scholarly journals Teratogenic Effect of Trypan Blue on Rat Embryos cultivated in vitro

Nature ◽  
1965 ◽  
Vol 206 (4984) ◽  
pp. 637-637 ◽  
Author(s):  
MYRON M. TURBOW
Teratology ◽  
1990 ◽  
Vol 42 (6) ◽  
pp. 611-618 ◽  
Author(s):  
M. Repetto ◽  
J. C. Maziere ◽  
D. Citadelle ◽  
R. Dupuis ◽  
M. Meier ◽  
...  

Development ◽  
1966 ◽  
Vol 15 (3) ◽  
pp. 387-395
Author(s):  
M. M. Turbow

Trypan blue is known to produce embryonic abnormalities in a wide variety of animals, including rats (Gillman, Gilbert, Gillman & Spence, 1948), mice (Waddington & Carter, 1953; Hamburgh, 1954), amphibians (Waddington & Perry, 1956), chickens (Beaudoin & Wilson, 1958;Stéphan & Sutter, 1961), rabbits (Ferm, 1956), and hamsters (Ferm, 1958). Studies on the teratogenic action of this dye have also been made in culture (Mulherkar, 1960). Since the first observation of the teratogenic action of trypan blue in rat embryos (Gillman et al. 1948), two questions that have remained unanswered are (1) whether the dye acts directly on the embryo or via the maternal system, and (2) what determines the period during which the rat embryo is most sensitive to the dye.


Development ◽  
1960 ◽  
Vol 8 (1) ◽  
pp. 1-5
Author(s):  
Leela Mulherkar

Various malformations in rats and mice have been observed to be caused by administration of the vital dye, Trypan blue (Gillman, Gilbert, Gillman, & Spence, 1948; Fox & Goss, 1956, 1957; Hamburgh, 1952, 1954; Waddington & Carter, 1952, 1953). Recently Waddington & Perry (1956) reported a teratogenic effect of Trypan blue on Amphibian embryos. The present paper deals with the effects of this dye on cultured chick embryos. Hen's eggs were incubated at 38°C. to the desired stage of development. Cultures were set up according to the ring technique described by New (1955). Precautions to maintain sterile conditions were observed throughout. An aqueous 1 per cent, solution of Gurr's vital Trypan blue was diluted with Pannett Compton saline to 0·05 per cent., which had been found to be a suitable concentration. A few drops of the dye solution were placed on the upper surface of the treated blastoderms.


2012 ◽  
Vol 34 (2) ◽  
pp. 151
Author(s):  
Francesca Di Renzo ◽  
Renato Bacchetta ◽  
Erminio Giavini ◽  
Elena Menegola
Keyword(s):  

2007 ◽  
Vol 192 (1) ◽  
pp. 207-214 ◽  
Author(s):  
Mattias Gäreskog ◽  
Parri Wentzel

Malformations and growth disturbances are two- to threefold more common in infants of diabetic mothers than in offspring of non-diabetic pregnancy. Several suggestions have emerged to explain the reasons for diabetic embryopathy, including enhanced mitochondrial production of reactive oxygen species leading to altered activation of protein kinase C. This study aimed to evaluate the effect of α-cyano-4-hydroxycinnamic acid (CHC) and N-acetylcysteine (NAC) addition on morphology and activity of protein kinase C-δ and protein kinase C-ζ in rat embryos exposed to a high glucose concentration in vitro. Day 9 embryos from normal rats were cultured in 10 or 30 mM glucose concentrations with or without supplementation of CHC, NAC, or protein kinase C inhibitors specific for protein kinase C-δ and protein kinase C-ζ. Embryos were evaluated for malformations, crown rump length, and somite number. Protein kinase C-δ and protein kinase C-ζ activities were estimated by western blot by separating membranous and cytosolic fractions of the embryo. We found increased malformations and growth retardation in embryos cultured in high versus low glucose concentrations. These abnormalities were diminished when CHC and NAC or specific protein kinase C-inhibitors were added to the culture medium. The activities of embryonic protein kinase C-δ and protein kinase C-ζ were increased in the high glucose environment after 24-h culture, but were normalized by the addition of CHC and NAC as well as respective inhibitor to the culture medium. These findings suggest that mitochondrial overproduction of reactive oxygen species is involved in diabetic embryopathy. Furthermore, such overproduction may affect embryonic development, at least partly, by enhancing the activities of protein kinase C-δ and protein kinase C-ζ.


Teratology ◽  
1982 ◽  
Vol 26 (3) ◽  
pp. 289-297 ◽  
Author(s):  
Amir P. Gulamhusein ◽  
Weiland J. Moore ◽  
Madhu Gupta ◽  
Felix Beck
Keyword(s):  

Development ◽  
1972 ◽  
Vol 27 (3) ◽  
pp. 543-553
Author(s):  
D. A. T. New ◽  
R. L. Brent

Rat embryos, explanted with their embryonic membranes during the early stages of organogenesis ( days gestation), were grown in culture in roller tubes. Yolk-sac antibody (sheep anti rat yolk-sac gamma globulin), known to be teratogenic when injected into pregnant rats, was added to the culture medium. At concentrations of 0·1 mg/ml or more the antibody caused gross retardation of growth and differentiation. Injection of antibody into the amniotic cavity so that it had direct contact with the embryo, or between the amnion and yolk sac so that it was in contact with the mesodermal surface of the yolk sac, had little or no effect on development of the embryo or its membranes. These in vitro experiments indicate that yolk-sac antibody has an effect on development independent of any immunological reaction of the mother, and the primary action is probably on the visceral yolk-sac endoderm.


Development ◽  
1964 ◽  
Vol 12 (1) ◽  
pp. 1-14
Author(s):  
Aeleta N. Barber ◽  
Jack C. Geer

Since the discovery of the teratogenicity of trypan blue by Gillman, Gilbert, Gilhnan and Spence (1948) the dye has offered a very concise and convenient method for studying teratogenesis in mammals. Dijkstra & Gillman (1960) fractionated the dye and found that the purple component stimulated the endothelial system in rats, thereby raising the speculation that the varied effects of the dye were caused by contamination. According to our previous experiments (1957, 1963) and those of Wilson, Beaudoin & Free (1959) one aspect of the problem has remained fairly constant, namely, the narrow time limit of the maximal effect of the dye and the stability of the pattern of malformations. Wilson and his associates suggest that the teratogenic effect is due to direct access of the dye to the embryo before the visceral yolk-sac is completely formed.


Teratology ◽  
1991 ◽  
Vol 43 (6) ◽  
pp. 575-582 ◽  
Author(s):  
Deborah K. Hansen ◽  
Thomas F. Grafton

Sign in / Sign up

Export Citation Format

Share Document