scholarly journals Effect of tannic acid on the synthesis of protein and nucleic acid by rat liver

1969 ◽  
Vol 113 (2) ◽  
pp. 307-313 ◽  
Author(s):  
A. A.-B. Badawy ◽  
Audrey E. White ◽  
G. H. Lathe

1. As early as 1hr. after the intraperitoneal administration of tannic acid to rats, it could be demonstrated in the liver. At 3hr. the nuclear fraction contained the largest amount of tannic acid. 2. Nuclear RNA synthesis was inhibited in vivo 2hr. after the administration of tannic acid. Induction by cortisol of tryptophan pyrrolase was 90% inhibited at 24hr. 3. Incorporation of [1−14C]leucine into protein by liver slices from treated rats was decreased by 50% after 24hr. Its incorporation into postmitochondrial supernatant from treated animals was not inhibited. Incorporation into slices and postmitochondrial supernatants were inhibited in vitro by tannic acid. 4. The sequence of events: concentration of tannic acid in nuclei, inhibition of nuclear RNA synthesis, inhibition of protein synthesis and production of necrosis, is discussed.

1972 ◽  
Vol 238 (84) ◽  
pp. 161-164 ◽  
Author(s):  
J. R. TATA ◽  
MARY JO HAMILTON ◽  
D. SHIELDS

1992 ◽  
Vol 1 (3) ◽  
pp. 37-56 ◽  
Author(s):  
Leonard Friedman ◽  
John Scalera ◽  
James E. Keys ◽  
Edmund L. Peters ◽  
Dennis W. Gaines ◽  
...  

The effects of 2-chioroethanol (2-CE) on rat tissue following in vitro and in vivo exposure were studied. At concentrations as low as 2.5 mg/ml, protein synthesis in liver slices was inhibited; at concentrations of 25 mg/ml and above, RNA synthesis and respiration were also impaired. Single oral doses of 2-CE to young adult rats at levels of 15-40 mg/kg body weight depressed liver nonprotein sulfhydryl (GSH) concentration and liver protein but not RNA synthesis. Liver lipid was increased by 7 hr after a single oral dose of 30 mg/kg. The time courses and dose-response relationship for GSH depletion and restoration and for protein synthesis inhibition and recovery were similar. The livers of female rats were more sensitive than the livers of male rats to the effects of 2-CE. Protein synthesis was also depressed in kidneys of 2-CE-treated male rats but at higher doses than those needed for this effect to occur in livers of the same animals. Liver polysome disaggregation also occurred after oral 2-CE doses of 20 mg/kg and greater. The effects of 2-CE on ribosome profiles and protein synthesis were at least partially reversed by concurrent intraperitoneal administration of cysteine. The possible relationship of these findings to a role of GSH in protein synthesis is discussed.


1985 ◽  
Vol 1 ◽  
pp. S17
Author(s):  
Sakae Yamagami ◽  
Hiroshi Onishi ◽  
Kyosuke Ohno ◽  
Koichi Mori ◽  
Yukio Kawakita

1987 ◽  
Vol 65 (3) ◽  
pp. 188-194 ◽  
Author(s):  
E. Schmedt ◽  
L. Kleiman

The production of [Formula: see text] during Friend cell erythroid differentiation has been studied. In vitro measurements of total nuclear RNA synthesis in nuclei isolated from Friend cells at different stages of differentiation show the total RNA synthesis increases 1.5-fold at day 1 of induction and then decreases through days 2 and 3 to approximately 75% of its rate of synthesis in the nuclei of uninduced cells. The synthesis of RNA polymerase III transcripts undergoes a similar fluctuation through day 2 of induction, but increases again at day 3. The specific synthesis of [Formula: see text] was measured by hybridization of labelled nuclear RNA to a [Formula: see text] gene probe. During erythroid differentiation the percentage of nuclear RNA represented by [Formula: see text] remains constant (0.065%), so that the absolute synthesis of [Formula: see text] fluctuates during differentiation, in parallel with the fluctuations in the synthesis of total nuclear RNA. The relative synthesis of [Formula: see text]in vivo was studied by labelling cells with 35Pi, isolating the resulting radioactive tRNA – 5S RNA population, and hybridizing this population to a [Formula: see text] gene probe. The ratio of [Formula: see text] in newly synthesized cytoplasmic RNA remains similar throughout differentiation (averaging 0.0171), implying that the fluctuations observed in the nuclear synthesis of [Formula: see text] during differentiation probably also occur for the nuclear synthesis of most tRNA and 5S RNA species. Attempts were made to measure the relative steady-state concentration of [Formula: see text] using both aminoacylation and in vitro end labelling of tRNA followed by hybridization to a [Formula: see text] gene probe. These two methods gave different results and we discuss the possible pitfalls of using enzymatic methods for quantitating tRNA concentrations in the cell.


1966 ◽  
Vol 122 (3) ◽  
pp. 847-850 ◽  
Author(s):  
J. Drews ◽  
P. K. Bondy

1986 ◽  
Vol 13 (6) ◽  
pp. 333-342 ◽  
Author(s):  
Fu-Li Yu ◽  
Irmanely H. Geronimo ◽  
Wanda Bender ◽  
Robert J. Dowe

1965 ◽  
Vol 49 (3_Suppl) ◽  
pp. S160 ◽  
Author(s):  
E. Stöcker ◽  
G. Dhom

2019 ◽  
Vol 20 (10) ◽  
pp. 2500 ◽  
Author(s):  
Vrathasha Vrathasha ◽  
Hilary Weidner ◽  
Anja Nohe

Background: Osteoporosis is a degenerative skeletal disease with a limited number of treatment options. CK2.3, a novel peptide, may be a potential therapeutic. It induces osteogenesis and bone formation in vitro and in vivo by acting downstream of BMPRIA through releasing CK2 from the receptor. However, the detailed signaling pathways, the time frame of signaling, and genes activated remain largely unknown. Methods: Using a newly developed fluorescent CK2.3 analog, specific inhibitors for the BMP signaling pathways, Western blot, and RT-qPCR, we determined the mechanism of CK2.3 in C2C12 cells. We then confirmed the results in primary BMSCs. Results: Using these methods, we showed that CK2.3 stimulation activated OSX, ALP, and OCN. CK2.3 stimulation induced time dependent release of CK2β from BMPRIA and concurrently CK2.3 colocalized with CK2α. Furthermore, CK2.3 induced BMP signaling depends on ERK1/2 and Smad1/5/8 signaling pathways. Conclusion: CK2.3 is a novel peptide that drives osteogenesis, and we detailed the molecular sequence of events that are triggered from the stimulation of CK2.3 until the induction of mineralization. This knowledge can be applied in the development of future therapeutics for osteoporosis.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sachiko Iwai ◽  
Hanako O. Ikeda ◽  
Hisashi Mera ◽  
Kohei Nishitani ◽  
Motoo Saito ◽  
...  

AbstractCurrently there is no effective treatment available for osteoarthritis (OA). We have recently developed Kyoto University Substances (KUSs), ATPase inhibitors specific for valosin-containing protein (VCP), as a novel class of medicine for cellular protection. KUSs suppressed intracellular ATP depletion, endoplasmic reticulum (ER) stress, and cell death. In this study, we investigated the effects of KUS121 on chondrocyte cell death. In cultured chondrocytes differentiated from ATDC5 cells, KUS121 suppressed the decline in ATP levels and apoptotic cell death under stress conditions induced by TNFα. KUS121 ameliorated TNFα-induced reduction of gene expression in chondrocytes, such as Sox9 and Col2α. KUS121 also suppressed ER stress and cell death in chondrocytes under tunicamycin load. Furthermore, intraperitoneal administration of KUS121 in vivo suppressed chondrocyte loss and proteoglycan reduction in knee joints of a monosodium iodoacetate-induced OA rat model. Moreover, intra-articular administration of KUS121 more prominently reduced the apoptosis of the affected chondrocytes. These results demonstrate that KUS121 protects chondrocytes from stress-induced cell death in vitro and in vivo, and indicate that KUS121 is a promising novel therapeutic agent to prevent the progression of OA.


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