Biomedical subjects

R A Seibert

Publications and source records attributed to R A Seibert.

18 recordsLinked to original sources

PubMed1979

Asynchrony of erythroblast maturation induced by riboflavin deficiency.

Ultrastructural studies indicate that galactoflavin-induced riboflavin deficiency induces asynchrony of rat erythroblast maturation. During the latter stages of maturation erythroblasts retain significantly larger numbers of ribosomes as compared to control cells. Nucleoli are not evident in erythroblasts whose nuclei indicate cells in the latter stages of development. Membrane whorls develop within the mitochondria of plasma cells, eosinophils and neutrophils during the fifth week of riboflavin deficiency. No further evidence of degeneration was noted among additional cell organelles.

Animals↗

PubMed1979

Lack of effect of riboflavin deficiency on vitamin B12-related metabolic pathways and fatty acid synthesis.

The neurological sequelae of riboflavin deficiency posed the possibility that this tissue injury was mediated by defective vitamin B12 function due to the requirement for riboflavin-dependent oxidoreductase systems in B12 coenzyme synthesis and function. Studies of the B12-dependent enzymatic reactions (5-methyltetrahydrofolic-homocysteine methyltransferase and methylmalonyl coenzyme A mutase) in a fiboflavin-deficient rat model documented normal B12 activity in liver and neural tissue. In addition, examination of neural lipids and separation and analysis of neural fatty acids failed to reveal the increased odd chain fatty acids characteristically seen in the B12-deficient state. Thus, the neural tissue sequelae of riboflavin deficiency do not appear to relate to B12 coenzyme function.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗

PubMed1977

Effects of galactoflavin-induced riboflavin deficiency upon rat hepatic cell ultrastructure.

The primary cytoplasmic effect of galactoflavin-induced riboflavin deficiency upon rat liver cells involved focal sites of degradation which were manifested by the formation of membranous whorls. The nuclear effect of riboflavin deficiency concerned fluctuations in the total number of perichromatin granules per nucleus. These granules increased in number during the deficiency reaching a peak at three weeks. Nucleoli appeared compact with no evidence for segregation of nucleolar components. The possible correlation between increased synthesis of perichromatin granules and altered protein synthesis is discussed.

Animals↗

PubMed1976

Effects of riboflavin deficiency on the ultrastructure of rat sciatic nerve fibers.

Ultrastructural studies indicate that riboflavin deficiency induced by either dietary restrictions alone or with the addition of the antagonist galactoflavin severely affects the structural integrity of myelin lamellae. The degenerative process induced by riboflavin deficiency is time dependent. Nonmyelinated nerve fibers are not affected ultrastructurally by the deficiency. Cellular organelles of both myelinated and nonmyelinated nerve fibers remain intact and presumably functional.

Animals↗

PubMed1975

Metabolism of methocarbamol (robaxin) in the isolated perfused rat liver and identification of glucuronides.

1. Permethylation and g.l.c.-mass spectrometric analysis of bile from an isolated rat liver perfusion to which methocarmol was added showed seven components not present in control bile: methocarbamol, glucuronides of methocarbamol and desmethyl-methocarbamol, and four glucuronides of hydroxylated methocarbamol metabolites. 2. An interesting rearrangement of a methyl group has been found in the mass spectrum of 3-(2-methoxyphenyloxy)-1,2-dimethoxypropane, the permethylation product from methocarbamol.

Animals↗

PubMed1973