| Literature DB >> 64646 |
Abstract
The formation of lipofuscin pigment under the extrinsic influence of maternal protein deprivation during most of the gestation period has been demonstrated in the cerebellum and motor cortex of the developing fetuses and neonates in squirrel monkeys. The controls maintained on high protein diets failed to show lipofuscin pigment in appreciable quantities. The dirty yellow to dark brown pigment bodies exist as homogeneous particulates as well as duplex structures, each with a thin, irregular, light brown cortex, studded with one or more darker granules, and a medulla filled with sharp yellow substance. The malnourished neonates, especially in the third and fifth laminae of motor cortex, show loose aggregations of lipofuscin bodies in the apical dendrite and occasionally in the body of the dendritic branches but not in the axon hillock or the body of the axon. Histochemically, the pigment is a complex of lipids, carbohydrates and proteins, showing strong reaction for non-specific esterase and acid phosphatase and mild activity of succinate and lactate dehydrogenase and monoamine oxidase, which puts the pigment observed in the same category as the typical aging pigment described in literature. It is clear that maternal protein deficiency during the critical period of the fetal brain development has an adverse effect on its biochemical maturation. The accumulation of lipofuscin pigment is probably one manifestation of the metabolic changes in the neurons, which may have the impact of hastening the aging process, if protein deprivation is continued into the postnatal period.Entities:
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Year: 1977 PMID: 64646 DOI: 10.1016/0047-6374(77)90002-1
Source DB: PubMed Journal: Mech Ageing Dev ISSN: 0047-6374 Impact factor: 5.432