Fructose-Enhanced Development and Growth of the N2-Fixing Cyanobiont Anabaena azollae

1988 ◽  
Vol 43 (5-6) ◽  
pp. 408-412 ◽  
Author(s):  
Anat Rozen ◽  
Mordechay Schönfeld ◽  
Elisha Tel-Or
Keyword(s):  
Nitrogenase Activity ◽  
Dark Respiration ◽  
Fold Increase ◽  
High Rate ◽  
Azolla Filiculoides ◽  
Anabaena Azollae ◽  
Energy Dependent ◽  
Fold Stimulation ◽  
Stimulation Of

Fructose supported the heterotrophic growth of the cyanobiont Anabaena azollae, isolated from the water fern Azolla filiculoides, and also enhanced its growth in the light by 2-3-fold. Fructose was taken up at a high rate in the light and in the dark, in an energy-dependent reaction. The photosynthetic and respiratory activities of the fructose grown cells were modified: O2 evolution in vivo was decreased by 40%, while PS I activity and dark respiration were 2-3-fold higher than in autotrophically grown cells. These changes were accompanied by 2-3-fold increase in heterocyst differentiation and by a 4-fold stimulation of nitrogenase activity.

Expression of Soluble Syndecan-1 or Heparanase by Myeloma Cells Enhances Levels of Angiogenic Growth Factors Present in Endothelial Cells.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3448-3448
Author(s):  
Yang Yang ◽  
Ashley Elizabeth Frith ◽  
Allison Theus ◽  
Veronica Macleod ◽  
Ralph D. Sanderson
Keyword(s):  
Endothelial Cells ◽  
Growth Factors ◽  
Growth Factor ◽  
Fold Increase ◽  
Conditioned Media ◽  
High Rate ◽  
In Vivo Studies ◽  
Angiogenic Growth Factors ◽  
Myeloma Cells

Abstract Multiple myeloma is a devastating cancer with a high rate of morbidity and mortality. Our previous in vivo studies demonstrate that both shed syndecan-1 and heparanase can promote myeloma tumor growth, metastasis and angiogenesis. To examine the mechanism underlying this enhanced angiogenesis, human umbilical vein endothelial cells (HUVEC) were cocultured with cells of the CAG myeloma cell line (vector-only controls, CAGcontrol) or CAG cells engineered to express high levels of either soluble syndecan-1 ectodomain (CAGssyn1 ) or heparanase ( CAGHPSE ). After coculture for 48 hours, levels of angiogenic growth factors present in the endothelial cells were examined. The goal was to determine if expression of either soluble syndecan-1 or heparanase by CAG myeloma cells altered growth factor levels relative to those present when control CAG cells were used. Co-culture with CAGssyn1 or CAGHPSE cells did not enhance endothelial levels of FGF-2, while levels of hepatoma-derived growth factor (HDGF) and hepatocyte growth factor (HGF) were elevated in endothelia growing in the presence of CAGssyn1 cells but not CAGHPSE cells or CAGcontrol cells. However, VEGF levels present in endothelial cells were substantially enhanced by the presence of CAGssyn1 (1.9-fold increase) or CAGHPSE cells (1.6-fold increase). Surprisingly, levels of VEGF in conditioned media of cocultures containing either CAGssyn1 or CAGHPSE cells was low. In contrast, when cultured in the absence of HUVECs, VEGF levels were elevated in conditioned media of both CAGssyn1and CAGHPSE cells. Addition of this conditioned media containing high levels of VEGF to HUVECs growing in the absence of CAG cells did not result in an elevation of VEGF levels in the endothelial cells. Together, these experiments suggest that VEGF expression is upregulated in CAG cells expressing high levels of shed syndecan-1 or heparanase and that VEGF becomes associated with the endothelial cells only when they are cultured in the presence of the myeloma cells. This cross-talk between myeloma and endothelial cells may lead to the enhanced angiogenesis that occurs in vivo in tumors formed by myeloma cells producing high levels of shed syndecan-1 and/or heparanase.

Stimulation of K-C1 cotransport in rat red cells by a hemolytic anemia-producing metabolite of dapsone

1989 ◽  
Vol 256 (2) ◽  
pp. C265-C272 ◽  
Author(s):  
M. Haas ◽  
J. H. Harrison
Keyword(s):  
Red Blood Cells ◽  
Hemolytic Anemia ◽  
Blood Cells ◽  
Pneumocystis Carinii ◽  
Fold Increase ◽  
Sh Groups ◽  
Splenic Uptake ◽  
Stimulation Of ◽  
In Cells

Dapsone, a sulfone compound used in the treatment of leprosy and, more recently, Pneumocystis carinii pneumonia, produces as a major side effect a hemolytic anemia. This anemia is characterized by oxidation of hemoglobin to methemoglobin and increased splenic uptake of red blood cells. Using a rat model, Grossman and Jollow (J. Pharmacol. Exp. Ther. 244: 118-125, 1988) found that dapsone hydroxylamine (DDS-NOH), a dapsone metabolite, is responsible for its hemolytic effect in vivo. DDS-NOH also promotes hemoglobin binding to SH groups on rat red cell membrane proteins (Budinsky et al., FASEB J. 2: A801, 1988). Since the binding of hemoglobin and other reagents (e.g., N-ethylmaleimide) to membrane SH groups has been associated with increased K transport in red blood cells, we examined the effect of DDS-NOH on K efflux from rat red blood cells in vitro. Cells shrink when exposed to DDS-NOH (100 microM) in media with plasma-like ionic composition. This shrinkage is prevented if extracellular K is raised to 110 mM or if intra- and extracellular Cl are replaced by methylsulfate (MeSO4), suggesting involvement of a K-Cl cotransport pathway. Indeed, 100 microM DDS-NOH produces a 4- to 5-fold increase in K efflux in cells containing Cl but less than a 2-fold increase in cells containing MeSO4. This stimulatory effect is specific for K; Na efflux is slightly inhibited by 100 microM DDS-NOH. The concentrations of DDS-NOH required for half-maximal stimulation of Cl-dependent K efflux (53 microM) is similar to its half-maximal hemolytic concentration in rats (approximately 100 microM). Furthermore, the stimulation of Cl-dependent K efflux by DDS-NOH is greater than 80% reversed by subsequent treatment of the cells with dithiothreitol, suggesting involvement of SH groups. Our results indicate that DDS-NOH exposure stimulates an apparent K-Cl cotransport in rat red blood cells, resulting in cell shrinkage under physiological ionic conditions. Since shrinkage of red blood cells renders them less deformable (Mohandas et al., J. Clin. Invest. 66: 563-573, 1980), this suggests a pathophysiological mechanism whereby DDS-NOH exposure in vivo could promote increased splenic uptake of red blood cells and hemolytic anemia.

Heparin Induces Synthesis and Secretion of Tissue Factor Pathway Inhibitor from Endothelial Cells In Vitro

2000 ◽  
Vol 83 (06) ◽  
pp. 937-943 ◽  
Author(s):  
Birgit Svensson ◽  
Randi Olsen ◽  
Mirella Ezban ◽  
Bjarne Østerud ◽  
Ruth Paulssen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Surface Membrane ◽  
Molecular Size ◽  
Fold Increase ◽  
Coagulation System ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Stimulation Of

SummaryTFPI is a potent inhibitor of the extrinsic coagulation system constitutively synthesized by endothelial cells. A major portion of intravascular TFPI is stored associated with endothelial cells, and administration of unfractionated heparin (UFH) in vivo causes a prompt mobilization of TFPI into the circulation. The present study was conducted to investigate how UFH affected the synthesis, secretion and anticoagulant potency of TFPI in endothelial cells in vitro. A spontaneously transformed immortal endothelial cell line was used (ECV304). Stimulation of ECV304 cells with UFH caused a prompt dose-dependent (0-5 IU UFH/ml) release of TFPI to the medium accompanied by no change of TFPI at the surface membrane assessed by immunocytochemical methods. Northern blot analysis revealed two mRNA transcripts for TFPI with a molecular size of 1.4 kb and 4.4 kb, respectively. Stimulation of ECV304 cells for 24 hrs with various concentrations of UFH caused a dose-dependent increase of TFPI in the medium (6.2-29.6 ng/106 cells within the concentration range 0-10 IU/ml). A similar dose-dependent increase in the expression of both TFPI mRNA species was observed. Long-term incubation of ECV304 cells with 5.0 IU/ml UFH caused a 5-10 fold increase in the TFPI concentration accumulated in the medium over 48 hrs. The increased TFPI mRNA expression induced by UFH appeared already after 10 min, peaked after 2-4 hrs, remained augmented throughout the entire period of UFH exposure, and preceeded the synthesis-dependent increase in TFPI release by 2-4 hrs. The procoagulant activity of the cells was downregulated by 36 % and the contribution of TFPI to the anticoagulant potency of ECV304 cells was moderately increased after 24 hrs heparin stimulation. It is suggested that these mechanisms are of major importance for the anticoagulant function of heparins.

MO010COLLAGEN TYPE VI PRODUCTION BY KIDNEY FIBROBLASTS IS DEPENDENT ON THE RIGHT STIMULI AND MAY SELF-PERPETUATE FIBROSIS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Alexandra Louise Møller ◽  
Daniel G. K. Rasmussen ◽  
Morten A. Karsdal ◽  
Federica Genovese
Keyword(s):  
Cell Model ◽  
Human Kidney ◽  
Fold Increase ◽  
Type I ◽  
Kidney Fibrosis ◽  
Collagen Formation ◽  
Ecm Proteins ◽  
Time Point ◽  
Stimulation Of

Abstract Background and Aims Accumulation of extracellular matrix (ECM) proteins is a hallmark of kidney fibrosis, which can lead to altered tissue homeostasis, kidney failure, and ultimately death. Many different cell types are involved in this process, but fibroblasts are the main source of ECM proteins such as collagen type I (COL I), III (COL III), and VI (COL VI). Recently, it was suggested that a fragment of COL VI, released during collagen maturation, is a bioactive molecule (endotrophin; ETP) with signaling potential, indicating that collagens are not just passive structural proteins. In this study, we investigated the effect of different pro-fibrotic stimulants on COL VI production and the effect of ETP itself on human kidney fibroblasts in the scar-in-a-jar (SiaJ) cell model. Method Cells were seeded in 48-well plates at 30.000 cells/well and incubated for 24h in DMEM + 10% FBS for adherence. Cells were then starved by incubating them for further 24h in DMEM + 0.4% FBS. To induce fibrogenesis, fresh medium was added at day 0 with 225/150 mg/mL Ficoll 70/400 and 1% ascorbic acid, containing either 7-, 0.7-, or 0.07 nM PDGF-AA, 8-, 0.8-, or 0.08 nM PDGF-BB, 4-, 0.4-, or 0.04 nM PDGF-CC, 7-, 0.7-, or 0.07 nM PDGF-DD, 0.9-, or 0.09 nM CTGF, 0.02 nM TGF-β or 30 nM ETP. Medium was changed and collected on days 3, 6, 10, and 13. Biomarkers of COL I (PRO-C1), III (PRO-C3), and VI (PRO-C6) formation were assessed in the medium by enzyme-linked immunosorbent assays developed at Nordic Bioscience. Results The stimulation of kidney fibroblasts with PDGF-AA, -BB, -CC, and -DD caused an increase in PRO-C6 compared to the unstimulated cells at every time point (P<0.0001). The increase in formation peaked at day 10, and a dose-dependent increase in COL VI levels was observed with PDGF-DD treatment. Interestingly, CTGF treatment did not enhance the synthesis of COL VI at any time point, and TGF-β treatment suppressed PRO-C6 levels compared to the untreated cells (not significant). The stimulation with 30 nM ETP caused an increase in PRO-C1 (P<0.0001) and PRO-C3 (P<0.0001) compared to the unstimulated cells on days 6, 10, and 13. The increase in collagen formation peaked at day 10 for both markers, with a 7.28-fold increase for COL I and a 4.13-fold increase for COL III. Conclusion The production of COL VI, an important mediator of fibrosis and inflammation through its bioactive fragment endotrophin, shows a differential expression after stimulation of kidney fibroblasts with different pro-fibrotic growth factors. Interestingly, members of the PDGF family induced COL VI production, whereas CTGF and TGF-β did not. Moreover, we confirmed that ETP itself could stimulate kidney fibroblasts to produce more ECM proteins; hence COL VI may self-perpetuate fibrosis. This SiaJ model, combined with ECM formation biomarkers, could be used to elucidate the mechanisms behind acute and sustained matrix production profiles in vivo.

Different responses in little and bigbig prolactin to metoclopramide in subjects with hyperprolactinemia due to 150–170 kD (bigbig) prolactin

1993 ◽  
Vol 128 (4) ◽  
pp. 308-312 ◽  
Author(s):  
T Bjøro ◽  
E Johansen ◽  
HH Frey ◽  
A Turter ◽  
PA Torjesen
Keyword(s):  
Menstrual Cycle ◽  
Luteal Phase ◽  
Male Subject ◽  
Fold Increase ◽  
Serum Prolactin ◽  
Maximal Response ◽  
Prolonged Stimulation ◽  
In Vivo Induction ◽  
Stimulation Of

We have studied in vivo induction of serum prolactin (PRL) levels in four females and one male, and regulation of PRL in the menstrual cycle in three females all with hyperprolactinemia with large amounts (72–92%) of bigbig PRL (MW 150–170 kD). Metoclopramide (MTC) iv induced a 4–29-fold increase in little PRL (25 kD PRL) at 30 min, while the increase in 150–170 kD PRL was 1.1–2.2-fold. The maximal response in 150–170 kD PRL was seen after 2–6 h, and the decrease after the maximal PRL values for 150–170 kD PRL was delayed compared to the decrease in 25 kD PRL. The different kinetics for 25 kD PRL and 150–170 kD PRL was responsible for the prolonged increase in total PRL seen in the subjects with large amounts of 150–170 kD PRL compared to the controls. The percentage of 1 50–170 kD PRL decreased to 29–60% at 30 min and returned to unstimulated values after 6–24 h. In contrast, prolonged stimulation of PRL secretion, as in the luteal phase, did not change the percentage of 150–170 kD PRL. In a male subject secreting large amounts of 1 50–170 kD PRL the increase in PRL after MTC was less, while the temporal changes in the 25 kD PRL levels were almost the same as in the females.

Immunomodulatory Drugs (IMiDs), Lenalidomide and Pomalidomide, Suppress Th1-Inducing Capacity of Dendritic Cells but Enhance Th2-Mediated Allergic Response

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 2520-2520
Author(s):  
Tomoki Ito ◽  
Phan Thi Xuan Vien ◽  
Muneo Inaba ◽  
Hideaki Yoshimura ◽  
Masaaki Hotta ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Molecular Mechanisms ◽  
Fold Increase ◽  
Allergic Response ◽  
High Rate ◽  
Th2 Cells ◽  
Immunomodulatory Drugs ◽  
Th2 Response

Abstract Background: Analogs of thalidomide, lenalidomide (LEN) and pomalidomide (POM), are novel anti-multiple myeloma (MM) drugs (so-called Immunomodulatory Drugs; IMiDs). LEN has been reported to enhance function of effector immune cells such as T cells and NK cells and to induce selective reduction of regulatory T cells. Meanwhile, LEN and POM treatments lead to relatively high rate onset of itchy skin with rash like allergic reaction. However, cellular and molecular mechanisms underlying their immunomodulatory effects still remain largely unclear. Although there is evidence indicating the immunomodulatory actions of LEN on mouse conventional dendritic cells (DCs), there are few reports showing their effects on human DC subsets. DCs are pivotal in orchestrating both innate and acquire immunity as the center of the immune regulatory system, and series of analyses have clarified a functional plasticity of DCs to induce Th1 or Th2 response. Therefore, we focused on the effects of LEN and POM on the function of human myeloid DCs (mDCs), which are the major regulators to induce Th1 or Th2 responses and play a pathogenic role in allergy by their dysregulated Th2-inducing function (Ito T. J Exp Med 2005; 202: 1213). Methods: Using cell sorting, flow cytometry, real-time PCR, and ELISA methods, function and signaling were analyzed in blood human CD11+ mDCs from healthy adult volunteers. Sera were obtained from 24 MM patients with before and after LEN therapy. Written informed consent was obtained for all patients. This study was approved by the Institutional Review Board of Kansai Medical University. Results: We found that both agents at clinical in vivo plasma concentration of 0.1 µM to 1 µM did not affect the mDC survival and their CD86 and OX40-ligand expression in response to toll-like receptor (TLR)-ligands (LPS, poly IC, or R848) and Th2-inducing cytokine, thymic stromal lymphopoietin (TSLP) for 24 h culture. Either LEN or POM inhibited dose-dependently mDC-derived Th1-associated cytokines, IL-12 in response to R848 (1 µM LEN; 5.2 % of cont. and 0.3 µM POM; 12 % of cont.), IFN-λ in response to poly IC (1 µM LEN; 5.4 % of cont. and 0.3 µM POM; 10 % of cont.), and TNFα in response to R848 (1 µM LEN; 36 % of cont. and 0.3 µM POM; 17 % of cont.), but enhanced IL-10 production in response to R848 (1 µM LEN; 4.8-fold increase and 0.3 µM POM; 7.5-fold increase). When mDCs were stimulated with TSLP, both agents significantly enhanced the production of Th2-recruiting chemokine CCL17/TARC (1 µM LEN; 2.4 fold increase and 0.3 µM POM; 3.9 fold increase), which functions as chemoattractant for memory Th2 cells and contribute to aggravation of allergic inflammation. These capacities of POM were stronger than those of LEN. In addition, we revealed that, in response to LPS or R848, both LEN and POM downregulated not only IRF4 mRNA in human mDCs as in LEN-treated myeloma cells, but also STAT4 mRNA, which is important for DC-mediated Th1 response and IL-12 production. In mDCs treated with TSLP, both agents were found to upregulate STAT6 mRNA, which is responsible for TSLP-mediated CCL17 secretion (Arima K. Sci Signal2010;3:ra4). Clinically, serum CCL17/TARC levels are associated with the disease activity of atopic dermatitis and sensitively reflect short-term changes in skin conditions. We also found, in MM patients, serum CCL17 levels at the onset of LEN-associated rash during 4 weeks (n=9; 1271 ± 376 pg/ml) were significantly higher (p <0.001) compared to those without rash in LEN treatment (n=15; 476 ± 236 pg/ml) and those before treatment (296 ± 172 pg/ml). Conclusion: Our data suggest that the IMiDs, while suppress the Th1-inducing capacity of DCs, rather lead to enhance allergic response at DC phase through modulation of signaling pathways in this stream of action. Thus, IMiDs could have the potential to shift DC-mediated response from Th1 to Th2, and our findings provide a plausible explanation for pathogenesis of IMiD-associated rash in the treatment for MM. Disclosures Ito: Celgene corporation: Honoraria; GSK: Patents & Royalties.

scholarly journals Stimulation of erythropoiesis by in vivo gene therapy: physiologic consequences of transfer of the human erythropoietin gene to experimental animals using an adenovirus vector

Blood ◽  
1994 ◽  
Vol 84 (9) ◽  
pp. 2946-2953 ◽  
Author(s):  
Y Setoguchi ◽  
C Danel ◽  
RG Crystal
Keyword(s):  
Gene Therapy ◽  
Blood Cell ◽  
Subcutaneous Administration ◽  
Adenovirus Vector ◽  
Fold Increase ◽  
Adenovirus Type ◽  
Stimulation Of Erythropoiesis ◽  
Adenovirus Type 5 ◽  
Stimulation Of

Abstract Erythropoietin (Epo), a 30.4-kD glycoprotein, is the principal regulator of erythropoiesis. To evaluate the concept that in vivo gene transfer might be used as an alternative to recombinant human Epo (rhEpo) in applications requiring a 1- to 3-week stimulation of erythropoiesis, the replication-deficient recombinant adenovirus AdMLP.Epo was constructed by deleting the majority of E1 from adenovirus type 5, and replacing E1 with an expression cassette containing the adenovirus type 5 major late promoter (MLP) and the human Epo gene, including the 32 cis-acting hypoxia response element. In vitro studies showed that infection of the human hepatocyte cell line Hep3B with AdMLP.Epo resulted in a 15-fold increase in Epo production in 24 hours that was enhanced to 116-fold in the presence of a hypoxic stimulus. One-time in vivo administration of AdMLP.Epo (7 x 10(9) plaque-forming units/kg) to the peritoneum of cotton rats caused a marked increase in red blood cell production, with a 2.6-fold increase in bone marrow erythroid precursors by day 4, and sevenfold increase in reticulocyte count by day 7. The hematocrit increased gradually, with a maximum of 64% +/- 4% at day 14 (compared with an untreated baseline of 46% +/- 2%), and a level of 55% +/- 1% at day 24. Furthermore, one-time subcutaneous administration of AdMLP.Epo caused an increase in hematocrit that peaked at 14 days (57% +/- 2%) and was still elevated at day 42. Hematocrit level in animals receiving subcutaneous administration of AdMLP.Epo sustained a long-term increase compared with animals receiving intraperitoneal administration. In the context of these observations, gene therapy with a single administration of an adenovirus vector containing the human EPO gene may provide a means of significantly augmenting the circulating red blood cell mass over the 1- to 3-week period necessary for many clinical applications.

scholarly journals A simplified protocol for in vitro rearing of human body lice

Parasite ◽  
2020 ◽  
Vol 27 ◽  
pp. 8
Author(s):  
Jose E. Pietri ◽  
Ritesh Ray
Keyword(s):  
Human Body ◽  
Laboratory Experiments ◽  
Fold Increase ◽  
High Rate ◽  
Regulatory Requirements ◽  
Pediculus Humanus ◽  
Hematophagous Insect ◽  
Body Lice

Human body lice (Pediculus humanus) are neglected ectoparasites and pathogen vectors. Difficulties in raising and maintaining colonies of body lice in a laboratory setting remain a barrier to fundamental studies of physiology and vector-pathogen interactions in these insects. Several in vivo and in vitro rearing systems have been previously described and used by multiple research groups. However, these methods suffer from drawbacks that still complicate the rearing of body lice relative to many other commonly studied hematophagous insects. Here, a simplified protocol for raising and maintaining body lice in vitro using the commercially available Hemotek apparatus is described. This protocol draws from published methods for rearing body lice as well as other hematophagous insect species to further reduce labor, time, costs, and regulatory requirements typically associated with keeping human body lice in the laboratory. Using this protocol, the insects consistently fed on commercially available rabbit blood with little mortality, reached adulthood at a high rate, and produced a significant number of viable eggs, resulting in a 4.8-fold increase in population over a period of 40 days. The data suggest that the process described here can propagate modest populations for ongoing laboratory experiments and is a useful alternative to existing methods. The use and further optimization of in vitro rearing systems may facilitate dynamic studies of body lice by a wider range of investigators, enabling new progress in combating lice infestations, and louse-borne infections.

scholarly journals Activation of adenylyl cyclase in Chlamydomonas reinhardtii by adhesion and by heat

1993 ◽  
Vol 122 (1) ◽  
pp. 137-147 ◽  
Author(s):  
T Saito ◽  
L Small ◽  
UW Goodenough
Keyword(s):  
Chlamydomonas Reinhardtii ◽  
Adenylyl Cyclase ◽  
Cell Body ◽  
Cyclase Activity ◽  
Defective Mutant ◽  
Adhesive Interactions ◽  
Fold Stimulation ◽  
Stimulation Of

Adhesion between Chlamydomonas reinhardtii gametes generates a rapid rise in cAMP levels which stimulates mating responses and zygotic cell fusion (Pasquale and Goodenough, 1987). We show here that sexual adhesion in vivo results in a twofold stimulation of flagellar adenylyl cyclase activity when the enzyme is subsequently assayed in vitro, a stimulation that is specifically blocked by Cd2+. A twofold stimulation is also elicited by the in vitro presentation of soluble cross-linking reagents (antisera and concanavalin A). In contrast, the 10-30-fold stimulation of the flagellar cyclase by in vitro exposure to 40 degrees C, first described by Zhang et al. (1991), is insensitive to Cd2+ but sensitive to such drugs as trifluoperizine and dibucaine. The capacity for twofold stimulation is displayed by the vegetative and gametic enzymes but is lost when gametes fuse to form zygotes; in contrast, the 10-fold stimulation is displayed by the gametic and zygotic enzymes but not the vegetative enzyme. The signal-defective mutant imp-3 fails to generate the normal mating-triggered cAMP production and can be rescued by exogenous dibutyryl cAMP. It displays normal basal rates of flagellar cyclase activity and a normal twofold stimulation by sexual adhesion and by soluble cross-linkers, but it is defective in 40 degrees C activation. The gametic cell-body adenylyl cyclase is stimulated when wild-type flagella, but not imp-3 flagella, undergo adhesive interactions in vivo, and it can be directly stimulated in vitro by cAMP presentation. We propose that the two levels of flagellar cyclase stimulation reflect either sequential steps in the activation of a single cyclase enzyme, with imp-3 blocked in the second step, or else the sequential activation of two different flagellar enzymes, with imp-3 defective in the second enzyme. We further propose that the cell-body enzyme is activated by the cAMP that is generated when flagellar cyclase activity is fully stimulated.

scholarly journals Stimulation of mouse liver glutathione S-transferase activity in propylthiouracil-treated mice in vivo by tri-iodothyronine

1986 ◽  
Vol 233 (2) ◽  
pp. 595-598 ◽  
Author(s):  
M T Williams ◽  
H Carrington ◽  
A Herrera
Keyword(s):  
Dehydrogenase Activity ◽  
Actinomycin D ◽  
Fold Increase ◽  
Transferase Activity ◽  
Glutathione S Transferase ◽  
Glycerol 3 Phosphate Dehydrogenase ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Stimulation Of

Female C57Bl/6J mice were given drinking water containing 0.05% propylthiouracil to induce a hypothyroid condition. Mitochondrial glycerol-3-phosphate dehydrogenase activity, used as an index of hypothyroidism, was 57.1 +/- 4.5 and 29.4 +/- 3.8 nmol/min per mg of protein for control and propylthiouracil-treated animals respectively. Administration of tri-iodothyronine resulted in an approx. 4.5-fold increase in dehydrogenase activity in propylthiouracil-treated animals. A dose-dependent increase in hepatic GSH S-transferase activity in propylthiouracil-treated animals was observed at tri-iodothyronine concentrations ranging from 2 to 200 micrograms/100 g body wt. This increase in transferase activity was seen only when 1,2-epoxy-3-(p-nitrophenoxy)propane was used as substrate for the transferase. Transferase activity with 1-chloro-2,4-dinitrobenzene and 1,2-dichloro-4-nitrobenzene as substrate was decreased by tri-iodothyronine. Administration of actinomycin D (75 micrograms/100 g body wt.) inhibited the tri-iodothyronine induction of transferase activity. Results of these studies strongly suggest that tri-iodothyronine administration markedly affected the activities of GSH S-transferase by inducing a specific isoenzyme of GSH S-transferase and suppressing other isoenzymic activities.

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