Possible mechanisms of human teratogenesis by imperfect potato

Summary The paper discusses some practical methods which may assist studies investigating the possible teratogenic effect of imperfect potatoes (if any). References are made to the possible changes in its nutrient components, and also to the solanidine steroidal properties which may have effects similar to the sex hormones.Changes in the fetal development due to maternal hormone inbalance, either of endogenous origin or induced by hormone therapy are shown through illustrative examples.

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Zusammenfassung Es werden einige praktikable Methoden diskutiert, die dazu dienen könnten, den möglichen teratogenen Effekt fehlerhafter Kartoffeln festzustellen. Es werden mögliche Veränderungen des Nährstoffanteils und auch die Steroideigenschaft des Solanidins, das ähnliche Wirkung wie Sexualhormone haben könnte, erörtert.Möglichkeiten einer Störung der fetalen Entwicklung infolge mütterlichen hormonellen Ungleichgewichts, entweder endogen bedingt oder infolge Hormontherapie, werden beispiel-half aufgezeigt.

     

Models and concepts derived from human teratogenesis and oncogenesis in early life

Several basic empirical facts are emphasized about human developmental oncology. The first is that teratogenesis and oncogenesis are intimately related and that indeed teratogenesis may be the more primitive reaction to the types of mutagenic injury giving rise to neoplasm. The second is that neoplasms of early life, particularly those initiated "in utero" are rare, and tend to spontaneously regress or cytodifferentiate. The theoretical models of carcinogenesis forwarded by Knudson and Matsunaga are enlisted in attempts to explain these phenomena and how the oncogene is expressed and modulated by the fetal or embryonal milieu.     

Some relations between teratogenesis and mutagenesis

The nonactinic environmental agents that have been found to induce mutations in laboratory mammals are almost without exception of a single chemical class, alkylating chemicals, whereas this class is only one of the numerous sorts of environmental agents that induce congenital structural malformations. Many other types of chemical teratogens as well as nonchemical teratogens exist. This conspicuous difference between the known means of producing these phenomena reflects the fact that the mechanism by which malformations and mutations arise are for the most part distinctly different from each other. Therefore, environmentally induced malformations and mutations cannot be equated with each other and used as mutual indicators in monitoring potential harmful effects of the environment.     

Salicylate-induced teratogenesis in the ferret

A single subcutaneous injection of 400 mg/kg sodium salicylate produced a high resorption rate on day 13 (91%) and on day 18 (66%) of gestation. Malformations were seen in the surviving fetuses. Pregnant ferrets injected with 250 mg/kg salicylate produced a lower resorption rate of between 31% and 43%. Malformations were seen in the surviving fetuses of animals injected with lower doses of sodium salicylate both at 13 and 18 days of gestation.Salicylate-induced teratogenicity at 400 mg/kg was compared with that produced in a closed colony of Wistar rats. The concentration of salicylate in whole blood (and serum) was determined after a single injection of 125 mg/kg or 400 mg/kg sodium salicylate. Although salicylate concentration in the blood in both species showed remarkable similarity at the doses tested and the times of sampling, the results indicated that the drug was far more embryo-toxic in ferrets than in rats. The inter-order variation in the embryotoxicity of sodium salicylate is such that it would be unwise to ignore its possible teratogenic activity in man.     

Maternal metabolism and teratogenesis in zinc-deficient rats

Embryos removed at 11.5 days gestation from pregnant rats allowed a zinc-deficient diet from the time of mating showed a high frequency of malformations of all organ systems. There were, however, large differences between litters of individual dams. Comparison of the daily food intake of zinc-deficient dams with the appearance of the embryos suggested that fluctuations in the maternal serum zinc levels induced by feeding or fasting influenced the availability of zinc to the embryos. By cyclically feeding zinc-deficient dams to a predetermined schedule, low maternal serum zinc levels were induced at selected stages of development. This was accompanied by specific malformations of the organs developing at that time.     

Glucocorticoid teratogenesis in the developing nephron

Although the induction of polycystic kidney disease by neonatal glucocorticoid treatment has been extensively documented, there are no data on induction of polycystic kidney disease with fetal exposure to glucocorticoids. We injected groups of pregnant Swiss Webster albino mice subcutaneously with 250 mg/kg of hydrocortisone acetate on individual days from days 1 to 19 of gestation. A control group received an equal volume of saline. Histologic analysis of 1,522 kidneys from the offspring of these animals revealed no evidence of polycystic kidneys in the control group or in offspring of animals injected before day 11 of pregnancy. A bimodal distribution of cystic kidney disease was noted in the remaining animals, with highest prevalence after injection on day 12 (50.8%) and day 17 (34.3%). We conclude that 250 mg/kg of glucocorticoids may induce polycystic kidney disease in utero, but possibly only during critical periods of metanephric development.