MMT, nanosilicate platelets were isolated in water to produce high surface areas and multiple ionic charges per platelets. After using these unique characteristics to bind to the surface of microorganism, it was demonstrated that the AB1010 790299-79-5 growth of various strains of bacteria was completely inhibited at 0.3% NSP by nonspecific binding. Furthermore, the surface of NSP modified by silver nanoparticles could improve the antibacterial activity but merely elicit slight immune response. The low cytotoxicity and genotoxicity of NSP have been verified by several methods, including comet assay, micronucleus test, and Salmonella gene mutation assay. A high lethal dose greater than 5,700 mg/kg body weight was also observed in rats with acute oral administration of NSP. Based on the strong binding ability and the low toxicity of NSP, we expect that NSP will act as a good mycotoxin adsorption agent when used as a feed additive. However, the effect of NSP on the development of embryos has not yet been reported. In this study, we evaluate the influences of NSP on the pre-implantation development of mouse embryos and the adsorption of FB1 by NSP via both in vitro and in vivo assays. Corn and soybean meal are major ingredients in animal feed. Corn is also the best medium to support Fusarium verticillioides growth. Almost all of the hog, broiler, and layer feed in Taiwan is reported to be contaminated by FB1 at up to 1.3 mg/kg on average. Therefore, how to prevent and reduce the deteriorated effects caused by FB1 is an important problem. Ceramide synthase can use sphinganine or sphingosine with fatty acyl-CoA to synthesize ceramide. Ceramide is a critical intermediate product during sphingolipid metabolism, producing sphingomyelin, sphingosine, or glycosphingolipid. However, due its chemical similarities with sphinganine and sphingosine, FB1 may inhibit the activity of ceramide synthase localized at the endoplasmic reticulum and disturb the metabolism of the sphingolipids that are important for stabilizing the structure and function of the cell membrane. In addition, free sphingoid bases were accumulated because of inhibition of ceramide synthase. The inhibition of ceramide synthase can promote free sphingoid base-induced cell death but inhibit cell death triggered by ceramide. Cells that are sensitive to sphingoid base-induced cell death will die and insensitive cells will survive. It has been hypothesized that FB1 can decrease the production of glycosphingolipids and thus lead to impaired function of the folate transporters on the cell membrane, and the intake of folate decreases after exposure to FB1. The low folate intake is responsible for the increased incidence of neural tube defects and the failure of neurulation during embryogenesis, particularly the exencephaly. However, a recent study held the opposite opinion which demonstrated that folate deficiency does not exacerbate NTD induction by FB1 in LM/Bc mice.