture after cell separation, the authors followed up the marker enzyme activities of golgi complex, mitochondria and biologic membrane. Thiamine pyrophosphatase, the marker enzyme of golgi complex, activity approached the level of long term culture at 4th day. Succinate dehydrogenase, the marker enzyme of mitochondria, activity decreased with time, then it maintained constant level after 4th day. Alkaline phosphatase, the marker enzyme of biological membrane, activity increased from 3rd day, and after 5th day it showed strong reaction. These data suggested that hepatocytes were stabilized and recovered normal activity 4 day after cell separation. But the main secretory function was speculated to be reduced in culture.

Effects of Dimethyl Sulfoxide on the Differentiation of Myocardial and Endothelial Cells / 영남의대학술지

To elucidate the effects of dimethyl sulfoxide on of myocardial and endothelial cells in culture, the cells were exposed to 10% dimethyl sulfoxide in culture medium for 1 hour at 48 hours after cell isolation. The general morphology and the cytochemical reaction of marker enzymes for mitochondria and Golgi complexes were investigated. The results were summarized as follows 1. DMSO induced elongation and narrowing of the cells and increase of mitochondrial reaction in myocardial cells. 2. DMSO induced destruction and disruption of myofibrils in myocardial cells resulting in increase of contractile activities. 3. In the endothelial cells, DMSO suppressed proliferative activities but thiamine pyrophosphatase reactions were enhanced indicating increase of Golgi complex activity. 4. DMSO seemed to hamper with the adhesiveness and motility of the endothelial cells causing the decrease of the number of cells in vitro.