Effects of phenylalanine on reproductive performance and teratogenesis in mice.

We evaluated the effects of phenylalanine on reproductive performance and teratogenesis in mice, as well as we assessed its protective effect in mice treated with an acute dose of cyclophosphamide. Animals were divided into 6 experimental groups (females N = 15/group, males N = 5/group): G1, the negative control group, phosphate-buffered saline; G2, the positive control group, 35 mg cyclophosphamide/kg body weight (b.w.); G3 and G4 received phenylalanine at doses of 150 and 300 mg/ kg b.w., respectively; G5 and G6 received phenylalanine at doses of 150 and 300 mg/kg b.w. co-administered with cyclophosphamide at a dose of 35 mg/kg b.w., respectively. Pregnant mice received phenylalanine from 8-12 days of pregnancy and cyclophosphamide on the 10th day of treatment or the respective vehicles. In animals treated with cyclophosphamide, offspring fetal weight significantly decreased. The G5 and G6 groups, which received cyclophosphamide co-administered with phenylalanine, showed a smaller reduction in weight. Based on this analysis, the offspring from groups G2, G5, and G6 showed low weight due to pregnancy age. Moreover, at the doses used, phenylalanine did not interfere with embryo-fetal development. However, further studies are necessary to increase the understanding of the effects of phenylalanine on mouse reproductive performance and teratogenesis.

Antigenotoxic and antimutagenic effects of glutamine supplementation on mice treated with cisplatin.

We evaluated the effects of glutamine on clastogenic and genotoxic damage prevention caused by the administration of cisplatin. Forty Swiss mice were divided into 8 experimental groups: G1 and G2, which were control groups; G3, G4, and G5, which were administered [2 doses of glutamine (orally)] separated by a 24-h period (150, 300, and 600 mg/kg, respectively), and a dose of phosphate-buffered saline by intraperitoneal injection; G6, G7, and G8, which were treated in the same manner as the previous groups, but received cisplatin rather than phosphate-buffered saline. The antimutagenicity groups showed damage reduction percentages of 79.05, 80.00, and 94.27% at the time point T1, 53.18, 67.05, and 64.74 at time point T2 for the 150, 300, and 600 mg/kg doses of glutamine, respectively. Antigenotoxic activity was evident for all 3 doses with damage reduction percentages of 115.05, 119.06, and 114.38 for the doses of glutamine of 150, 300, and 600 mg/ kg, respectively. These results suggest that further studies are needed to confirm the clastogenic activity of glutamine. However, our results may lead to rational strategies for supplementation of this antioxidant as an adjuvant in cancer treatment or for preventing genomic lesions.