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S Sanyal

Publications and source records attributed to S Sanyal.

At least 127 records · Page 7Linked to original sources
PubMed1981

Absence of receptor outer segments in the retina of rds mutant mice.

In mice homozygous for the newly reported rds (retinal degeneration slow) gene, a progressive loss of visual cells occurs throughout life. Histogenesis of the retina proceeds normally with the exception of the receptor layer which remains rudimentary. Electron microscopic observations of the retina at different stages of development have revealed that the outer segments of the visual cells in this mutant fail to develop and that the receptor layer consists of inner segments only. In the absorption spectra of the retinal extract from the mutant the characteristic rhodopsin peak is lacking.

Animals↗
PubMed1981

Turnover rate of molecular species of sphingomyelin in rat brain.

Turnover rate of individual molecular species of sphingomyelin of adult rat brain myelin and microsomal membranes was determined after an intracerebral injection of 100 microCi of [C3H3]choline. Myelin and microsomal membrane sphingomyelins were isolated from the rest of the lipids. The individual molecular species of benzoylated sphingomyelin were separated and quantitated by reversed-phase high performance liquid chromatography. All individual major molecular species of microsomal and myelin sphingomyelin had maximum incorporation at 6 and 15 days, respectively, after the injection. The specific radioactivity of all the various molecular species of both myelin and microsomal sphingomyelin declined at a similar rate after reaching a maximum. There was no significant difference in the turnover rate of short chain (16:0, 18:0) and long chain (greater than 22:0) fatty acid containing sphingomyelin. The average apparent turnover rate of myelin and microsomal sphingomyelin molecular species was about 14-16 days for the fast pool and about 45 days for the slow pool. It is concluded that individual molecular species of sphingomyelin of myelin and microsomal membranes turned over at a similar rate. Thus, turnover rate of sphingomyelin in myelin and microsomal membranes is not affected by the fatty acyl composition of the lipid.

Animals↗
PubMed1981

Acute dieldrin toxicity: effect on the uptake of glucose and leucine and on brush border enzymes in monkey intestine.

Administration of a single oral dose of dieldrin (20 mg/kg body wt.) to rhesus monkeys considerably elevated the uptake of glucose and the activities of brush border sucrase, lactase, maltase and alkaline phosphatase in intestine compared to control animals. Leucine uptake and leucine amino peptidase activity was significantly depressed in pesticide-treated animals. Kinetic studies with brush border sucrase revealed that augmentation of enzyme activity in pesticide-fed animals was due to an increase in the disaccharidase content.

Alkaline Phosphatase↗
PubMed1981

Effect of a single oral dose of DDT on lipid metabolism in rat.

A single oral dose of 1,1,1-trichloro-2-2-bis (p-chlorophenyl)ethane (DDT) (600 mg/kg body weight) was given to rats and the levels of various lipids in adipose tissue, liver and plasma were studied. No alteration was observed in the levels of various lipid classes in these tissues except for a decrease in the phospholipid and triglyceride fractions in liver. Lipoprotein lipase activity of post-heparin plasma (protamine-sensitive and -resistant) was significantly decreased, whereas in liver and adipose tissue, the activity of this enzyme remained unchanged.

Adipose Tissue↗
PubMed1981

Prolactin suppression and spermatogenic developments in maturing rats. A quantitative study.

Prolonged suppression of prolactin (PRL) in immature male rats inhibits the spermatocyte-spermatid conversion process, alters leydig cell morphology, decreases accessory sex organ weight and increases serum LH levels without a significant alteration in serum FSH concentration. Amelioration of these effects by exogenous PRL strongly indicates that in the absence of PRL excess titers of endogenous LH fail to exert an influence on the spermatogenic activity of maturing testes.

Animals↗
PubMed1980

Development and degeneration of retina in rds mutant mice: light microscopy.

Changes during the development and degeneration of the retina in 020/A mice, which are homozygous for the newly reported rds (retinal degeneration slow), gene were studied by histological and enzyme-histochemical methods with Balb/c mice carrying the normal allele as control. During normal development the total thickness of the retina grows from the time of birth till the age of 21 days and thereafter gradually diminishes, while the thicknesses of the component layers show a characteristic and differential change in course of their histogenesis. In the normal retina the perikarya of the cones are more frequent in the central than in the peripheral areas. The cone frequency in the central retina, but not in the periphery, increases with age and implies selective loss of rod cells in older animals. In the homozygous rds mice, the receptor layer remains rudimentary, but the other retinal layers show a normal trend of growth during the first 2 weeks after birth. Thereafter th morphological layers containing visual cell structures--the receptor, the outer nuclear, and the outer plexiform layers--begin to reduce. The loss of visual cells is readily marked by the reduction of the outer nuclear layer and is first evident at 2 weeks after birth. Degeneration is more rapid up to the age of 2-3 months, when the outer nuclear layer is reduced to half of its original thickness; thereafter degeneration progresses more slowly. The receptor and the outer plexiform layers are also simultaneously reduced. At 9 months, the peripheral parts of the retina, and at 12 months, the entire retina is completely lacking in visual cells. In the central retina of the mutant, rod and cone cell populations are equally affected up to the age of 6 months, as their relative frequency remains similar to the normal. In the peripheral retina, where cell loss is more pronounced, and in the central retina at 9 months an increase in relative frequency of cones is recorded and indicate increased susceptibility of the rods to later degenerative changes. The inner parts of the retina, including inner nuclear, inner plexiform, and ganglion cell layers, remain morphologically unaffected until irregular vascularization follows total loss of visual cells. The pigment epithelium is also affected at this late stage and appears depleted and patchy. In the normal retina, macrophages which are positively stained for the enzyme N-acetyl-beta-glucosaminidase appear in the inner layers with the growth of the retinal vasculature. In the mutant, increased frequency and stainability of the macrophages are discernible in the inner retina at 11 days. The macrophages migrate outwards and are observed in the outer nuclear layer and in the optic ventricle during the period of degeneration. These findings are compared with the observations in the other retinal degeneration mutants in rodents, and in retinitis pigmentosa in humans. The suitability of the rds mice as an animal model system for the human disease is emphasized.

Animals↗
PubMed1979

Histochemical studies of testicular delta5-3beta-hydroxysteroid dehydrogenase and 17beta-hydroxysteroid dehydrogenase after chronic indomethacin administration in rats pretreated with clomiphene-citrate.

Histochemical studies of testicular delta5-3beta-Hydroxysteroid Dehydrogenase and 17beta-Hydroxysteroid Dehydrogenase in sexually immature rats treated chronically with simultaneous Indomethacin and Clomiphene revealed greater inhibition in the enzyme activities when compared to Clomiphene treated animals alone. This suggests prostaglandin-inhibitors may be directly inhibitory to NAD-requiring enzymes involved in testicular steroid biosynthesis.

17-Hydroxysteroid Dehydrogenases↗
PubMed1979

Dysgenetic lens (dyl)--a new gene in the mouse.

A new autosomal recessive gene, dysgenetic lens (dyl), in the mouse is described. Homozygotes are fully viable and exhibit smaller eye, corneal opacity, adhesion of the iris, cataractous degeneration, and extrusion of the lens nucleus and persistent lens-epithelium attachment. Developmental failure of lens vesicle--ectoderm separation is recognized as the earliest expression of the genetic defect. Possible significance of this mutant in the understanding of Peter's anomaly is indicated.

Animals↗