Fetal development influences

Marks, T.A., G.L. Kimmel, and R.E. Staples. 1981. Influence of symmetrical polychlorinated biphenyl isomers on embryo and fetal development in mice. I. Teratogenicity of 3,3, 4,4, 5,5 -hexachlorobiphenyl. Toxicol. Appl. Pharmacol. 61 269-276. 

Marks TA, Fisher PW, Staples RE. 1980. Influence of -hexane on embryo and fetal development in mice. Drug Chem Toxicol 3(4) 393-406. 

Giroud A, Tuchmann-Duplessis H, Mercier-Parot L. Influence de la thalidomide sur le developpement foetal. [Influence of thalidomide on fetal development.] Bmi Acad Natl Med 1962 146 343-5. 

The Dutch Hunger Winter, in short, provided one of the major sources of evidence for a new idea in the understanding of later health and disease. This idea forms the hypothetical background for this chapter s focus on specific factors inside and outside the fetal environment that influence, and sometimes disrupt, fetal development. 

Rees S. Harding R. (2004). Brain development during fetal life influences of the intra-uterine environment. Neurosci. Lett. 2004 361 111—114. 

Wadhwa, P. D. (2005). Psychoneuroendocrine processes in human pregnancy influence fetal development and health. Psycho-neuroendocrinol. 30 724—743. 

Prenatal influences. 2. Fetus—Abnormalities—Etiology. I. Title. [DNLM 1. Embryonic and Fetal Development—drug effects. 

The induction of damage by influences in embryonic or fetal development, causing malformations or embryonic death, is a problem of the toxicity rather than mutagenicity of the inducing agent (Gebhart et al. 

Hydroxylated PCBs can influence T4 metabolism by a strong inhibition of T4 sulfation (Schuur et al., 1998). As sulfation is a major regulation pathway ofT4 in the fetus, the interference of these metabolites with T4 sulfation may have consequences for fetal development, and in particular for brain development (Brouwer et al., 1998). 

The effects of severe iodine deficiency on fetal brain and somatic development were found to be more severe but similar to those observed by McIntosh et al (10) when thyroidectomy was performed on fetal sheep at 50-60 days. Fetal thyroidectomy later in gestation at 98 days caused less severe effects (11). Further investigations by McIntosh et al (12), following earlier indications (13) that the maternal thyroid could exert an influence on fetal development in early pregnancy, revealed that a combination of maternal thyroidectomy before conception and fetal thyroidectomy at 98 days gestation produced more severe effects than those of iodine deficiency (Fig. 1). 

This reaction is catalyzed by the enzyme rhodanese. Thiosulfate and colloidal sulfur are the only compounds so far discovered that react to form thiocyanate. One useful function of this reaction is that it serves to detoxify cyanide, traces of which are also formed endogenously in the metabolism of the mammal. The enzyme rhodanese is widely distributed in animal tissues, the activity in liver being particularly high. Gal, Fung, and Greenberg found that rhodanese activity increases with fetal development up to the time of birth. The rhodanese activity of the mother was not influenced by pregnancy. 

Thus it would appear that a moderate reduction of the maternal food intake does not materially influence the fetus. However, recent studies in man based on a better knowledge of nutritional requirements and evaluated by statistical methods have shed new light on the influence of maternal diet on fetal development. They have shomi that quantitative and qualitative factors of the maternal diet affect the condition of the infant at birth without causing inanition of the mother. These studies will be discussed later in a special section (p. 91). 

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