Mutational analysis of AXIN2, MSX1, and PAX9 in two Mexican oligodontia families.

The genes for axin inhibition protein 2 (AXIN2), msh homeobox 1 (MSX1), and paired box gene 9 (PAX9) are involved in tooth root formation and tooth development. Mutations of the AXIN2, MSX1, and PAX9 genes are associated with non-syndromic oligodontia. In this study, we investigated phenotype and AXIN2, MSX1, and PAX9 gene variations in two Mexican families with non-syndromic oligodontia. Individuals from two families underwent clinical examinations, including an intra-oral examination and panoramic radiograph. Retrospective data were reviewed, and peripheral blood samples were collected. The exons and exon-intronic boundaries of the AXIN2, MSX1, and PAX9 genes were sequenced and analyzed. Protein and messenger RNA structures were predicted using bioinformative software programs. Clinical and oral examinations revealed isolated non-syndromic oligodontia in the two Mexican families. The average number of missing teeth was 12. The sequence analysis of exons and exon-intronic regions of AXIN2, MSX1, and PAX9 revealed 11 single-nucleotide polymorphisms (SNPs), including seven in AXIN2, two in MSX1, and three in PAX9. One novel SNP of MSX1, c.476T>G (Leu159Arg), was found in all of the studied patients in the families. MSX1 Leu159Arg and PAX9 Ala240Pro change protein and messenger RNA structures. Our findings suggested that a combined reduction of MSX1 and PAX9 gene dosages increased the risk for oligodontia in the Mexican families, as in vivo investigation has indicated that interaction between Msx1 and Pax9 is required for tooth development.

Vitamin E improves antioxidant status but not lipid metabolism in laying hens fed a aged corn-containing diet.

OBJECTIVE: The objective of this study was to determine whether a dietary vitamin E (VE) supplement could alleviate any detrimental effects of aged corn on lipid metabolism and antioxidant status in laying hens. METHODS: The experiment consisted of a 2×3 factorial design with two corn types (normal corn and aged corn (stored for 4 yr) and three concentrations of VE (0, 20, and 100 IU/kg). A total of 216 Lohmann laying hens (50 wk of age) were randomly allocated into six treatment diets for 12 wk. Each treatment had 6 replicates of 6 hens per replicate. RESULTS: The results show that aged corn significantly decreased the content of low-density lipoprotein cholesterol (p<0.05), and reduced chemokine-like receptor 1 (CMKLR1) mRNA expression (p<0.05) in the liver compared to controls. Diet with VE did not alter the content of crude fat and cholesterol (p>0.05), or acetyl-CoA carboxylase, lipoprotein lipase, fatty acid synthase or CMKLR1 mRNA expression (p>0.05) in the liver among treatment groups. Aged corn significantly increased the content of malondialdehyde (MDA) (p<0.05) and decreased superoxide dismutase (SOD) activity (p<0.05) in the liver. The VE increased the content of MDA (p<0.05) but decreased glutathione peroxidase (GSH-Px) activity in serum (p<0.01) and in the ovaries (p<0.05). Adding VE at 20 and 100 IU/kg significantly increased GSH-Px activity (p<0.05) in liver and in serum (p<0.01), 100 IU/kg VE significantly increased SOD activity (p<0.05) in serum. Aged corn had no significant effects on GSH-Px mRNA or SOD mRNA expression (p<0.01) in the liver and ovaries. Addition of 100 IU/kg VE could significantly increase SOD mRNA expression (p<0.01) in the liver and ovary. CONCLUSION: Aged corn affected lipid metabolism and decreased the antioxidant function of laying hens. Dietary VE supplementation was unable to counteract the negative effects of aged corn on lipid metabolism. However, addition of 100 IU/kg VE prevented aged corninduced lipid peroxidation in the organs of laying hens.