Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma glycoprotein synthesis in normal and vitamin A-deficient rats was investigated by injecting the rats with labeled carbohydrate precursors and then fractionating their plasmas on DEAE-Sephadex. Plasma from deficient rats showed a consistent depression of 30% in the uptake of label into a peak eluting with 0.23 M NaCl. The major component of this peak was identified as the rat alpha1-macroglobulin, based on its molecular weight (800,000), its mobility on cellulose acetate electrophoresis and its ability to bind trypsin. Although the alpha1-macroglobulin synthesis appeared to be depressed by 30%, its fractional turnover rate was not affected by vitamin A deficiency (t 1/2 = 18 hours). The trypsin-binding ability of this glycoprotein was used as a comparative measure of its concentration, and the results confirmed that serum levels of this glycoprotein were lower in deficient rats. In severe deficiency, alpha1-macroglobulin levels dropped to between 10% and 20% of normal levels.
 ...
PMID:A plasma glycoprotein depressed in vitamin A deficiency in the rat: alpha 1-macroglobulin. 6 42

Serum samples were obtained from 43 children 14 years old or younger in Malaysia and Guatemala. The levels of the serum glycoprotein alpha 2-macroglobulin (alpha 2-M) were assayed by two methods: the trypsin-binding assay of Ganrot (Clin. Chim. Acta 14:493, 1960) and a radial immunodiffusion assay against alpha 2-M antiserum. The two methods gave the same results. When serum alpha 2-M levels were plotted against serum vitamin A concentrations, they were significantly correlated (r = 0.505, P less than 0.001); children with serum vitamin A levels greater than 40 micrograms/100 ml had alpha 2-M levels of 3.71 +/- 0.79 mg/ml (mean +/- SD, n = 13), while those with level less than 40 micrograms/100 ml had alpha 2-M levels of 2.78 +/- 0.51 mg/ml (n = 30); the difference was significant (P less than 0.001). Normal, apparently healthy children had alpha 2-M levels of 3.90 +/- 0.39 mg/ml. Most of the children sampled suffered from a variety of infections; of these, measles appeared to counteract the effect of vitamin A deficiency by elevating alpha 2-M levels. Vitamin A-deficient children with measles had alpha 2-M levels not significantly lower than those of normal children. The difference between deficient and normal values of alpha 2-M was still significant (P less than 0.05) when expressed per milligram of serum protein, showing that the effect was not caused by lowered serum protein concentrations associated with protein-calorie malnutrition, from which most of the deficiency children suffered.
 ...
PMID:alpha 2-Macroglobulin in vitamin A-deficient children. 8 10

Previous studies have shown that disruption or damage to the seminiferous tubules by radiation, antiandrogen, vitamin A deficiency or experimental cryptorchidism causes Leydig cell hypertrophy and hyperplasia, suggesting that Sertoli cells secrete a mitogenic factor(s) that stimulates Leydig cell proliferation. To study the possible paracrine regulation of Leydig cell proliferation by Sertoli cells, highly purified Leydig cells and Sertoli cells were co-cultured in a two-chambered co-culture system. Our results revealed that co-culture of immature rat Sertoli cells with Leydig cells stimulated Leydig cell DNA synthesis by 19-fold, increased cell number by about 3.9-fold and increased the labeling index from 0.5% to 15.8%. In addition to these changes, co-culture reduced Leydig cell testosterone formation and luteinizing hormone (LH) receptor levels, and dramatically altered the morphology of Leydig cells. The addition of concentrates from Sertoli cell conditioned medium (SCCM) mimicked these biological effects. The Leydig cell mitogenic activity in SCCM was trypsin sensitive and inactivated by boiling for 2 h, suggesting that it is a protein. However, it was resistant to acid and dithiothreitol. The molecular weight of this putative factor(s) is above 10 kDa. The responsiveness of Leydig cells to this mitogenic protein(s) decreased with age, whereas the secretion of this protein(s) by Sertoli cells in culture did not change with age. The addition of 10 ng/ml of follicle stimulating hormone (FSH) dramatically decreased the mitogenic activity in SCCM, indicating that the secretion of this mitogenic factor(s) is inhibited by FSH. This paracrine factor(s) may be as yet an unidentified testicular growth factor(s) because it differs in molecular weight, stability and other characteristics from all previously reported Sertoli cell-produced or expressed growth factors.
 ...
PMID:A Sertoli cell-secreted paracrine factor(s) stimulates proliferation and inhibits steroidogenesis of rat Leydig cells. 789 20

Hybrid chickens Astra S fed vitamin A deficiency diet containing 11 or 19% protein were infected with 500 invasive eggs of Ascaridia galli. One part of them received vitamin A in a dose corresponding to daily requirement, other part in double dose. After 7 weeks the extensity and intensity of ascaridiosis were determined. In pancreas and intestinal contents the activities of alpha-amylase, lipase and trypsin were measured. The invasion index was the highest in the group of chickens fed the protein and vitamin A deficiency diet. Vitamin A in a requirement dose lowered the parasite index. The results with double dose of vitamin A were worse in comparison with single dose. The activities of digestive enzymes were lower in infected animals than in the control groups. Vitamin A acted as moderator of the enzymatic changes during ascaridiosis.
 ...
PMID:[Effect of vitamin A and protein levels in the diet of chickens infected with Ascaridia galli on activity of digestive enzymes in pancreas and small intestine]. 883 7