Search PubMed⌕ Search

Biomedical subjects

S P Sharma

Publications and source records attributed to S P Sharma.

At least 127 records · Page 7Linked to original sources

Experimental protein malnutrition in squirrel monkeys: cytochemical interaction of nucleolus and cytoplasm in the anterior horn cells of the spinal cord of Saimiri sciureus.

Nuecleolo-cytoplasmic relationships have been studied using histochemical techniques in the spinal cord of healthy neonates compared with those born to mothers malnourished through most of the gestation period, and healthy and severely protein-malnourished young adult squirrel monkeys. Formaldehyde-fixed as well as fresh frozen tissues were used for histological study and for histochemical techniques to demonstrate lipids, carbohydrates, nucleic acids and enzymes of various metabolic cycles. Changes in the neuronal cytoplasm of the low protein animals appear to be related to impaired protein metabolism and energy transport. The nucleolus reacts to cytoplasmic changes by enlarging its size and by active synthesis of secretion of nucleolar material, which is then passed into the cytoplasm through an evagination of the nuclear envelope. The greater the degree of chromatolysis in the cytoplasm, the more active the nucleolus appears to be in terms of its enlarged size and transfer of secretion products into the cytoplasm. It is believed that the perinuclear accumulation of secretion products in the neuronal cytoplasm of the protein-deficient animals has its origin in the nucleolus. Such an accumulation in the severely malnourished animals appears to be a compensatory mechanism for the increased cytoplasmic catabolism and loss of ribonucleoprotein material in order to facilitate additional protein synthesis for cell survival.

Age Factors↗

Nucleolar changes in response to dietary protein malnutrition in the neurons of the motor cerebral cortex and cerebellum of squirrel moneky Saimiri sciureus.

Nucleolo-cytoplasmic relationships have been studied in healthy squirrel monkeys and those subjected to a known degree of protein malnutrition. In the latter group, thirty-two pregnant animals starting from 35 days of gestation and 24 young adult animals were given a diet containing 7.5% and 2.0% protein content, respectively, compared to a diet with 25% protein for the controls. The motor cortex and the cerebellum removed from neonates as well as young adult animals sacrificed after 9, 11, 13 and 15 weeks of feeding schedules were investigated. Four animals after 15 weeks of dietary protein deprivation were rehabilitated with a balanced diet over a year's period. Formaldehyde-fixed as well as fresh frozen tissues were used for the histological study and to employ histochemical techniques for the demonstration of lipids, carbohydrates, nucleic acids and enzymes of various metabolic cycles. As a result of protein malnutrition, the nucleolus in a majority of the neurons from the motor cortex and the Purkinje cells of the cerebellum undergoes a series of morphological and cytochemical transformations in response to cytoplasmic changes related to impaired protein metabolism. The greater the level of protein deprivation, the greater is the degree of cytoplasmic chromatolysis and more pronounced are the nucleolar transformation in terms of enlarged size, secretory activity and transfer of nucleolar material in the cytoplasm. The nucleolar buds located close to the periphery of the nuclear membrane and the nucleolar material in the cytoplasm show identical cytochemical nature except for the presence of DNA in the former. It appears that during migration through the nuclear membrane the nucleolar material loses its DNA component and only aggregates of ribosomes and protein pass into cytoplasm, which aid in the synthesis of specific proteins lost as a result of catabolic processes initiated by protein malnutrition. Most of the observed changes in the adult squirrel monkeys are reversed when they are rehabilitated with a balanced diet.

Aged↗

Reversibility of lipofuscin accumulation caused by protein malnutrition in the motor cortex of squirrel monkeys, Saimiri scireus.

Lipofuscin pigment has been demonstrated histochemically in the motor cortex by the use of several histochemical and cytochemical methods in the healthy (maintained on a diet with 25% protein content) and protein malnourished (maintained on a diet with 2% protein content) adult animals. 4 animals in the latter category were rehabilitated over a period of 11 months and various histochemical techniques were repeated on the motor cortex of these animals. The healthy animals showed a somewhat uniform distribution of lipofuscin pigment in the neuronal perikarya with the perineuronal glia showing only slight occurrence of pigment bodies. The malnourished animals exhibited a significantly larger number of lipofuscin bodies in the neuronal as well as glial perikarya. The neurons, especially, showed aggregations of lipofuscin bodies characterized by a large increase in the activity of acid phosphatase and simple esterases. The rehabilitated animals, however, showed a decrease of lipofuscin pigment in the neuronal perikarya with a concomitant loss of lysosomal enzymes, while a significant increase of these bodies was observed in the perineuronal glial cells. It is evident that the formation of lipofuscin pigment gets accelerated under the extrinsic influence of dietary protein deprivation in the adult animals, but the process is reversed at least to some extent by halting the dietary deficiency or its correction by rehabilitation. The perineuronal glial cells appear to play a significant role in the removal of lipofuscin bodies from the neuronal perikarya. The significance of these observations has been discussed.

Animals↗

Experimental protein malnutrition in primates: electronmicroscopic observations on the cerebellum of healthy and malnourished squirrel monkeys (Saimiri sciureus).

Eight young adult squirrel monkeys were maintained on a protein deficient (2% calories from proteins) diet for a period of 15 weeks during which the animals lost wieght steadily and developed varying degrees of sensory and motor impairments as evidenced by lack of interest in the surrounding environment and changes in posture and gait. An additional eight animals were maintained on a high protein diet (25% calories from proteins) to serve as controls. Two animals each from the experimental and control groups were sacrificed at 9, 11, 13 and 15 weeks of special feeding schedule. The Purkinje cells of the cerebellum of malnourished animals showed significant changes in the ribosomes, endoplasmic reticulum and Golgi zone indicating greatly disturbed protein metabolism. The granule cells, especially of the pale variety show prominent watery swellings with scant cell organelles. The most prominent change appeared in various types of neurons related to the multiplication of various types of lysosomes, multivesicular lamellar bodies and the lipofuscin pigment bodies. In the animals sacrificed at different intervals, the relatively more malnourished animals showed significantly larger number of lipofuscin pigment in the various types of neurons of the cerebellar cortex. The dendritic changes included honey-comb formation in the lumen. The astrocyte glial fibers were greatly increased. The pericytes of the blood vessels showed irregular outlines and were greatly enlarged with numerous osmiophilic bodies (presumably lipofuscin) in the experimental animals as compared to the controls.

Animals↗

Experimental protein malnutrition as a causative factor in the histological and histochemical disruption of the ependymal cells of the third ventricla and cervical central canal of squirrel monkeys.

The histologic disturbances of the cuboidal and columnar ependymal cells of the neonates under the extrinsic influence of maternal protein deprivation during most of the gestation period have been demonstrated in the central canal of the cervical spinal cord and III ventricle of the squirrel monkey brain. The control animals whose mothers were maintained on high protein diets showed an unbroken ependymal layer with an intact glial fiber layer and the subependymal cell plate. Taking birth-weight as an indication of the degree of malnutrition, maximum disruption of the ependymal layer was observed in those animals born around 80 g birth-weight. In the latter, most of the ependymal cells lost their characteristic arrangement and columnar shapes. The ependymal cells of the manourished animals show a marked reduction of oxidative enzyme content and relatively active glycogen metabolism as compared to the healthy controls. The significance of these changes has been discussed in the light of parallels in the embryological development and, to some extent, functions between the orinary neurons, ependymal cells of the choroid plexus, other ependymal cells and the glial cells. In this context, the changes observed in the present studies under the effect of protein malnutrition must be taken as part of overall changes experienced by various kinds of cells comprising the nervous system.

Animals↗

Pyridine as an unmasking reagent for lipoprotein complexes in the nervous system of protein deficient squirrel monkeys.

Acid hematin test with pyridine and Sudan black B controls was employed on selected areas of the brains of 115, 140 days fetuses, neonates and adult squirrel monkeys maintained on low and high protein diet. Our histochemical findings indicate that the reduction of phospholipids in the low protein fetuses and neonates is related to myelination, wereas in the adults, most of the lipids are bound to proteins and/or cerebrosides to form complexes, as revealed by the unmasking action of pyridine.

Animals↗