STEROIDS AND THE STIMULATION OF SEXUAL REPRODUCTION OF A SPECIES OF PYTHIUM

1964 ◽  
Vol 10 (2) ◽  
pp. 187-195 ◽  
Author(s):  
R. H. Haskins ◽  
A. P. Tulloch ◽  
R. G. Micetich

The fatty acid compositions of the mycelia of a parasitic species of Pythium and of various hosts are reported. The Pythium spp. contained high concentrations of myristic acid and low concentrations of linoleic and linolenic acids in comparison with concentrations in other fungi tested. Appreciable amounts of unsaturated C20 acids, uncommon in fungi, were found in the Phycomycetes tested. Vegetable oils and other fats of widely varying fatty acid compositions were all effective in stimulating sexual reproduction of the Pythium sp. It was concluded that substance(s) other than fatty acids present in the vegetable oils were responsible for the stimulation observed. The most active fraction in sunflower seed oil was isolated and identified as a phytosterol, probably β-sitosterol. The results of testing for stimulatory activity a series of structurally related compounds indicated that the sexual reproduction of the Pythium sp. studied required the presence of a substance such as β-sitosterol or cholesterol or one with similar structure and which similarly satisfied certain specific structural requirements regarding length of the C17 side chain, stereochemistry, and position of the oxygenated function. β-Sitosterol and cholesterol were effective at 0.2 γ/ml in potato dextrose agar.


1972 ◽  
Vol 128 (5) ◽  
pp. 1057-1067 ◽  
Author(s):  
E. D Saggerson

1. 0.5mm-Palmitate stimulated incorporation of [U-14C]glucose into glyceride glycerol and fatty acids in normal fat cells in a manner dependent upon the glucose concentration. 2. In the presence of insulin the incorporation of 5mm-glucose into glyceride fatty acids was increased by concentrations of palmitate, adrenaline and 6-N-2′-O-dibutyryladenosine 3′:5′-cyclic monophosphate up to 0.5mm, 0.5μm and 0.5mm respectively. Higher concentrations of these agents produced progressive decreases in the rate of glucose incorporation into fatty acids. 3. The effects of palmitate and lipolytic agents upon the measured parameters of glucose utilization were similar, suggesting that the effects of lipolytic agents are mediated through increased concentrations of free fatty acids. 4. In fat cells from 24h-starved rats, maximal stimulation of glucose incorporation into fatty acids was achieved with 0.25mm-palmitate. Higher concentrations of palmitate were inhibitory. In fat cells from 72h-starved rats, palmitate only stimulated glucose incorporation into fatty acids at high concentrations of palmitate (1mm and above). 5. The ability of fat cells to incorporate glucose into glyceride glycerol in the presence of palmitate decreased with increasing periods of starvation. 6. It is suggested that low concentrations of free fatty acids stimulate fatty acid synthesis from glucose by increasing the utilization of ATP and cytoplasmic NADH for esterification of these free fatty acids. When esterification of free fatty acids does not keep pace with their provision, inhibition of fatty acid synthesis occurs. Provision of free fatty acids far in excess of the esterification capacity of the cells leads to uncoupling of oxidative phosphorylation and a secondary stimulation of fatty acid synthesis from glucose.



PEDIATRICS ◽  
1968 ◽  
Vol 41 (3) ◽  
pp. 640-645
Author(s):  
Paulus Zee

Triglyceride, cholesterol and cholesteryl ester concentrations in the cord serum of 10 infants were determined and found to be considerably lower than in the mother's serum. The fatty acid compositions of the cord serum triglycerides and cholesteryl esters were significantly different from those of the mothers. The linoleate fraction of these esters was especially low. Plasma triglyceride concentrations in full-term, healthy infants rose significantly 9 hours after birth. The fatty acid distribution of these triglycerides at 12 hours varied from that at birth; this difference was also reflected in reported plasma free fatty acids and suggests a precursory relationship. The plasma total cholesterol concentrations did not alter in the first 12 hours, nor did the fatty acid distribution of the cholesteryl esters change significantly. A method to measure low concentrations of triglycerides in small samples is described. The differences between maternal and cord serum lipids suggest that fetal lipids do not originate directly in the mother. The rise in plasma triglycerides is part of an increased fat mobilization occurring after birth.



1989 ◽  
Vol 67 (9) ◽  
pp. 999-1006 ◽  
Author(s):  
Njanoor Narayanan ◽  
Philip Bedard ◽  
Trilochan S. Waraich

In the present study, the effects of the cytosolic Ca2+ transport inhibitor on ATP-dependent Ca2+ uptake by, and unidirectional passive Ca2+ release from, sarcoplassmic reticulum enriched membrane vesicles were examined in parallel experiments to determine whether inhibitor-mediated enhancement in Ca2+ efflux contributes to inhibition of net Ca2+ uptake. When assays were performed at pH 6.8 in the presence of oxalate, low concentrations (<100 μg/mL) of the inhibitor caused substantial inhibition of Ca2+ uptake by SR (28–50%). At this pH, low concentrations of the inhibitor did not cause enhancement of passive Ca2+ release from actively Ca2+-loaded sarcoplasmic reticulum. Under these conditions, high concentrations (>100 μg/mL) of the inhibitor caused stimulation of passive Ca2+ release but to a much lesser extent when compared with the extent of inhibition of active Ca2+ uptake (i.e., twofold greater inhibition of Ca2+ uptake than stimulation of Ca2+ release). When Ca2+ uptake and release assays were carried out at pH 7.4, the Ca2+ release promoting action of the inhibitor became more pronounced, such that the magnitude of enhancement in Ca2+ release at varying concentrations of the inhibitor (20–200 μg/mL) was not markedly different from the magnitude of inhibition of Ca2+ uptake. In the absence of oxalate in the assay medium, inhibition of Ca2+ uptake was observed at alkaline but not acidic pH. These findings imply that the inhibition of Ca2+ uptake observed at pH 6.8 is mainly due to decrease in the rate of active Ca2+ transport into the membrane vesicles rather than stimulation of passive Ca2+ efflux; at alkaline pH (pH 7.4), enhanced Ca2+ efflux contributes substantially, if not exclusively, to the decrease in Ca2+ uptake observed in the presence of the inhibitor. It is suggested that if the cytosolic inhibitor has actions similar to those observed in vitro in intact cardiac muscle, acid–base status of the intracellular fluid would be a major factor influencing the nature of its effects (inhibition of Ca2+ uptake or stimulation of Ca2+ release) on transmembrane Ca2+ fluxes across the sarcoplasmic reticulum.Key words: sarcoplasmic reticulum, Ca2+ uptake, Ca2+ release, endogenous inhibitor, heart muscle.



2016 ◽  
Vol 2016 ◽  
pp. 1-6
Author(s):  
Zhan-jun Li ◽  
Feng-jian Yang ◽  
Lei Yang ◽  
Yuan-Gang Zu

Oil extracted from the seeds ofCaesalpinia spinosa(common name: tara) can be used in a number of applications. In the present study, tara seed oil was obtained by ultrasonic extraction. The effects of different solvents, particle sizes in the ground seed samples, extraction times, ultrasonication powers, extraction temperatures, and liquid–solid ratios on the yield of tara seed oil were investigated. The yield from the ultrasonic extraction was compared with that from traditional Soxhlet extraction. The results showed that ultrasonic extraction could be completed in a shorter time with reduced solvent consumption. The yield of tara seed oil increased with increasing ultrasonication power and extraction temperature. Gas chromatography was used to analyze the fatty acid compositions of the oils extracted by the two methods. The fatty acid compositions of the oils from both extraction methods were similar, which indicates that ultrasonic extraction is a viable alternative means of extraction. It is a rapid, efficient, and simple method for production of lipids from tara seeds.



1974 ◽  
Vol 137 (3) ◽  
pp. 435-442 ◽  
Author(s):  
Owen A. Young ◽  
John W. Anderson

1. Short-chain fatty acyl-CoA synthetase from seeds of Pinus radiata was examined by acetate- and propionate-dependent PPi–ATP exchange. Reaction mixtures came to equilibrium almost instantly as judged by rates of exchange and analysis of an incubation mixture. 2. The activity of the enzyme was correlated with the concentration of MgP2O72- but not with the concentration of Mg2+, as judged by PPi–ATP exchange and fatty acyl AMP-dependent synthesis of ATP in the presence of PPi. In PPi–ATP exchange assays, no clear relationship between activity and any single species of ATP was apparent. 3. High concentrations of fatty acid inhibited PPi–ATP exchange. PPi–dATP exchange was less than PPi–ATP exchange at low concentrations of fatty acid, but at higher concentrations PPi–dATP exchange exceeded PPi–ATP exchange. The rate of synthesis of fatty acyl-CoA in the presence of dATP was less than with ATP. 4. ATP and propionate inhibited the synthesis of ATP from propionyl-AMP and PPi. The inhibition by ATP was competitive with respect to propionyl-AMP and non-competitive with respect to PPi. The inhibition by propionate was non-competitive with respect to propionyl-AMP and PPi. 5. AMP was a competitive inhibitor of propionyl-AMP-dependent synthesis of ATP and competitively inhibited propionate-dependent PPi–ATP exchange when ATP was the variable substrate. 6. It was concluded that the first partial reaction catalysed by the enzyme is ordered; ATP is the first substrate to react with the enzyme and PPi is probably the only product released.





1986 ◽  
Vol 251 (2) ◽  
pp. C238-C246 ◽  
Author(s):  
B. Espinoza ◽  
W. Wharton

Cholera toxin produced a dose-dependent decrease in the restimulation of G0/G1 traverse in density-arrested human fibroblasts but did not inhibit the stimulation of cells arrested in G0 after serum starvation at low density. In addition, cholera toxin did not inhibit the proliferation of sparse logarithmically growing human fibroblasts, even when low concentrations of the phosphodiesterase inhibitor isobutylmethylxanthine (IBMX) were also present. However, the final density to which sparse cells grew was limited by cholera toxin, when added either alone or together with low concentrations of IBMX. In contrast, high concentrations of the phosphodiesterase inhibitor alone produced a profound inhibition in the growth of sparse human fibroblasts. IBMX produced an inhibition both in the G1 and in the G2 phases of the cell cycle by a mechanism(s) that was not related to the magnitude of the increases in adenosine 3',5'-cyclic monophosphate concentrations.



1990 ◽  
Vol 259 (4) ◽  
pp. H1079-H1085 ◽  
Author(s):  
J. J. McVeigh ◽  
G. D. Lopaschuk

We have previously shown that high concentrations of fatty acids depress reperfusion recovery of ischemic rat hearts as a result of a fatty acid inhibition of glucose oxidation. In this study, we determined whether dichloroacetate, an activator of pyruvate dehydrogenase, could overcome fatty acid inhibition of glucose oxidation and thereby improve mechanical recovery of hearts reperfused after a period of transient global ischemia. Isolated working rat hearts, perfused with 11 mM glucose, 1.2 mM palmitate, and 500 microU/ml insulin, were subjected to a 30-min period of no flow ischemia, followed by a 30-min period of reperfusion. Under these conditions, control hearts recovered 37% of preischemic function. The addition of 1 mM dichloroacetate to the perfusate at reperfusion resulted in a significant improvement in recovery of mechanical function (to 73% of preischemic function). When dichloroacetate was added before the onset of ischemia, however, this protective effect was lost, and a significant increase in myocardial lactate accumulation during ischemia was observed. The effects of dichloroacetate on glucose oxidation rates in both nonischemic and reperfused ischemic hearts was determined by perfusing hearts with 11 mM [U-14C]glucose and 1.2 mM palmitate and quantitatively collecting 14CO2 produced by the heart. In nonischemic hearts, 1 mM dichloroacetate increased steady-state glucose oxidation rates from 298 +/- 69 to 1,223 +/- 135 nmol.g dry wt-1.min-1. The addition of dichloroacetate to hearts reperfused after a 25-min period of ischemia also increased glucose oxidation rates from (112 +/- 25 to 561 +/- 83 nmol.g dry wt-1.min-1).(ABSTRACT TRUNCATED AT 250 WORDS)



Trees ◽  
1997 ◽  
Vol 12 (2) ◽  
pp. 57 ◽  
Author(s):  
R. L. Wolff ◽  
Laurent G. Deluc ◽  
Anne M. Marpeau ◽  
Bernard Comps


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