Reaction patterns of cell organelles in vitamin B6 deficiency. Ultrastructural-morphometric analysis of the liver parenchymal cell.
Under the influence of seven weeks of vitamin B6-free nutrition, the hepatocyte single volume is diminished in the face of an unchanged nuclear single volume, posing the question of whether there is proportional atrophy of all cell organelles or single organelle atrophy with counter-regulatory hyperplasia in other cellular compartments. The nucleoli hypertrophy, as the result of segregation and protein synthesis inhibition. The rough endoplasmic reticulum experiences hypoplasia, but the ultrastructural-morphometric analysis does not determine which metabolic steps are attacked. By contrast one observes hyperplasia in the smooth endoplasmic reticulum, which may be regarded as a counter-regulatory mechanism to the choking of protein synthesis. As with the rough endoplasmic reticulum, the mitochondria also show hypoplasia. This is due to the dependency of the mitochondria upon the endoplasmic protein synthesis. The disturbed functional output of the endoplasmic reticulum is seen in the reduced number of orthoperoxisomes as well. The Golgi apparatus experiences hypoplasia as a result of B6 hypovitaminosis, and this must be considered in the context of fatty change in the liver.
D000818:Animals; D001284:Atrophy; D002466:Cell Nucleolus / Q000648:ultrastructure; D004721:Endoplasmic Reticulum / Q000648:ultrastructure; D006056:Golgi Apparatus / Q000648:ultrastructure; D006984:Hypertrophy; D008099:Liver / Q000648:ultrastructure*; D008297:Male; D008930:Mitochondria, Liver / Q000648:ultrastructure; D009940:Organoids / Q000648:ultrastructure*; D051381:Rats; D026681:Vitamin B 6 Deficiency / Q000473:pathology*