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[Mitochondrial heredity in hydatidiform moles]
H Márquez Monter1, F Castelán Montalban
1Departamento de Medicina Experimental, Facultad de Medicina, UNAM México, D.F.
Abstract:
A mitochondrial DNA study of seven hydatidiform moles and seven full term placentas as controls was carried out to determine the role played by mitochondrial DNA as the only maternal genome participating in the pathogenesis of these trophoblastic growths. Mitochondrial DNA was digested by restriction enzymes Eco R1 and Hind III, processed by electrophoresis and stained by ethidium bromide. Molar mitochondrial DNA showed two restriction bands at 9416 and 2322 kbs with Eco R1 and one band at 2322 kbs with Hind III, whereas the controls showed three bands of 9416, 4361 and 2322 kbs with Eco 1, and two bands at 4361 and 2322 kbs with Hind III. The results were interpreted as a DNA alteration consistent with a mutation at level of tARN genes, initiating the reading of gen ND2 of Complex I, NADH dehydrogenase and affecting Complex CO III that transcribe cytochrome c and oxidoreductase genes. The alterations are considered as mutations probably resulted from folic acid deficiency at threshold levels during nuclear and mitochondrial DNA synthesis in oogenesis and meiosis that renders anucleated ova (cytoplasts), fertilized, and further accelerated development of a zygote bearing an entire androgenic genome.