The Inhibitory Action of Antimycin A in the Early Chick Embryo

Development ◽  
1960 ◽  
Vol 8 (3) ◽  
pp. 314-320
Author(s):  
J. McKenzie ◽  
J. D. Ebert

Antimycin A, an antibiotic obtained from an undetermined species of streptomyces, was isolated, crystallized, and described by Dunshee, Leben, Keitt, & Strong (1949), and its biological action has been studied by many workers since then. Ahmad, Schneider, & Strong (1950) demonstrated its effects on the growth and metabolism of yeast, on enzyme activities in the succinoxidase system, and on rats given the drug orally. Potter & Reif (1952) confirmed the inhibitory effect of antimycin A on the succinoxidase system in liver, suggested the presence of an ‘antimycin A-blocked factor’, identical, probably, with the ‘Slater factor’ and showed that, in certain tissues, there is an antimycin A-insensitive pathway for DPN oxidation. The same workers, Reif & Potter (1954), used the drug to characterize the pathways of DPN oxidation in different tissues. Green, Mii, & Kahout (1955) and Thorn (1956) argue from their experiments that the BAL-sensitive (Slater) factor and the antimycin A-sensitive factor are not identical.

Development ◽  
1962 ◽  
Vol 10 (1) ◽  
pp. 88-98
Author(s):  
Patricia Barron ◽  
J. Mckenzie

The list of effective teratogenic agents has become embarrassingly long: physical agents, metabolic inhibitors, vitamin deficiency, hypervitaminosis, and hormones, to mention only a few, are all known to produce congenital abnormalities. These substances have been administered at different times and in varying doses to nearly every group of animals, from amphibians to mammals, but there has been little effort to examine their mode of action. All too often, investigation ceases with the demonstration of a statistically significant number of abnormalities, enough to label the agent teratogenic. Sometimes a section of the work describes the histology of the lesions but does not indicate the primary action of the teratogen. Occasionally a drug has a well-recognized metabolic or chemical effect, e.g. cyanide on cytochrome oxidase, iodoacetate on triosephosphate dehydrogenase (Spratt, 1950), and we learn, by deduction, a little of the normal metabolism of development. Relatively few substances fall into this category, however.


1968 ◽  
Vol 37 (3) ◽  
pp. 650-659 ◽  
Author(s):  
Judson D. Sheridan

Electrophysiological evidence is presented for the exchange of small ions directly between cells interiors, i.e. "electrical coupling," in the early chick embryo. Experiments with intracellular marking show that coupling is widespread, occurring between cells in the same tissue, e.g. ectoderm, notochord, neural plate, mesoderm, and Hensen's node, and between cells in different tissues, e.g. notochord to neural plate, notochord to neural tube, notochord to mesoderm. The coupling demonstrates the presence of specialized low-resistance intercellular junctions as found in other embryos and numerous adult tissues. The results are discussed in relation to recent electron microscopical studies of intercellular junctions in the early chick embryo. The function of the electrical coupling in embryogenesis remains unknown, but some possibilities are considered.


1957 ◽  
Vol 41 (2) ◽  
pp. 279-288 ◽  
Author(s):  
Toshio Ito ◽  
G. Fraenkel

The effect of γ-butyrobetaine alone and with the addition of carnitine on the development of the early excised chick embryo has been studied. γ-Butyrobetaine in appropriate amounts exerts an inhibitory effect which can be relieved or annulled by the inclusion of appropriate amounts of carnitine. This has been interpreted as a metabolite-antimetabolite relationship, in which the normal metabolite, carnitine, is antagonized by the structurally closely related γ-butyrobetaine, and is regarded as evidence of an important role of carnitine in the metabolism of the developing chick embryo.


Development ◽  
1996 ◽  
Vol 122 (5) ◽  
pp. 1523-1534 ◽  
Author(s):  
D. Psychoyos ◽  
C.D. Stern

We have used carbocyanine dyes to fate map the primitive streak in the early chick embryo, from stages 3+ (mid-primitive streak) to 9 (8 somites). We show that presumptive notochord, foregut and medial somite do not originate solely from Hensen's node, but also from the anterior primitive streak. At early stages (4- and 4), there is no correlation between specific anteroposterior levels of the primitive streak and the final position of their descendants in the notochord. We describe in detail the contribution of specific levels of the primitive streak to the medial and lateral halves of the somites. To understand how the descendants of labelled cells reach their destinations in different tissues, we have followed the movement of labelled cells during their emigration from the primitive streak in living embryos, and find that cells destined to different structures follow defined pathways of movement, even if they arise from similar positions in the streak. Somite and notochord precursors migrate anteriorly within the streak and pass through different portions of the node; this provides an explanation for the segregation of notochord and somite territories in the node.


1984 ◽  
Vol 52 (03) ◽  
pp. 333-335 ◽  
Author(s):  
Vider M Steen ◽  
Holm Holmsen

SummaryThe inhibitory effect of cAMP-elevating agents on shape change and aggregation in human platelets was studied to improve the understanding of the sequential relationship between these two responses.Human platelet-rich plasma was preincubated for 2 min at 37° C with prostaglandin E1 or adenosine, agents known to elevate the intracellular level of cAMP. Their inhibitory effects on ADP-induced shape change and aggregation were determined both separately and simultaneously. The dose-inhibition patterns for shape change and aggregation were similar for both PGE1 and adenosine. There was no distinct difference between the inhibitory action of these two inhibitors.These observations suggest that elevation of the intracellular concentration of cAMP interferes with an early step in the stimulus-response coupling that is common for aggregation and shape change.


1986 ◽  
Vol 55 (01) ◽  
pp. 012-018 ◽  
Author(s):  
Paolo Gresele ◽  
Jef Arnout ◽  
Hans Deckmyn ◽  
Jos Vermylen

SummaryDipyridamole inhibits platelet aggregation in whole blood at lower concentrations than in plasma. The blood cells responsible for increased effectiveness in blood are the erythrocytes. Using the impedance aggregometer we have carried out a series of pharmacological studies in vitro to elucidate the mechanism of action of dipyridamole in whole blood. Adenosine deaminase, an enzyme breaking down adenosine, reverses the inhibitory action of dipyridamole. Two different adenosine receptor antagonists, 5’-deoxy-5’-methylthioadenosine and theophylline, also partially neutralize the activity of dipyridamole in blood. Enprofylline, a phosphodiesterase inhibitor with almost no adenosine receptor antagonistic properties, potentiates the inhibition of platelet aggregation by dipyridamole. An inhibitory effect similar to that of dipyridamole can be obtained combining a pure adenosine uptake inhibitor (RE 102 BS) with a pure phosphodiesterase inhibitor (MX-MB 82 or enprofylline). Mixing the blood during preincubation with dipyridamole increases the degree of inhibition. Lowering the haematocrit slightly reduces the effectiveness.Although we did not carry out direct measurements of adenosine levels, the results of our pharmacological studies clearly show that dipyridamole inhibits platelet aggregation in whole blood by blocking the reuptake of adenosine formed from precursors released by red blood cells following microtrauma. Its slight phosphodiesterase inhibitory action potentiates the effects of adenosine on platelets.


1982 ◽  
Vol 92 (1) ◽  
pp. 37-42 ◽  
Author(s):  
H. M. A. MEIJS-ROELOFS ◽  
P. KRAMER ◽  
L. GRIBLING-HEGGE

A possible role of 5α-androstane-3α,17β-diol (3α-androstanediol) in the control of FSH secretion was studied at various ages in ovariectomized rats. In the rat strain used, vaginal opening, coincident with first ovulation, generally occurs between 37 and 42 days of age. If 3α-androstanediol alone was given as an ovarian substitute, an inhibitory effect on FSH release was evident with all three doses tested (50, 100, 300 μg/100 g body wt) between 13 and 30 days of age; at 33–35 days of age only the 300 μg dose caused some inhibition of FSH release. Results were more complex if 3α-androstanediol was given in combined treatment with oestradiol and progesterone. Given with progesterone, 3α-androstanediol showed a synergistic inhibitory action on FSH release between 20 and 30 days of age. However, when 3α-androstanediol was combined with oestradiol a clear decrease in effect, as compared to the effect of oestradiol alone, was found between 20 and 30 days of age. Also the effect of combined oestradiol and progesterone treatment was greater than the effect of combined treatment with oestradiol, progesterone and 3α-androstanediol. At all ages after day 20 none of the steroid combinations tested was capable of maintaining FSH levels in ovariectomized rats similar to those in intact rats. It is concluded that 3α-androstanediol might play a role in the control of FSH secretion in the immature rat, but after day 20 the potentially inhibitory action of 3α-androstanediol on FSH secretion is limited in the presence of oestradiol.


1966 ◽  
Vol 44 (4) ◽  
pp. 661-676 ◽  
Author(s):  
Robert P. Thompson

To demonstrate the phenomenon of homologous inhibition by clearly interpretable results in a readily reactive system, experiments were carried out to study the effect of chick whole eye extract on the development of the vesicular lens of the chick embryo in vitro. The heads of embryos of 11 through 13 somites were explanted onto nutrient medium diluted with varying amounts of the extract, and cultured for 30 hours. A total of 35 embryos exposed to concentrations of 1:1, 1:2, and 1:4 (extract to medium) showed complete inhibition of lens vesicle formation. Of a total of 53 embryos on concentrations of 1:8, 1:16, 1:32, and 1:64, more than 50% showed inhibition of vesicle formation. The inhibitory effect disappeared at a concentration of 1:128. Control material exposed to some equivalent concentrations of nutrient medium – saline mixtures showed inhibition of vesicle formation in only 15% of 33 embryos. Of a total of 27 control embryos exposed to ventricular muscle extract, approximately one-third showed inhibition of vesicle formation at concentrations of 1:8 and 1:16, with the inhibitory effect disappearing at 1:32. The implications of this result are discussed. Other factors and control experiments are described and their value is assessed.


Cells ◽  
2018 ◽  
Vol 7 (2) ◽  
pp. 9 ◽  
Author(s):  
José Serrado Marques ◽  
Vera Teixeira ◽  
António Jacinto ◽  
Ana Tavares

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