Protein synthesis is not required for the inhibitory effect of selenite on cell colony formation and RNA synthesis

1994 ◽  
Vol 40 (2) ◽  
pp. 181-187 ◽  
Author(s):  
Lin Yan ◽  
Gerald D. Frenkel
Keyword(s):  
Protein Synthesis ◽  
Colony Formation ◽  
Rna Synthesis ◽  
Inhibitory Effect ◽  
Cell Colony

scholarly journals A comparative study of the effect of aflatoxin B1 and actinomycin D on HeLa cells

1969 ◽  
Vol 114 (2) ◽  
pp. 289-298 ◽  
Author(s):  
E. H. Harley ◽  
K. R. Rees ◽  
A. Cohen
Keyword(s):  
Protein Synthesis ◽  
Ribosomal Rna ◽  
Mechanism Of Action ◽  
Aflatoxin B1 ◽  
Hela Cells ◽  
Rna Synthesis ◽  
Actinomycin D ◽  
Inhibitory Effect ◽  
Cytotoxic Effects ◽  
Rna Precursor

1. The cytotoxic effects of aflatoxin B1 on HeLa cells were examined and effects of short exposures of the cells to the toxin were found to be reversible. 2. Aflatoxin B1 inhibited the synthesis of both ribosomal and heterodisperse RNA. It is proposed that the toxin's mechanism of action on ribosomal RNA synthesis is related to its inhibitory effect on the maturation of the 45s-ribosomal-RNA precursor. 3. Protein synthesis is inhibited to a greater extent by aflatoxin B1 than by actinomycin D. In contrast with actinomycin D, aflatoxin B1 was shown to disaggregate polyribosomes directly.

scholarly journals Time-dependent effects of α-amanitin on nuclear maturation and protein synthesis in mammalian oocytes

Development ◽  
1983 ◽  
Vol 73 (1) ◽  
pp. 317-338
Author(s):  
J. C. Osborn ◽  
R. M. Moor
Keyword(s):  
Protein Synthesis ◽  
Rna Synthesis ◽  
Cumulus Cell ◽  
Cumulus Cells ◽  
Inhibitory Effect ◽  
Time Dependent ◽  
Meiotic Maturation ◽  
Inhibitory Effects ◽  
Nuclear Maturation ◽  
Cytoplasmic Maturation

The addition of α-amanitin to extrafollicular, cumulus-enclosed ovine oocytes at explantation inhibits meiotic maturation and prevents many of the changes in protein synthesis that normally accompany maturation. By contrast, these inhibitory effects are considerably reduced by eitherdelaying the addition of the drug for 1–4 h or by denuding the oocytes of all associated cumulus cells at the onset of culture. The observations that the inhibitory effect of cordycepin onnuclear maturation is also time-dependent and cumulus-cell-dependent and that the oocyte is susceptible to cordycepin for longer than its sensitivity to α-amanitin are consistent with the differential effects of these drugs on RNA synthesis. It is concluded that a transcriptional event at the onset of maturation is essential for the initiation of those changes in protein synthesis required for the regulation of nuclear and cytoplasmic maturation. It is uncertain, however, whether this transcriptional event occurs within the cumulus cells or within the oocyte.

FEMALE ENDOCRINE CONTROL MECHANISMS DURING THE NEONATAL PERIOD

1972 ◽  
Vol 70 (2) ◽  
pp. 396-408 ◽  
Author(s):  
K.-D. Schulz ◽  
H. Haarmann ◽  
A. Harland
Keyword(s):  
Protein Synthesis ◽  
Reproductive System ◽  
Rna Synthesis ◽  
Neonatal Period ◽  
High Dose ◽  
Female Reproductive System ◽  
Endocrine Control ◽  
Hypothalamic Region ◽  
Rna And Protein Synthesis ◽  
Physiological Dose

ABSTRACT The present investigation deals with the oestrogen-sensitivity of the female reproductive system during the neonatal period. Newborn female guinea pigs were used as test animals. At different times after a single subcutaneous injection of a physiological dose of 0.1 μg or an unphysiologically high dose of 10 μg 17β-oestradiol/100 g body weight, the RNA- and protein-synthesis was examined in the hypothalamic region, pituitary, cerebral cortex, liver, adrenal gland, ovary and uterus. With a physiological dose an increase in organ weight, protein content, RNA-and protein-synthesis was found only in the uterus. These alterations turned out to be dose-dependent. In addition to the findings in the uterus an inhibition of the aminoacid incorporation rate occurred in the liver following the injection of the high oestradiol dose. As early as 1 hour after the administration of 0.1 μg 17β-oestradiol an almost 100% increase in uterine protein synthesis was detectable. This result demonstrates a high oestrogen-sensitivity of this organ during the neonatal period. All the other organs of the female reproductive system such as the hypothalamus, pituitary and ovary did not show any oestrogen response. Therefore the functional immaturity of the uterus during post partem life is not the result of a deficient hormone sensitivity but is correlated with the absence of a sufficient hormonal stimulus at this time. The investigation on the effects of actinomycin resulted in different reactions in the uterus and liver. In contrast to the liver a paradoxical actinomycin effect was found in the uterus after treatment with actinomycin alone. This effect is characterized by a small inhibition of RNA-synthesis and a 50% increase in protein synthesis. The treatment of the newborn test animals with actinomycin and 17β-oestradiol together abolished the oestrogen-induced stimulation of the uterine RNA-and protein-synthesis. Consequently, the effect of oestrogens during the neonatal period is also connected with the formation of new proteins via an increased DNA-directed RNA-synthesis.

Rotundic Acid Regulates the Effects of Let-7f-5p on Caco2 Cell Proliferation

2020 ◽  
Vol 20 ◽  
Author(s):  
Yuan Feng ◽  
Xinran Liu ◽  
Yueqing Han ◽  
Mantian Chen ◽  
Lin Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Colony Formation ◽  
Cancer Cell Line ◽  
Human Colon ◽  
Colon Cancer Cell Line ◽  
Inhibitory Effect ◽  
Human Colon Cancer ◽  
Caco2 Cell ◽  
Study Results ◽  
Rotundic Acid

Background & Objective: Nowadays, the interaction between natural products and microRNAs provides a promising field for exploring the chemo preventive agents for various cancers.As a member of microRNAs, the expression of let-7f-5p is universally down regulated in colorectal cancer (CRC). The present study aimed to uncover the function of let-7f-5p in the proliferation of human colon cancer cell line Caco2 and explored chemo preventive agents from natural resources that can prevent the development of CRC. Methods: Herein, Caco2 cells were transfected with let-7f-5p mimic and inhibitor to manipulate let-7f-5p levels, and the expression of let-7f-5p wasper formed by RT‑qPCR. Next, we determined how let-7f-5p regulates Caco2 cell proliferation by using MTT, wound-healing, cell cycle,and colony formation assays.Besides, to further understand the effect of let-7f-5p, we evaluated the protein level of AMER3 and SLC9A9 by using western blotting assays. Results: The results showed a suppressive function of let-7f-5p on Caco2 cell proliferation and then put forward a triterpenoid (rotundic acid, RA) which significant antagonized the effect of cell proliferation, restitution after wounding,and colony formation caused by let-7f-5p. Moreover, the western blot results further indicated that the inhibitory effect of RA might be due to its suppressive role in let-7f-5p-targeted AMER3 and SLC9A9 regulation. Conclusion: Our validation study results confirmed that let-7f-5p was a potent tumor suppressor gene of Caco2 cell proliferation,and RA showed as a regulator of the effect oflet-7f-5p on cell proliferation and then could be a potential chemo preventive agent for CRC treatment.

Lipopolysaccharide-induced sensitization of adenylyl cyclase activity in murine macrophages

2006 ◽  
Vol 290 (1) ◽  
pp. C143-C151 ◽  
Author(s):  
Y. Osawa ◽  
H. T. Lee ◽  
C. A. Hirshman ◽  
D. Xu ◽  
C. W. Emala
Keyword(s):  
Protein Synthesis ◽  
Adenylyl Cyclase ◽  
Actinomycin D ◽  
Inhibitory Effect ◽  
Cytokine Release ◽  
Adenylyl Cyclase Activity ◽  
Phosphorylation State ◽  
Murine Macrophages ◽  
Dependent Pathway ◽  
New Protein

LPS is known to modulate macrophage responses during sepsis, including cytokine release, phagocytosis, and proliferation. Although agents that elevate cAMP reverse LPS-induced macrophage functions, whether LPS itself modulates cAMP and whether LPS-induced decreases in proliferation are modulated via a cAMP-dependent pathway are not known. Murine macrophages (RAW264.7 cells) were treated with LPS in the presence or absence of inhibitors of prostaglandin signaling, protein kinases, CaM, Giproteins, and NF-κB translocation or transcription/translation. LPS effects on CaMKII phosphorylation and the expression of relevant adenylyl cyclase (AC) isoforms were measured. LPS caused a significant dose (5–10,000 ng/ml)- and time (1–8 h)-dependent increase in forskolin-stimulated AC activity that was abrogated by pretreatment with SN50 (an NF-κB inhibitor), actinomycin D, or cycloheximide, indicating that the effect is mediated via NF-κB-dependent transcription and new protein synthesis. Furthermore, LPS decreased the phosphorylation state of CaMKII, and pretreatment with a CaM antagonist attenuated the LPS-induced sensitization of AC. LPS, cAMP, or PKA activation each independently decreased macrophage proliferation. However, inhibition of NF-κB had no effect on LPS-induced decreased proliferation, indicating that LPS-induced decreased macrophage proliferation can proceed via PKA-independent signaling pathways. Taken together, these findings indicate that LPS induces sensitization of AC activity by augmenting the stimulatory effect of CaM and attenuating the inhibitory effect of CaMKII on isoforms of AC that are CaMK sensitive.

METABOLISM OF LEPTOSPIRES: II. THE ACTION OF 8-AZAGUANINE

1967 ◽  
Vol 13 (12) ◽  
pp. 1621-1629 ◽  
Author(s):  
Russell C. Johnson ◽  
Palmer Rogers
Keyword(s):  
Nucleic Acids ◽  
Ribonucleic Acid ◽  
Rna Synthesis ◽  
Inhibitory Effect ◽  
Relative Increase ◽  
Purine Biosynthesis ◽  
Low Concentrations

Both the pathogen Leptospira pomona and the saprophyte L. biflexa Patoc I can convert exogenous adenine, guanine, and 8-azaguanine to the corresponding nucleotide and incorporate them into nucleic acids. L. pomona is inhibited by low concentrations of 8-azaguanine (50 μg/ml) and this inhibition is associated with less than a 5% replacement of the ribonucleic acid (RNA) guanine residues by the analogue. Guanine possessed the highest activity for antagonizing the inhibitory effect of 8-azaguanine. The biosynthetic process of L. pomona most affected by the analogue was a relative increase in RNA synthesis. The analogue-resistant L. biflexa incorporated 1/10 as much 8-azaguanine as L. pomona. The higher rate of purine biosynthesis, in addition to the lesser amount of 8-azaguanine incorporated, may account for the analogue resistance of L. biflexa.

scholarly journals Immunoregulation of B lymphocyte colony formation by T cell subsets in patients with chronic lymphocytic leukemia

Blood ◽  
1986 ◽  
Vol 67 (2) ◽  
pp. 294-298
Author(s):  
LA Fernandez ◽  
JM MacSween ◽  
GR Langley
Keyword(s):  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Colony Formation ◽  
B Lymphocyte ◽  
Normal Subjects ◽  
Colony Growth ◽  
Lymphocytic Leukemia ◽  
T Cell Subsets ◽  
Cell Colony

Normal B lymphocytes are activated, proliferate, and then differentiate into plasma cells and secrete immunoglobulin (Ig). We have reported that chronic lymphocytic leukemia (CLL) T4 cells help and CLL T8 cells lack suppressor effects on Ig synthesis by normal B cells (Blood 62:767, 1983). We have now explored the earlier phase, proliferation, using B cell colony formation; in semisolid media. B lymphocyte colonies from normal individuals and from patients with CLL were grown in 0.3% agarose overlayed with T cells or T cell subsets and the B cell mitogen staphylococcal protein A. Enriched T cells, OKT4 or OKT8, were obtained either by sheep erythrocyte rosettes or depletion of OKT8 or OKT4 cells by monoclonal antibody or complement, respectively. Twenty thousand B cells from normal subjects yielded 65 +/- 9, 64 +/- 7, and 19 +/- 6 colonies with autologous unfractionated T-, OKT4-, or OKT8- positive cells, respectively. This compared to 29 +/- 11, 81 +/- 11, and 15 +/- 4 colonies from patients with CLL with added autologous unfractionated T-, OKT4-, or OKT8-positive cells. To determine whether the fewer number of colonies in both normal subjects and patients with CLL with OKT8-positive cells was due to suppression or lack of help, the number of OKT4-positive cells was held constant, and OKT8-positive cells were added in increasing numbers. No suppression of colony formation could be demonstrated. Furthermore, the addition of increasing numbers of concanavalin A (Con A)-activated OKT8-positive cells did not suppress colony formation. These results suggest that the CLL T cell subsets behave in a functionally similar manner to normal T cell subsets, namely, (1) that normal and CLL B cell colony growth is helped by OKT4 cells; and (2) in contrast to immunoglobulin secretion by B cells, neither normal nor CLL OKT8 cells, unstimulated or activated by Con A, suppress B cell colony growth.

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