scholarly journals The effects of galactosamine on UTP levels in the livers of young, adult and old rats.

2000 ◽  
Vol 47 (2) ◽  
pp. 349-353 ◽  
Author(s):  
Z Kmieć ◽  
R T Smoleński ◽  
M Zych ◽  
A Myśliwski

Galactosamine (GalN), a well-known hepatotoxin that depletes the cellular pool of uracil nucleotides, was previously shown to have greater impact on the inhibition of protein synthesis in hepatocytes of old rats as compared with young animals (Kmieć 1994, Ann. N.Y. Ac. Sci. 717, 216-225). In the present study we compared the effects of GalN on the nucleotide content (measured by ion-exchange HPLC) in the livers of young (4 months), adult (12 months), and old (24-26 months old) rats two hours after its intraperitoneal administration. UTP content of the livers of old control rats was significantly lower (by 28%) than that of young animals. GalN administration decreased the UTP content in the livers of young, adult and old rats by, respectively, 55%, 65% and 89%, and increased the content of UDP-sugars by 189%, 175% and 305%. The hepatic content of ATP, ADP, AMP, NAD, GTP except CTP did not differ significantly among the age groups of rats studied, and was not changed by GalN treatment. The content of CTP was significantly higher in old rats (P < 0.03) upon GalN treatment. The lower hepatic content of UTP may partially explain the increased sensitivity of hepatocytes and livers of old rats to the action of galactosamine, and possibly to other hepatotoxic compounds that decrease transcription in the liver.

1980 ◽  
Vol 41 (1) ◽  
pp. 273-289
Author(s):  
B. Ashour ◽  
M. Tribe ◽  
P. Whittaker

The effects of cycloheximide, chloramphenicol and ethidium bromide on the blowfly Calliphora erythrocephala were studied. In the first set of experiments, toxic levels were determined by examining activity and mortality of flies after injection of various doses of each drug. In the second set of experiments, the effect of drug treatment on flight muscle mitochondrial protein synthesis was determined in relation to age by following the incorporation of radioactively labelled amino acid, [3H]leucine, into mitochondrial protein in vivo. To confirm the developmental changes in flight muscle mitochondria, mitochondrial protein content per fly was estimated from emergence to 30 days of age; the highest protein level was recorded between 6 and 10 days of age. Maximum incorporation of labelled amino acid was found in newly emerged flies, and this age group was also the most sensitive to drug treatment. By the time flies had reached 6–10 days of age, amino acid incorporation had declined to about two-thirds of the rate obtained with newly emerged flies. With 6–10-day old flies, however, the highest value for flight muscle mitochondrial protein per fly was recorded, and these flies also displayed the greatest resistance to drug treatment of any age group investigated. For example, inhibition of protein synthesis following injection of 300 micrograms/fly of chloramphenicol was only about 15% below the untreated control in 6–10-day-old flies, whereas in all other age groups investigated, inhibition ranged between 30 and 50% of the controls. At 15–20 days of age, protein synthesis decreased to a third of the newly emerged flies' rate and continued to decrease further in the 30–35-day-old group, where it was less than one sixth of the youngest age group. The effect of drug treatment on these older flies was also less than that observed with newly emerged flies, especially after chloramphenicol and ethidium bromide injections. The effect of cycloheximide however, was much the same in all age groups, with inhibition of protein synthesis being 80–90% of controls. Surprisingly, cycloheximide (1–10 micrograms/fly) had little initial effect on mortality of young flies, despite almost complete blockage in the synthesis of mitochondrial proteins at these concentrations. 95% mortality occurred only when doses of 20 micrograms/fly were given. In contrast, high doses of chloramphenicol (400 micrograms/fly) and ethidium bromide (15 micrograms/fly) caused almost total mortality a few hours after injection, although such doses never induced more than about 50% inhibition of mitochondrial protein synthesis. Each drug therefore has a different site of inhibition and induces different mortality effects. Possible explanations for these differences in mortality are discussed.


1999 ◽  
Vol 277 (4) ◽  
pp. E608-E616 ◽  
Author(s):  
L. Mosoni ◽  
T. Malmezat ◽  
M. C. Valluy ◽  
M. L. Houlier ◽  
D. Attaix ◽  
...  

Sarcopenia could result from the inability of an older individual to recover muscle lost during catabolic periods. To test this hypothesis, we compared the capacity of 5-day-refed 12- and 24-mo-old rats to recover muscle mass lost after 10 days without food. We measured gastrocnemius and liver protein synthesis with the flooding-dose method and also measured nitrogen balance, 3-methylhistidine excretion, and the gene expression of components of proteolytic pathways in muscle comparing fed, starved, and refed rats at each age. We show that 24-mo-old rats had an altered capacity to recover muscle proteins. Muscle protein synthesis, inhibited during starvation, returned to control values during refeeding in both age groups. The lower recovery in 24-mo-old rats was related to a lack of inhibition of muscle proteolysis during refeeding. The level of gene expression of components of the proteolytic pathways did not account for the variations in muscle proteolysis at both ages. In conclusion, this study highlights the role of muscle proteolysis in the lower recovery of muscle protein mass lost during catabolic periods.


1970 ◽  
Vol 118 (4) ◽  
pp. 659-666 ◽  
Author(s):  
G. Turnock

A mutant of Escherichia coli with increased sensitivity to streptomycin has been studied. This strain differed from a normal strs strain in that streptomycin produced inhibition of protein synthesis and loss of viability with almost no lag period. Chloramphenicol protected a normal strs strain but not the mutant against the bactericidal action of streptomycin. The results obtained support the idea that access of streptomycin to its site of action in a normal cell is restricted, and that this restriction, which is much less effective in the mutant, probably involves a permeability barrier. Comparison of the inhibition of protein synthesis by streptomycin with concomitant changes in the distribution of polyribosomes in both strains suggested that the antibiotic can directly inhibit the translation of mRNA.


1957 ◽  
Vol 35 (1) ◽  
pp. 759-766 ◽  
Author(s):  
W. F. Perry ◽  
Helen F. Bowen

The effect of growth hormone on the in vitro incorporation of C14 acetate into fatty acids, carbon dioxide, and cholesterol by liver and adipose tissue from young, adult, and old rats was studied.In all three age groups of animals, growth hormone was found to depress the incorporation of acetate into fatty acids by liver slices but the CO2 production was unaffected. In both young and old animals growth hormone did not significantly alter the incorporation of acetate into fatty acids and CO2 by preparations of adipose tissue, but did result in a decline in the fat content of the adipose tissue. It was noted that the CO2 production from acetate was much less with adipose tissue from old rats than with similar preparations from young rats.Incorporation of acetate into cholesterol was unaffected by growth hormone in young and old animals but was significantly increased in liver slices from adult animals.


1957 ◽  
Vol 35 (9) ◽  
pp. 759-766 ◽  
Author(s):  
W. F. Perry ◽  
Helen F. Bowen

The effect of growth hormone on the in vitro incorporation of C14 acetate into fatty acids, carbon dioxide, and cholesterol by liver and adipose tissue from young, adult, and old rats was studied.In all three age groups of animals, growth hormone was found to depress the incorporation of acetate into fatty acids by liver slices but the CO2 production was unaffected. In both young and old animals growth hormone did not significantly alter the incorporation of acetate into fatty acids and CO2 by preparations of adipose tissue, but did result in a decline in the fat content of the adipose tissue. It was noted that the CO2 production from acetate was much less with adipose tissue from old rats than with similar preparations from young rats.Incorporation of acetate into cholesterol was unaffected by growth hormone in young and old animals but was significantly increased in liver slices from adult animals.


1975 ◽  
Vol 229 (2) ◽  
pp. 512-517 ◽  
Author(s):  
I Gil-Ad ◽  
G Udeschini ◽  
D Cocchi ◽  
EE Muller

2-Deoxy-D-glucose (2-DG), a glucose analogue, blocks glycolysis and induces intracellular glucoprivation. In the adult rat intraperitoneal administration of 2-DG or its injection into the lateral ventricle (IVT) of the brain induces hyperglycemia which is divorced from a rise in plasma insulin (IRI). In the present study, responsiveness to 2-DG-induced glucoprivation, after central or intraperitoneal injection of the drug, was studied in rats of 7, 14, 21, and 28 days of age and compared to that of the adult rat (50 days old). In 7-, 14-, 21-, and 28-day-old rats, the overall blood glucose (BG) response to IVT-injected 2-DG was equivalent to 4, 3.3, 17, and 33%, respectively, of the BG response present in the adult rat. Following intraperitoneal injection of 2-DG , the BG response evoked in the same age groups corresponded to 27, 31, 41, and 93%, respectively, of the adult response. Base-line plasma IRI levels were significantly lower in pups than in adults and increased progressively with age, but no difference was present in IRI levels between 2-DG-treated and control pups whether the 2-DG was given via the laterl ventricle or intraperitoneally. These results demonstrate the presence in the infant rat of clear-cut hyporesponsiveness to 2-DG-induced glucoprivation. The different response pattern between experiments involving central and peripheral 2-DG administration supports the existence of separate peripheral glucoreceptors for 2-DG and their earlier ontogenic activation. Since the infant mammal glucose is of minor relevance as an energy substrate, an interrelationship appears to be present between requirements for fuel(s) and homeostatic response to fuel deprivation.


1990 ◽  
Vol 258 (1) ◽  
pp. H207-H211 ◽  
Author(s):  
R. B. Biggs ◽  
F. W. Booth

The purpose of these experiments was to determine whether mixed protein synthesis rates in hearts of Fischer 344 rats were decreased from maturity to senescence. When compared with 12-mo-old rat hearts, hearts from 23- to 25-mo-old rats had 13% lower concentrations of noncollagen protein, 9% less non-collagen protein per heart, 10% higher ratio of heart wet weight-to-body weight, and no difference in the basal rate of mixed protein synthesis, when expressed as fractional rate per day. Despite the 9% decrease in total noncollagen protein in 23- to 25-mo-old rat hearts, the derived value for milligrams protein synthesized per day was not different between age groups. When triiodothyronine was given for 3 days to mature and senescent rats, fractional rates of mixed protein synthesis were increased by similar percents (57–70%) in hearts from these two age groups. Basal and triiodothyronine-stimulated RNA concentrations in hearts of 12-mo-old and 23- to 25-mo-old rats were not different. These observations showed no decrease in either the basal or the maximal thyroid-stimulated rates of mixed protein synthesis in the hearts between mature and senescent rats. Thus an aging-programmed downregulation of mixed protein synthesis rates within cardiac muscle did not occur in the senescent Fischer 344 rat heart in this study.


Sign in / Sign up

Export Citation Format

Share Document