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R S Bedwal

Publications and source records attributed to R S Bedwal.

10 recordsLinked to original sources
PubMed2000

SDS-PAGE analysis of caput epididymis proteins in rats receiving a zinc deficient diet.

Caput epididymis proteins from control, pairfed and zinc deficient (ZD) wistar weanling albino rats after 2-, 4-, 6- and 8-weeks were examined using SDS-PAGE followed by densitometric scanning of the gels. In comparison to the control and pairfed rats, ZD rats displayed new proteins. These included a Mr 42 kDa from 2ZD, Mr 47.5, 27.5, 23.2 and 16.0 kDa from 4ZD and Mr 87 and 14.2 kDa from 6ZD group. The 8ZD group, however, revealed no additional protein bands over controls. Further, several other proteins were missing from ZD rats. These included Mr 93 and 71 kDa from 2ZD; 93, 90, 79, 67, 62, 55 and 15.3 kDa from 4ZD; 60, 45.5, 34, 30 and 24 kDa from 6ZD and 41.5, 33 and 27.5 kDa bands from 8ZD group. The results indicate that the induced Zn-deficient state may be responsible for the altered protein patterns in the caput epididymis. The duration of low Zn uptake period also appears to influence the protein pattern in caput epididymis.

Animals↗
PubMed1998

Zinc, copper and hydrolytic enzymes in epididymis of hydrocortisone treated rat.

Administration of glucocorticoid (1, 2 and 4 mg) in excess leads to degeneration of epididymides as supported by cellular degeneration, sperm density and morphometric measurements. Zinc level increased statistically after 1, 2 and 4 mg hydrocortisone treatment while copper increased after 1 and 2 mg treatment. Cholesterol, protein and leucine aminopeptidase levels increased and decreased significantly in caput and cauda respectively. Activity of alkaline phosphatase reduced significantly while the treatment of hydrocortisone at different doses elevated acid phosphatase, aryl sulphatase and lactate dehydrogenase activities. Evidently, these changes are as a result of onset of cellular degeneration leading to impairment of metabolic/secretory activity of epididymal cells. The possible involvement of pituitary-testis axis in hydrocortisone induced epididymal degeneration and functional inhibition has been discussed.

Acid Phosphatase↗
PubMed1995

Light and electron microscopic changes in the ovary of zinc deficient BALB/c mice.

Female BALB/c strain of mice fed on Zn deficient diet for 2-, 4- and 6- weeks exhibited prolonged diestrous phase with only VII types of follicles instead of VIII as compared to their respective control and pairfed. Light microscopic studies displayed increased atresia, cessation of oogenesis and ovulation, degeneration of follicular cells of zona granulosa, clumped chromatin of oocyte and disrupted zona pellucida and corona radiata. Ultrastructural studies of peripheral follicular and theca interstitial cells of type VI and VII follicles revealed swollen mitochondria, dilated ERs (free of RNP particles), increased lysosomes, several necrotic areas of cytoplasm and pyknotic nuclei. Conclusively, Zn deficiency may lead to (1) reduction in energy, protein intake and in secretion of GnRH by hypothalamus and LH and FSH by hypophysis, (2) increased synthesis and/or secretion of prolactin. (3) reduced output of estrogen, and (4) eventually slow growth or arrest of ovulation or atresia of the growing follicles in the ovary.

Animals↗
PubMed1995

Effect of adrenalectomy and adrenalectomy+hydrocortisone treatment on histopathological, biochemical and zinc and copper profiles in rat testes.

Degenerative changes such as decreased seminiferous tubule diameter, Leydig cell nuclear diameter, spermatogenic arrest, oedematous fluid in the interstitium and lumen of seminiferous tubules and increased levels of zinc, copper and enzymes (lactate dehydrogenase, LDH; leucine aminopeptidase, LAP; and aryl sulphatase) in adrenalectomised rats suggest a possible role of adrenal cortex and its hormones in spermatogonial cell proliferation and subsequent differentiation, homeostasis of biological trace elements and behaviour of enzymes. Atrophy of Leydig cells and the degenerative changes in testes of adrenalectomised rats can be attributed to reduced supply of testosterone. Hydrocortisone, administered through a single dose acted as hyperstate of hydrocortisone for a short duration, thereby inhibiting steroidogenesis either directly by affecting Leydig cell testosterone production or indirectly by affecting the release of LH from pituitary gland and thus caused degeneration of germinal epithelium. Once hydrocortisone (half life < 12 hr) was metabolized, the animals returned to adrenalectomised state, the degeneration persisted. Thus, hydrocortisone administered through a single dose was insufficient to sustain spermatogenesis. Chronic administration at physiological dose may renew spermatogenesis. Increased levels of LDH, LAP and arylsulphatase are, probably, necessary for cellular degeneration. Zinc and copper exhibited an increase and the rise can be corroborated to (1) failure of regulatory mechanism(s) that control the flow of the elements across the blood-testes barrier; and (2) increased oedematous fluid formed by cellular deaths of the germinal epithelium.

Adrenal Cortex↗
PubMed1994

Zinc, copper and selenium in reproduction.

Of the nine biological trace elements, zinc, copper and selenium are important in reproduction in males and females. Zinc content is high in the adult testis, and the prostate has a higher concentration of zinc than any other organ of the body. Zinc deficiency first impairs angiotensin converting enzyme (ACE) activity, and this in turn leads to depletion of testosterone and inhibition of spermatogenesis. Defects in spermatozoa are frequently observed in the zinc-deficient rat. Zinc is thought to help to extend the functional life span of the ejaculated spermatozoa. Zinc deficiency in the female can lead to such problems as impaired synthesis/secretion of (FSH) and (LH), abnormal ovarian development, disruption of the estrous cycle, frequent abortion, a prolonged gestation period, teratogenicity, stillbirths, difficulty in parturition, pre-eclampsia, toxemia and low birth weights of infants. The level of testosterone in the male has been suggested to play a role in the severity of copper deficiency. Copper-deficient female rats are protected against mortality due to copper deficiency, and the protection has been suggested to be provided by estrogens, since estrogens alter the subcellular distribution of copper in the liver and increase plasma copper levels by inducing ceruloplasmin synthesis. The selenium content of male gonads increases during pubertal maturation. Selenium is localized in the mitochondrial capsule protein (MCP) of the midpiece. Maximal incorporation in MCP occurs at steps 7 and 12 of spermatogenesis and uptake decreases by step 15. Selenium deficiency in females results in infertility, abortions and retention of the placenta. The newborns from a selenium-deficient mother suffer from muscular weakness, but the concentration of selenium during pregnancy does not have any effect on the weight of the baby or length of pregnancy. The selenium requirements of a pregnant and lactating mother are increased as a result of selenium transport to the fetus via the placenta and to the infant via breast milk.

Animals↗
PubMed1994

Histological and biochemical changes in testis of zinc deficient BALB/c strain of mice.

Zinc, protein, cholesterol, phospholipids, alkaline phosphatase (AlPase), acid phosphatase (AcPase), adenosine-5-triphosphatase(ATPase) and histology were studied in testis of zinc-deficient mice. Zinc and protein decreased in the 3-week experiment whereas they increased in the 6-week experiment. Zinc is involved in several functions of the cell and is regulated by hormones. Inhibition of spermatogenesis indicates for decreased zinc levels in 3-week whereas the increase in 6-week experiment indicates for accumulation of zinc in oedomatous fluid and uncontrolled diffusion of zinc across the blood testis barrier. Glycogen decreased in the 3-week as well as 6-week experiments due to blockage of androgen and spermatogenesis. Cholesterol and phospholipids increased in the 3-week experiment and decreased in 6-week experiment as both the parameters are related to steroidogenesis. Zinc deficiency leads to aspermatogenic condition and comparatively less injury to non-germinal cells. This could have blocked the transport of material across the testis barrier and therefore might have increased AlPase levels. Increased AcPase, probably represents lysosomal enzymes, as the cell debris of disorganised epithelium are to be digested and removed. ATPase increased in 3-week experiment and can be correlated to increased demands of energy of testicular cells to overcome the insults of zinc deficiency whereas the decrease in 6-week experiment could be as a result of inhibition of spermatogenesis.

Acid Phosphatase↗
PubMed1993

Selenium--its biological perspectives.

Selenium is an essential trace element at lower concentrations and toxic at higher concentration. Animals can metabolize both inorganic and organic forms and convert non methylated Se to mono--or di--or tri--methylated forms, of which, mono-methylated forms are most toxic. Glutathione reductase converts selenoglutathione to H2S in liver and erythrocytes and is ultimately excreted. Se effects the toxicities of xenobiotic agents, provides antagonistic effect to Sulphur and co-administration with Zn increase Se retention in certain organs. At its toxic level (4-8 ppm) it increases Cu contents of heart, liver and kidney and has detoxifying or protecting effect against Cd and Hg. It is a prosthetic group of several seleno metalloenzymes. The concentration of the element is decreased in serum/plasma or erythrocytes of patients of AIDS, trisomy-21, Crohn's and Down's syndrome, phenylketonurea, Keshan's disease and cancer. Rather, the element has antiproliferative and cancer protecting effect. Se content of testes increases considerably during pubertal maturation and, during Se deficiency, the supply to the testes has priority over the other tissues. The element is localized in the mitochondrial capsule protein (MCP) and is involved in biosynthesis of testosterone. Neither the age of mother nor the concentration of Se during pregnancy has any effect on weight of baby or the length of pregnancy. Se levels in human milk is affected by maternal intake and its requirements by infants and young children are higher for their rapid growth. Clinical symptoms of its toxicity include severe irritations of respiratory system, metallic taste in mouth, formication of nose, signs of rhinitis, lung edema and brancho-pneumonia. The typical garlic odour of breath and sweat is due to dimethyl-selenide.

Animals↗
PubMed1983

Langerhans cell and leprosy.

Langerhans cell population was counted in 44 patients of different types of leprosy and compared with 12 normal volunteers. Significant reduction in LC count was observed in cases of LL (253.44 +/- 136.83/mm2) and BL (349.36 +/- 121.67/mm2). Whereas in TT (854.60 +/- 332.01/mm2) and BT (715.76 +/- 235.33/mm2) there was no significant difference, as compared to Normal (927.43 +/- 103.87/mm2). Treatment had no influence on LC population in both the polar types of leprosy. Role of these immunocompetent dendritic cells in the pathogenesis of leprosy is discussed.

Adolescent↗
PubMedDate not supplied

Ultrastructural study of epidermal Langherhans cells in leprosy.

ATPase staining and ultrastructural study of skin biopsies from six patients of leprosy (2TT, 4LL) and three normal subjects was carried out to study Langherhans Cells (LC). ATPase staining showed normal counts of LCs in tuberculoid patients, while significant reduction was observed in lepromatous cases. Electron microscopy revealed morphological changes in LL cases in the form of dense matrix and indistinct cristae of mitochondria; decreased number of lysosomes and rough endoplasmic reticulum; and numerous vacuoles in cytoplasm. TT cases showed normal morphology. Possible role of Langerhans Cells in pathogenesis of leprosy is discussed.

Humans↗