Potential involvement of yolk sac in teratogenesis

European Journal and Rcpraluctive

ELSEVIER

of Obstetrics & Gynecology Biology 66 (1996) 201

Letter to the editor

Potential involvement of yolk sac in teratogenesis Gian Mario Clinica

Ginecologica

e Ostetrica.

Tiboni*, Umberto Bellati

Universita’

“G. d’Annwr;io

111

0

1996 Elsevicr

Scbcnrx

Iretand

Ltd.

AU rights

1976;

KE, Roberts of pinocytosis

G. K&ton ME. Beck in rat yolk sac by trypau

[31

141

161

yolk

sac cndoderm Pcdiatr Rcs 1983:

Ihnidmoa BRG, Denkcr L. Transfer of drugs to and fetus atIer plaanution. In: Nau H, Scott WJ Phamtacokinctics in tetatomis. Vol. I. Bocs CRC Press, 1987. Raxsd IR. Dnwsti IE. Manual M. Inhibition of

the embryo Jr., editors. Ra~oa. FL: rat yolk

sac

pinocytosis by cadmium and its rwenal by zinc. 3 Nutr 1982: 112: 1994-2001. Jwbau MR. Lee QP, Fantel A. Xeaobiotic biotransfomtatiowttiowtivatioo in organoe cotissues: implications for embryotoxicity and tcratogmesis. Chwg Mctab RN 1992; 24: 195-238. Di llio C, Tiboai GM, Sacchctta P, Angelucci S, BucciarcUi A, Bdlati 0, Aceto A. Ti rsodependtat md tirsuc-spccifiivtiatioa of glutathiooe Mcch A&g Dcv

rescnal

F, Lloyd JB. blw. Teratol-

14: 343-354.

Leung CCK. Anti swum to rat tisczral iaducu! aboonual embryonic dentopmcnt. 17: 313-316.

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f5(96)02402-3

Williams inhibition ogy

The accumulation of cadmium in yolk sac as we11as in cborioallantoic placenta may at least partly account for the embryotoxicity induced by this metal. Cadmium accumulation, would affect embryonic development by preventing important nutrients, like zinc and vitamine B12, to gain accessto the embryonic compartment [3,4].

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References

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PII:

66/00-ChLli.

Recent studies have shown that the low levels of metabolic activities detectable in embryonic tissues, may be able to generate reactive intermediates with embryotoxic potential [S]. Maximum levels of these catalytic activities have been detected in the yoIk sac [S], as also confirmed by our recent fmdings (61. Also in this respect, as stressed by Jucbau and-co-workers [5], the yolk sac may have a crucial role in xenobiotic-induced teratogenesis.

We read with interest the review from Dr N. Exalt0 (Ear/y human nufrition. Eur J Obstet Gynecol Reprod Biol 1995; 61: 3-6). As emphasized by the author, there is an increasing body of literature to suggest that yolk sac plays a crucial role during ontogenesis. An interesting point was that yolk sac impairment can be of significance in teratogenesis. The article was focused on human yolk sac, and we feel it could be of interest to mention other experimental studies which, in agreement with that reported by Dr Exalto on diabetes-induced embryopathy, are supportive of the concept that the yolk sac could be the primary target of developmental toxicants. In 1976, Williams et al. [ll reported that trypan blue, a molecule which is unable to cross the yolk sac barrier, elicits embryotoxicity by inhibition of yolk sac pinocytosis. Trypan blue-induced embryotoxicity has being considered a compelling evidence that xenobiotics can impair normal development without having direct access to embryonic tissues. Another evidence of yolk sac involvement in teratogenesis, was the finding that malformations are inducibte by anti-serum to endodermal cells of yolk sac

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tmnsfcrasc duriag 1995; 78: 47-62.

gestation

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mouse.