Isolation of a respiratory inhibitor from alfalfa

1959 ◽  
Vol 84 (2) ◽  
pp. 405-410 ◽  
Author(s):  
Ralph A. Shaw ◽  
Horace D. Jackson
Author(s):  
Cláudia A. Ribeiro ◽  
Luke A. Rahman ◽  
Louis G. Holmes ◽  
Ayrianna M. Woody ◽  
Calum M. Webster ◽  
...  

AbstractThe spread of multidrug-resistance in Gram-negative bacterial pathogens presents a major clinical challenge, and new approaches are required to combat these organisms. Nitric oxide (NO) is a well-known antimicrobial that is produced by the immune system in response to infection, and numerous studies have demonstrated that NO is a respiratory inhibitor with both bacteriostatic and bactericidal properties. However, given that loss of aerobic respiratory complexes is known to diminish antibiotic efficacy, it was hypothesised that the potent respiratory inhibitor NO would elicit similar effects. Indeed, the current work demonstrates that pre-exposure to NO-releasers elicits a > tenfold increase in IC50 for gentamicin against pathogenic E. coli (i.e. a huge decrease in lethality). It was therefore hypothesised that hyper-sensitivity to NO may have arisen in bacterial pathogens and that this trait could promote the acquisition of antibiotic-resistance mechanisms through enabling cells to persist in the presence of toxic levels of antibiotic. To test this hypothesis, genomics and microbiological approaches were used to screen a collection of E. coli clinical isolates for antibiotic susceptibility and NO tolerance, although the data did not support a correlation between increased carriage of antibiotic resistance genes and NO tolerance. However, the current work has important implications for how antibiotic susceptibility might be measured in future (i.e. ± NO) and underlines the evolutionary advantage for bacterial pathogens to maintain tolerance to toxic levels of NO.


1988 ◽  
Vol 66 (4) ◽  
pp. 635-641 ◽  
Author(s):  
S. Jana ◽  
M. K. Upadhyaya ◽  
S. N. Acharya

Seven crosses, involving either nondormant × dormant or dormant × dormant pure lines of wild oats (Avena fatua L.), were made. Selfing of the hybrid and further hybridization were carried out to produce the F2 and reciprocal backcross generations. The seed germination time-course curves of the parents, their F1, and segregating generations over a 20-week period were studied. Differences in time course of germination in these generations were interpreted in terms of a minimum of three interacting loci. Two pure lines, AN51 and MO73, differed in their response to sodium azide, a respiratory inhibitor, with the former being more responsive. In crosses between these lines, the F1 seeds were also more responsive when AN51 was used as the maternal parent. This differential response of two dormant pure lines and their reciprocal F1s suggests maternal influence in germination response to sodium azide.


1980 ◽  
Vol 58 (5) ◽  
pp. 403-409 ◽  
Author(s):  
D. C. S. Hutchison ◽  
R. Desai ◽  
D. Bellamy ◽  
H. Baum

1. The lysosomal enzymes of circulating polymorphonuclear leucocytes contain a potent elastase; release of this enzyme within the lung is thought to be responsible for the destruction of elastic tissue in pulmonary emphysema. 2. The release of lysosomal enzymes from blood leucocytes of normal and emphysematous subjects during phagocytosis of particulate material was studied In vitro. Acid phosphatase and acid ribonuclease were used as markers of lysosomal enzyme release, no sufficiently sensitive assay for elastase being available. Cigarette smoke was separated into ‘particulate’ and ‘soluble’ fractions. In a preliminary study, the particulate fraction stimulated enzyme release; in the experiments reported here, latex particles were used to produce this effect. 3. Approximately one-third of the total lysosomal enzyme content was released to the exterior of the cell during phagocytosis of latex particles. In this respect there was no difference between normal and emphysematous subjects. 4. The effects of the non-particulate soluble fraction of cigarette smoke on phagocytosis-induced enzyme release were studied. This fraction inhibited enzyme release from polymorphonuclear leucocytes of normal subjects but not from those of emphysematous patients. When the ‘cigarette-smoke solution’ was replaced by the respiratory inhibitor, antimycin A, a similar inhibition of enzyme release occurred. The inhibition of phagocytosis in cells of normal subjects is presumed to be due to a respiratory inhibitor such as carbon monoxide in the soluble fraction of the smoke. We postulate that the polymorphonuclear leucocytes of emphysematous patients are adapted to hypoxic conditions so that inhibition of enzyme release does not occur.


1938 ◽  
Vol 15 (1) ◽  
pp. 132-142
Author(s):  
W. L. FRANCIS ◽  
O. GATTY

The oxidative biochemistry of living frog skin in so far as it is concerned with the maintenance of the electrical potential across the skin has been investigated by the use of the respiratory inhibitor iodoacetate. It appears that internal supplies of carbohydrate and external supplies of dl-lactate, pyruvate, acetate, propionate, n-butyrate, iso-butyrate and possibly crotonate can all be oxidized to precursors of the potential. This is not so for external supplies of formate, glycollate, succinate, acrylate, malonate, dl-β-hydroxybutyrate, and acetoacetate.


1991 ◽  
Vol 260 (3) ◽  
pp. C383-C391 ◽  
Author(s):  
C. M. Hohl ◽  
R. A. Altschuld

Isolated adult canine ventricular myocytes incubated in the absence of glucose with the respiratory inhibitor rotenone retained 67% of ATP (control, 26.0 +/- 0.9 nmol/mg protein) during 3-h incubation, yet phosphocreatine fell to 23% of initial content. Lactate production proceeded at a constant rate of 5 nmol.mg-1.min-1 in rotenone-treated glucose-free myocytes. A 36% decline in rod-shaped cells and an increase in percent 22Na permeation from 37% in aerobic cells (approximately 13 mM intracellular sodium) to 68% in rotenone-treated glucose-free myocytes paralleled the loss of ATP. Total exchangeable calcium was maintained at control aerobic levels. Exposure of canine cells to 3-h hypoxia in the absence of glucose followed by 5-min reoxygenation resulted in a 73% decrease in ATP, a rise in calcium from 3.3 +/- 0.2 to 6.6 +/- 1.6 nmol/mg, and an increase in 22Na permeation to 111%. Under these conditions the number of rod-shaped myocytes declined by 77%, with corresponding increases in viable contracted and hypercontracted myocytes. The response of canine myocytes to severe hypoxia and reaeration contrasts greatly to earlier studies using adult rat cardiac myocytes [see Hohl et al. Am. J. Physiol. 242 (Heart Circ. Physiol. 11): H1022-H1030, 1982]. Species differences with respect to basal metabolism, rates of ATP production and degradation, and regulation of cation movements are most likely responsible for the observed differences.


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