Sulphydryl and Disulphide Levels in Protein Fractions from Hydrated and Dry Leaves of Resurrection Plants

Significant changes in sulphydryl (‘SH’) and disulphide(‘SS’) levels during air-drying in leaves of ‘resurrection’plants (whose protoplasm survives dehydration) stemmed mainlyfrom protein turnover effects. No significant changes were foundin the SH, SS levels in leaves of the desiccation sensitivespecies Sporobolus pyramidalis following air-drying. The three tolerant species studied differed in the directionof change. Some data were consistent with Levitt's SH, SS hypothesis:increases in protein-SS levels in Sporobolus stapfianus (desiccationtolerant) were consistent with a stabilization of new proteinby SS bonds; lower reactivity of protein-SH in the tolerantspecies Talbotia elegans (which on the other hand has decreasedprotein-SS) is consistent with a second mechanism of decreasingprotein denaturation proposed in Levitt's hypothesis. Evidence of some conversion of SH to SS in the soluble proteinsof Xerophyta viscosa (a tolerant species) would on Levitt'shypothesis indicate an injurious process. Some degree of proteindenaturation might be indicated by partial inactivation of thesoluble enzyme ribulose bisphosphate carboxylase in this species,and loss of some soluble isoenzymes (peroxidase and alkalinephosphatase). An apparent lack of SH conversion to SS in thesensitive species Sporobolus pyramidalis was not consistentwith the SH, SS hypothesis. Resurrection plants, Sporobolus pyramidalis, Sporobolus stapfianus, Talbotia elegans, Xerophyta viscosa, drought resistance, desiccation tolerance, protein turnover, sulphydryl groups     

Genetic mapping of the G101 bacteriophage (Pseudomonas aeuruginosa by temperature-sensitive mutations

Temperature-sensitive (ts) mutations of the G101 phage were isolated after mutagenesis with hydroxylamine. A complementation analysis of 61ts mutants showed that these mutants may be divided into at least 12 complementation groups. Twots mutants probably originated in genes which control lytic functions of the G101 phage. It was shown by three factor crosses that all of the 12ts mutations tested are localized on that side of the “c” region where the probablecI repressor gene is positioned. Sevents mutations is closely linked to thecI ₂₆ clear marker, three exhibit a closer linkage and two do not exhibit any linkage withcI. All mutations isolated until now can be arrange linearly. According to the present knowledge the preliminary genetic map of the G101 phage is linear.     

An inexpensive photosynthetic irradiance sensor for ecological field studies

The design and characteristics of inexpensive and simply constructed equal-energy response photosynthetic irradiance sensors is described for use particularly where several cells are required in comparative ecological studies either above or below water. The dimensions of the sensors can be changed proportionally to suit different applications or components. The response of the sensor to irradiance at varying angles corresponds very closely to that required by the cosine law. The sensor is comparatively insensitive to other environmental variables in field use and gave a stable output; the long term drift was proportional to electrical output but in continuous use, drift is regular and could reach -0.08 year^-1 of the total. The spectral range and cosine response is discussed in comparison to other more expensive (x 5–10) commercially available, sensors and to local standards.     

Suppression of A-type potassium current in pyramidal neurons of the rat hippocampus, induced by pinacidil and its fluorine derivatives

With the use of a patch-clamp technique in the whole-cell configuration, we studied the effects of pinacidil and its fluorine derivatives on A-type potassium current (I _A) through the membrane of pyramidal neurons of the rat hippocampus. Hydrogen peroxide (10 mM) exerted no influence on the rate of inactivation ofI _A; therefore, this current is probably mediated by Shal Kv4.2 potassium channels. Pinacidil demonstrated the properties of a weakI _A blocker: in the 500 μM concentration it blocked about 45% of the current, while 50 μM of pinacidil fluorine derivatives were capable of blocking up to 30% ofI _A. The effects of pinacidil and its derivatives showed no dependence on the stimulating potential. A similar pattern of the effects of pinacidil fluorine derivatives, which are an order of magnitude stronger than those of pinacidil itself, allows us to suppose that the imine nitrogen of the tested compounds is significantly more involved in the molecular interaction with the site of an A-type potassium channel than the pyridine nitrogen.     

Mitochondrial glutathione modulates TNF-alpha-induced endothelial cell dysfunction.

The effect of glutathione (GSH) depletion by L-buthionine-[S,R]-sulphoximine (BSO) on tumor necrosis factor-alpha (TNF-alpha)-induced adhesion molecule expression and mononuclear leukocyte adhesion to human umbilical vein endothelial cells (HUVECs) was investigated. Cells with marked depletion of cytoplasmic GSH, but with an intact pool of mitochondrial GSH, only slightly enhanced TNF-alpha-induced E-selectin and vascular cell adhesion molecule-1 (VCAM-1) expression, compared with the control. However, TNF-a-induced expression of both molecules was markedly enhanced when the mitochondrial GSH pool was diminished to <15% of the control. In contrast, TNF-alpha-induced intercellular adhesion molecule-1 (ICAM-1) expression was not affected by the depletion of either cytoplasmic or mitochondrial GSH. Marked enhancement of TNF-alpha-induced adhesion molecule expression by the depletion of mitochondrial GSH resulted in increased in mononuclear leukocyte adhesion to treated HUVECs, compared with the control. These effects parallel reactive oxygen species (ROS) formation by the depletion of mitochondrial but not cytoplasmic GSH. Our findings demonstrate that depletion of mitochondrial GSH renders more ROS generation in HUVECs, and mitochondrial GSH modulates TNF-alpha-induced adhesion molecule expression and mononuclear leukocyte adhesion in HUVECs.