L-Glutamic acid monosodium salt reduces the harmful effect of lithium on the development of Xenopus laevis embryos.

Many xenobiotics in the environment affect the human body in various ways. Among those xenobiotics, lithium chloride (Li, LiCl) and monosodium glutamate (L-glutamic acid monosodium salt, MSG) compounds affect the crucial processes of stem cell differentiation, cell proliferation, developmental gene expression, and overall development in animals. In this study, we aimed to examine the developmental effects of exposure to flavor enhancer MSG and LiCI medicament on Xenopus embryos using the frog embryo teratogenesis assay of Xenopus test. To this purpose, Xenopus laevis embryos were exposed to four different concentrations of MSG (120, 500, 750, 1000 mg/dL) and Li (0.02 g/L) alone and in combinations for a period of 96 h, and then normal, abnormal, and death ratios were determined in all exposure groups. Besides, length values of all groups and membrane potentials of fertilized and non-fertilized oocyte groups treated with 120- and 500-mg/dL MSG doses and 0.02-g/L LiCI dose were measured. Treatment with ADI (acceptable daily intake) dose of MSG alone did not lead to a substantial effect on the development of Xenopus laevis embryos. But, exposure to daily doses exceeding the ADI level (500, 750, 1000 mg/dL) caused significant harmful effects. Besides, Li-involving treatments caused dramatic deleterious effects on embryo development. MSG attenuated harmful effects of Li in MSG+Li combined treatments. Membrane potentials of non-fertilized oocytes and fertilized eggs were significantly changed in all groups that their membrane potentials were measured. Extrapolating these results into humans require similarly designed studies conducted on human embryos.

Evaluating the Teratogenicity of Ritodrine and Nifedipine using a Frog Embryo Teratogenesis assay (FETAX).

The Frog Embryo Teratogenesis Assay-Xenopus (FETAX) was used to assess the teratogenic potential of two tocolytics. Embryos of the South African clawed frog, Xenopus laevis, were exposed to ritodrine or nifedipine. Exposure media were changed and monitored at 24-hour intervals. The 96-hour LC50 (Lethal concentration), the 96-hour EC50 (Malformation), and the No Observable Adverse Effect Concentrations (NOAEC) and the Lowest Observable Adverse Effect Concentration (LOAEC) for mortality, malformation and length were determined for each drug. Nifedipine was determined to be the more toxic and teratogenic than ritodrine, with a LC50 of 0.606 µg/L, an EC50 of 0.006 µg/L, and a teratogenicity Index (TI) value (LC50/EC50) of 101. On the other hand, the LC50 of ritodrine was 28.571 mg/L. In addition; the LC50, EC50 and TI values for nifedipine in the 5 mg/L ritodrine + nifedipine combination group were determined as 1.050 µg/L, 0.868 µg/L and 1.5 respectively. For ritodrine, the NOAEC and LOAEC values were determined as 2 mg/L and 4 mg/L, respectively. For the nifedipine and the ritodrine + nifedipine groups; while the LOAEC values of these groups were 0.0001 µg/L and 0.1 µg/L, respectively. NOAEC value couldn't be determined. Our results demonstrated that nifedipine administration was associated with higher levels of teratogenic and toxic effects. However, the ritodrine + nifedipine combination form reduced the toxic and teratogenic effects of nifedipine on Xenopus embryos. Further studies should be conducted in order to investigate the optimal combination concentrations of these substances for the treatment of preterm labor.