Monosodium glutamate in the chick embryo: lack of obvious toxic or teratogenic effects when administered at 24 hours incubation

The administration of monosodium glutamate (MSC) to chick embryos at 24 hours did neither produce gross developmental defects nor influence growth by 72 hours total incubation. The concentration of MSG administered ranged from 0.3 to 46.6 percent, the volumes injected being 0.05, 0.1, or 0.2 ml. Several injection methods were evaluated. It is suggested that injection into the centre of the yolk is the most effective way to give water-soluble treatments during this period of development (AU).

Teratogenicity of hypoglycin-A: some morphological and biochemical aspects

Hypoglycin-A is a toxic, non-proteinogenic amino acid of considerable biochemical interest. It is obtained fron the fruit of Blighia sapida K., and is the causative factor of the Jamaican "vomiting sickness". The toxicity of hypoglycin-A is attributed to the formation of a metabolic methylenecycclopropaneacetic acid which inhibits the oxidation of long-chain fatty acids. Hypoglycin-A induced in pregnant rats a significantly high incidence of congenital abnormalities and reabsorption. It did not reduce the fertility in mice, malformations were absent and only a small increase in reabsorption sites was observed after the adminstration of large doses. Hypoglycin-A administered to pregnant rabbits resulted in a high incidence of foetal reabsorption and overall stunting. Injected into the yolk sac of 24 and 48 hour chick embryos, hypoglycin-A was not teratogenic. Leucine, administered to pregnant rats simutaneously with hypoglycin-A, afforded no protection against the teratogenic action of hypoglycin-A. Leucine was shown to be highly teratogenic and exaggerated the teratogenicity of riboflavin and hypoglycin-A to pregnant rats the occurrence of congenital abnormalities. Inhibition of long-chain fatty acid oxidation may represent a basic cellular mechanism involved in the teratogenicity of hypoglycin-A, because of its influence on oxidative phosphorylation and the electron transport system. Reversal of the hypoglycin-induced teratogenic effects by riboflavin, suggests that inhibition of the acyl dehydrogenase flavin-dependent-oxidation reaction, occurring during the degradation of fatty acids, is the site of action of hypoglycin-A (AU)