Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ETHIONINE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1980

Poly(A) polymerase activity in ethionine-intoxicated rats: the relative effectiveness of disaggregated and intact polyribosomes as primers for poly(A) polymerase.

Ethionine intoxication causes a change in the metabolism of poly(A) sequences on the 3' OH terminus of mRNA in rat liver in vivo. In an attempt to determine the factors responsible for these changes, nuclear and cytoplasmic poly(A) polymerase activities and the state of the primer were examined in vitro. Requirements for optimal enzyme activities were determined. The nuclear and cytoplasmic enzymes had different K+, Mn2+, and poly(A) primer optima. The levels of nuclear and cytoplasmic poly(A) polymerase activity were shown to decrease following ethionine intoxication. Poly(A)+ RNA isolated from the livers of saline- and ethionine-treated rats served equally well as primers for the cytoplasmic poly(A) polymerase. Disaggregated polysomes were seven times more effective as primers than were intact polysomes. The results suggest that the mRNP particle which is released from polysomes as a result of ethionine intoxication functions better as a poly(A) polymerase primer than does the intact polysome.

Animals↗
PubMed1976

The effect of egg phospholipid administration upon liver enzymic activities during ethionine treatment.

Female rats were injected subcutaneously with ethionine, and enzymic activities of liver membranes (Na+-k+-stimulated ATPase, Mg2+-stimulated ATPase, glucose-6-phosphatase, NADPH: cytochrome c oxido-reductase and NAD-nucleosidase) examined at proper intervals, during the intraperitoneal treatment of an egg phospholipid preparation (EPL). It is shown that EPL is unable to overcome the enzymic changes due to severe ethionine treatment, but is able to facilitate the recovery times after drug withdrawal for all the enzymic activities, except for NAD-nucleosidase. At lower dosage of the drug, the ethionine treatment is able to prevent the observed change of the glucose-6-phosphatase activity but not that of the Mg2+-ATPase. It is suggested that the EPL treatment may modify the chemical composition ahd/or architecture of liver membranes, altered by the ethionine injection, thus acting, at least partially, on the enzymic changes.

Adenosine Triphosphatases↗
PubMed1977

Ethionine and the phosphorylation of ribosomal protein S6.

Ribosome phosphorylation was studied by monitoring the phosphorylation state of small subunit protein S6 as visualized on two-dimensional electrophoretograms of ribosomal proteins isolated from rat liver. No phosphorylation of S6 was observed under conditions of ethionine-induced inhibition of protein synthesis. Moderate phosphorylation, detected as the appearance of S6 and four or five phosphorylated derivatives, was observed in saline-treated animals. Reversal of ethionine-induced inhibition of protein synthesis by treatment with adenine led to extensive phosphorylation of S6. A model for protein synthesis which includes requisite phosphorylation of ribosomes during initiation is proposed. Cyclic adenosine 3':5'-monophosphate concentration was significantly elevated in liver of both ethionine- and ethionine plus adenine-treated rats, relative to that of saline-treated animals.

Adenine↗
PubMed1990

Effects of ATP depletion with DL-ethionine on biliary excretion of indocyanine green in the rat.

To clarify the energy-dependency of biliary excretion of a diagnostic dye, the effect of ATP depletion on biliary excretion was investigated. Biliary excretion of indocyanine green (ICG) in rat liver reached a maximum 20 min after intravenous application. The level of ATP in the liver was lowered to 35.4% of the control value about 5 h after administration of DL-ethionine (100 mg/100 g body weight). The rate of bile flow and the amount of ICG excreted in initial 10 min into the bile of ethionine-treated rats were lowered to 67.5% and 61.3% of the control values, respectively. The amount of ICG excreted for 10 min from 30 min to 40 min after application of ICG in ethionine-treated rats was comparable to that of the control. The level of ICG in blood 5 min after application of ICG was raised by 59.2% of the control value. These results suggest that ATP depletion in the liver caused by treatment with ethionine suppresses the initial rate of uptake and biliary excretion of ICG.

Adenosine Triphosphate↗
PubMed1973

Effect of ethionine on carbohydrate and lipid metabolism.

In ethionine-treated rats, the ATP content of adipose tissue was not decreased whereas in liver it was drastically reduced to about one-fifth of the control level. Shortly after the injection of ethionine, hepatic glycogen was depleted and the blood glucose concentration fell from 120 to 80 mg/100 ml. This was followed by a two- to threefold elevation of the plasma fatty acid level. Hepatic glucose-6-phosphate was decreased and was not elevated by administration of 2 mmoles of glucose unless ATP was partially restored to normal levels. When hepatic ATP was decreased, the disappearance of [(14)C]glucose from the blood and its incorporation into glycogen and glyceride-glycerol and the incorporation of [3-(14)C]pyruvate into glyceride-glycerol were reduced. 6 hr after ethionine injection the plasma triglyceride level fell but there was no significant change in the liver triglyceride concentration, but by 24 hr it had increased markedly. Lipogenesis in adipose tissue was depressed in vivo, possibly due to decreased glycerol-3-phosphate concentrations. A marked decrease of glycerol-3-phosphate in both liver and adipose tissue was noted. Administration of glucose effectively depressed plasma free fatty acid concentration and elevated the glycerol-3-phosphate levels. Ethionine injection to fasted animals further depressed the blood glucose and elevated the plasma free fatty acid level.

Adenosine Triphosphate↗
PubMed1971

Studies on acute methionine toxicity. I. Nucleolar disaggregation in guinea pig hepatic cells with methionine or ethionine and its reversal with adenine.

The effects of methionine and ethionine on the fine structure of hepatic cell nucleoli of guinea pigs and rats were investigated. A single intraperitoneal injection of methionine into guinea pigs results in the disruption of nucleolonema as early as 2 hours after the injection. By 4 hours, nucleoli show complete fragmentation consisting of many small fragments and small remnants of nucleoli. Large aggregates of interchromatinic granules and condensation of chromatin appear in the nucleoplasm. These changes are remarkably similar to the lesions induced by ethionine in the liver of the rat or the guinea pig. The methionine-induced nuclear and nucleolar lesions persist up to 10 hours after the injection. The administration of adenine 4 hours after the methionine injection reverses the nucleolar lesions by 8 hours. The appearance of incompletely reconstructed nucleoli with twisted ropelike structures suggests a pattern of recovery very similar to the adenine-induced nucleolar reformation in ethionine-treated rats. Injecting methionine into rats induced no nucleolar abnormalities. It is suggested that the mechanism of nucleolar fragmentation induced by methionine or ethionine is related to the accumulation of S-adenosyl compounds with concomitant ATP deficiency in the liver.

Adenine↗
PubMed1981

The effect of prostaglandin E2 on ethionine-induced pancreatitis in the rat.

Prostaglandins have been reported to exert a protective effect against short-term experimental pancreatic injury. We evaluated the protective effect of PGE2 using a model designed to maintain pancreatitis over a period of 5-10 days. Acute pancreatitis was induced by daily intraperitoneal injections of DL-ethionine in rats maintained on a protein-free diet. Test periods of 10 and 5 days (parts I and II, respectively) were employed. In parts I and II, PGE2 0.1 microgram/g body wt was given subcutaneously 30 min before ethionine. In part II, a second daily dose of PGE2 0.1 microgram/g body wt was given 7 h after ethionine. PGE2 did not protect against the weight loss, decrease in food consumption, alteration in serum amylase, pancreatic necrosis, or mortality induced by ethionine. This study indicates that the protective effect of PGE2 observed in short-term experimental pancreatitis is not reproducible in a model in which pancreatitis is maintained for 5 and 10 day periods.

Amylases↗
PubMed1981

Blocking by the carcinogen, L-ethionine, of SOS functions in a tif-1 mutant of Escherichia coli B/r.

In Escherichia coli, DNA damage by carcinogenic agents results in the coordinate expression of a diversity of functions (SOS functions), many of which are thermally inducible without any damage to DNA in a tif-1 mutant. These include prophage induction, filamentous growth, and an error-prone DNA repair activity, which is responsible for ultraviolet-induced mutagenesis. Ethionine causes hepatic carcinoma in rats after prolonged feeding but is not a mutagen in the Ames test. The present study shows that 10 mM ethionine prevents the thermal induction of lambda-prophage in a tif-1 derivative of E. coli. The enhancement of mutation, which normally occurs at high temperature after a low dose of ultraviolet light, is also blocked by ethionine. Ethionine does not block, to any appreciable extent, the incorporation of radioactive precursors into RNA, DNA, or protein.

DNA↗
PubMed1983

Comparison of the effects of basal and methionine-supplemented recovery diets on the liver of ethionine-pretreated rats.

Alterations in the liver of rats during ethionine administration and subsequent recovery on basal or methionine-supplemented diets were examined by light and electron microscopy and by the point counting technique. After administration of 1% DL-ethionine diet for 34 days, adult female rats showed a significant decrease (P less than 0.01) in the percentage volume of hepatocytes and a significant increase (P less than 0.002) in the percentage volume of duct cells compared with control animals. When the carcinogen diet was replaced by either basal or methionine-supplemented diet, the percentage volumes of proliferated duct cells fell. The hepatocytes appeared almost normal in the rats on basal recovery diet, whereas those on methionine diet showed extensive fat accumulation in the central hepatocytes. Similar lipid deposition was observed in rats given either methionine plus ethionine diet or basal diet followed by methionine diet as a recovery diet. The percentage volumes of hepatocytes and duct cells in rats transferred to basal recovery diet did not differ significantly from those placed on methionine diet or on methionine plus ethionine diet. Some possible causes of methionine-induced fat deposition are discussed.

Animals↗
PubMed1984

Effect of ethionine on dolichyl phosphate-dependent transglycosylation reactions in rat liver.

Dolichyl phosphates of different chain length (C35, C55 , C75 , Dol-mixture of C90 , 95, 100, 105 and C110 ) were tested as lipid acceptors in transglycosylation reactions. In the absence of exogenously added dolichyl phosphates there were no differences in the rate of synthesis in liver of dolichyl phosphate mannose, dolichyl phosphate glucose and dolichyl pyrophosphate N-acetylglucosamine between normal and ethionine-treated animals. Addition of exogenous dolichyl phosphates of different chain length stimulated the synthesis of dolichyl phosphate mannose and dolichyl pyrophosphate N-acetyl-glucosamine 2 to 4 times depending on the chain length of dolichols , both in normal and ethionine-treated animals. In liver of ethionine-treated rats the formation of dolichyl phosphate glucose was not stimulated. Following ethionine treatment the concentration of free and esterified with fatty acids dolichols was increased.

Animals↗
PubMed1983

Ethionine-dependent inhibition of acute-phase plasma protein synthesis in the rat.

Ethionine administered intraperitoneally to rats suffering from turpentine-induced inflammation preferentially reduced incorporation of 14C-leucine into fibrinogen, haptoglobin and other acute-phase proteins. The inhibitory effect was observed both in vivo and in liver slices obtained from ethionine-treated donors, while addition of ethionine to liver slices in vitro led to general reduction of synthesis of all liver and plasma proteins, including albumin. For comparison, the effects of galactosamine and actinomycin D on plasma protein synthesis in injured rats were also examined. It has been concluded that ethionine acts in the early phases of the acute-phase response, probably by inhibition of trauma-induced transcription of liver mRNA specific for acute-phase proteins.

Animals↗
PubMed1978

Inhibition of ethionine pancreatitis in the rabbit by DL-BETA-3 thienylalanine pretreatment.

Beta-3 thienylalanine, an inhibitor of zymogen formation, was studied in the experimental model of ethionine pancreatitis in the rabbit. Beta-3TA pretreated and nonpretreated rabbits were given ethionine for six days and controls were given chow only. Animals were killed and serum amylase values determined. Pancreatic tissue was studied by light and electron microscopy. Beta-3TA pretreated rabbits on ethionine showed normal amylase values, while those receiving only ethionine showed high values. Microscopic examination showed severe pancreatitis in the nonpretreated group but only mild vacuolization of cells in the Beta-3TA pretreated animals. Electron microscopy demonstrated integrity of rough endoplasmic reticulum in pretreated animals and severe distortion of cytoplasmic organelles in nonpretreated animals.

Alanine↗
PubMed1979

Stability of messenger ribonucleic acid of free and membrane-bound polyribosomes of the livers of rats treated with ethionine.

Administration of ethionine to female rats results in disaggregation of free and membrane-bound polyribosomes and inhibition of protein synthesis in the liver. The administration of adenine and methionine to ethionine-treated rats reverses these effects, even after actinomycin D treatment which inhibits new RNA synthesis. The membrane-bound polyribosomes show greater recovery of the state of aggregation and of in vitro protein synthesis than do the free polyribosomes of rat liver. The messenger RNA (mRNA) in the recovering membrane-bound polyribosomes appears to come from endoplasmic reticulum membranes and is not related to increased nucleocytoplasmic translocation of existing mRNA. Initiation factors-dependent stimulation of polyphenylalanine synthesis by ribosomes and by initiation factors of membrane-bound polyribosomes is increased more than the synthesis by ribosomes and by initiation factors of free polyribosomes in the livers of ethionine-treated rats receiving actinomycin D and adenine plus methionine. Our results suggest that stable mRNA associated with membranes remains in the rat liver after injury by ethionine, and during recovery induced by adenine and methionine, the mRNA is utilized to reform membrane-bound polyribosomes.

Adenine↗
PubMed1976

Enhancement of pancreatic tumorigenesis of 4-hydroxyaminoquinoline 1-oxide by ethionine in rats.

The effect of ethionine on pancreatic tumorigenesis of 4-hydroxyaminoquinoline 1-oxide (4-HAQO) in rats was studied. The high incidence of hyperplastic nodules developed in the exocrine pancreas of animals receiving a single injection of 4-HAQO only or protein-deficient diet containing 0.5% ethionine for 4 days followed by 4-HAQO. The incidence of adenoma was higher than that of hyperplastic nodules and well-differentiated adenocarcinoma developed in 1 out of 12 animals receiving protein-deficient diet containing ethionine for 18 days followed by 4-HAQO. No tumor was found in the pancreas of animals that received 0.005N HCl without 4-HAQO. These results suggest that the pancreatic tumorigenesis of 4-HAQO is enhanced by ethionine.

4-Hydroxyaminoquinoline-1-oxide↗
PubMed1993

Liver carcinogenesis associated with feeding of ethionine in a choline-free diet: evidence against a role of oval cells in the emergence of hepatocellular carcinoma.

In an attempt to clarify the role of oval cells in the emergence of hepatocellular carcinoma, we fed rats a choline-free diet containing 0%, 0.05% or 0.1% ethionine. The incidence and nature of premalignant and malignant hepatic lesions were then related to the degree of oval cell proliferation. Intake of choline-free diet alone for up to 12 mo was associated with minimal oval cell proliferation; cholangiofibrosis, hepatocellular nodules and hepatocellular carcinoma were observed in 55%, 23% and 14% of the animals, respectively. When rats were given the choline-free diet with 0.05% ethionine, proliferation of oval cells was more pronounced; after a 6- to 12 mo feeding period, cholangiofibrosis (57%) was again observed. However, hepatocellular nodules (91%) and hepatocellular carcinoma (74%) were the most common lesions seen with this feeding regimen. Finally, rats fed the choline-free diet with 0.1% ethionine had massive oval cell proliferation and progressive loss of parenchymal liver tissue. Most of these animals died before they had consumed the choline-free diet with 0.1% ethionine for 12 mo. Rats in this group (96%) exhibited large and numerous cholangiofibrotic lesions, but hepatocellular nodules and carcinoma were not detected. In all animals of each experimental group, hyperplastic bile duct cells in areas of cholangiofibrosis and oval cells were positive for cytokeratin 19, an intermediate filament protein present only in bile duct cells in normal liver. Hepatocellular nodules and hepatocellular carcinoma were invariably negative for cytokeratin 19. We interpret these findings to suggest that oval cells are not involved in the histogenesis of hepatocellular carcinoma.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1974

Control of Free Methionine Production in Wild Type and Ethionine-resistant Mutants of Chlorella sorokiniana.

Mutants of Chlorella sorokiniana selected for resistance to the methionine analogue ethionine took up ethionine at the same rate as did the wild type strain. Cells of two ethionine-resistant mutants produced severalfold higher levels of free methionine and cysteine than did wild type cells.Exogenous methionine had no apparent effect on free methionine production in a mutant that produces excessive levels of free methionine. Under the same conditions, production of free methionine was relatively inhibited in wild type cells and in a mutant that produces wild type levels of free methionine.The results suggest that free methionine production in the wild type strain is subject to endproduct control, and that this control is lacking in one class of ethionine-resistant mutants.

Journal Article↗
PubMed1990

The serum activities of AP, gamma-GT, GlDH and GPT after bile duct obstruction and ethionine in the rat.

The increase of activity of the enzymes AP, Gamma-GT, GlDH and GPT was investigated in this study with regard to its pathomechanism. The increase of AP is known to be caused by a de novo-protein synthesis in the liver, as several investigators have demonstrated using protein synthesis inhibitors. In this study female Wistar rats were partly sham-operated, partly bile duct-obstructed. One half of each group received the protein synthesis inhibitor ethionine, 24 h after bile duct obstruction in the group with ethionine the following enzyme activities were measured in the serum: AP 216 +/- 80 U/l; gamma-GT 4.5 +/- 1.9 U/l; GlDH 85 +/- 26 U/l; GPT 375 +/- 163 U/l. In the group without ethionine the activities were: AP 459 +/- 69 U/l; gamma-GT 4 +/- 0.9 U/l; GlDH 120 +/- 81 U/l; GPT 417 +/- 191 U/l. Because the differences between the groups with and without ethionine were not significant with the exception of AP, it is concluded that in the early phase of bile duct obstruction up to 24 h no influence of de novo-protein synthesis can be demonstrated in the elevation of the activities of gamma-GT, GlDH and GPT.

Alanine Transaminase↗
PubMed1962

Enzyme distribution in the rat fetus and palcenta following the adminstration of ethionine.

Enzyme changes which accompany ethionine-induced resorption of the rat conceptus have been studied by both histochemical and biochemical techniques. Pregnant rats were injected with ethionine over a 3-day period prior to autopsy on day 12 of pregnancy. Sections of the whole conceptus were studied for acid phosphatase with both the Burstone and Gomori methods and for succinoxidase activity with nitro-BT. Biochemical determinations of cathepsins, acid phosphatase, and succinoxidase were performed on homogenates of the fetuses, placentae, and deciduas basalis from ethionine-treated and saline-treated rats. The histochemical study has shown that resorption is accompanied by an increase in the size and number of acid phosphatase granules in the decidual tissues and a concurrent loss of acid phosphatase granules in the fetal tissues. Biochemical methodology indicated that there was no increase in total cathepsin or acid phosphatase activities in the resorbing tissues. No change in succinoxidase activity was found with either histochemical or biochemical techniques. The significance of these results was discussed with reference to the lysosome hypothesis.

Acid Phosphatase↗