Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “STARVATION”

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 343 records · Page 19Linked to original sources
PubMed1981

Effect of supplemental dietary chromium or nicotinic acid on carbohydrate metabolism during basal, starvation, and refeeding periods in poults.

A series of experiments were conducted with turkey poults to ascertain the effects of supplemental chromium or excess of nicotinic acid on growth and carbohydrate metabolism. A 23% protein starter diet was selected to emphasize the effect of chromium under basal, starvation for 48 hr, and refeeding periods. Thirty percent protein diets were also used to determine if the effects were compounded by protein levels. Supplemental chromium (20 ppm) significantly increased (P less than .05) weight at 3 weeks of age of poults consuming 23% protein diets, while an additional 250 ppm of nicotinic acid had little effect on poult weight at 3 weeks (P greater than .05). Supplemental chromium did not increase (P greater than .05) feed consumption of poults consuming both 23 and 30% protein diets. Supplemental chromium increased liver glycogen at 3 weeks of age and following refeeding after the 48 hr fast (P less than .05). Blood glucose was significantly affected by starvation-refeeding (P less than .05) but was not affected by either chromium or nicotinic acid. Supplemental chromium increased (P less than .01) active glycogen synthetase, while nicotinic acid increased (P less than .01) active phosphorylase at both protein levels. Synthetase was not decreased by starvation but was increased (P less than .01) by refeeding regardless of protein level fed. Phosphorylase was not affected by a starvation-refeeding regimen. Chromium supplementation increased in the vitro incorporation of (14C) glucose into glycogen during basal, starvation and refeeding periods (P less than .01), again, regardless of protein level.

Animal Feed↗
PubMed2005

Growth history influences starvation-induced expression of uspA, grpE, and rpoS and subsequent cryotolerance in Escherichia coli O157:H7.

In this study, we investigated the effect of starvation on cryotolerance of Escherichia coli O157:H7 grown in tryptic soy broth (TSB) and Luria-Bertani broth (LB). Starved cells (cells suspended in water at 37 degrees C for 6 h) and control cells (cells in TSB or LB) were frozen at -18 degrees C for up to 240 h in their respective growth media. The E. coli grown in TSB showed a greater starvation effect (the difference in percent survival of starved and control cells) and cryotolerance. The starved E. coli grown in TSB showed a 30% increase in their ability to survive frozen storage for 24 h at -18 degrees C. The corresponding increase in survival for LB-grown E. coli was only 3.8%. Cryotolerance induced by starvation of TSB- and LB-grown E. coli was correlated with the expression of genes involved in general stress response pathways, such as uspA, grpE, and rpoS. The expression of uspA, grpE, and rpoS was quantified by measuring the green fluorescence generated from autofluorescent E. coli harboring puspA::gfp, pgrpE::gfp, and prpoS::gfp gene fusions. The results obtained in this study indicate that uspA, grpE, and rpoS were induced on starvation when E. coli was grown in TSB, and their expression correlated well with subsequent induction of cryotolerance developed at -18 degrees C. In contrast, cells grown in LB and subsequently exposed to starvation conditions showed no increase in expression of uspA, grpE, or rpoS, and, as expected, these cells did not exhibit increased cryotolerance at -18 degrees C. Knowledge of molecular mechanisms involved in cross-protection might make it possible to devise strategies to limit their effects and lead to ways to predict the survival of foodborne pathogens in stressful environments.

Adaptation, Physiological↗
PubMed1975

Cytochemistry of gastrodermal autophagy following starvation in Schistosoma mansoni.

The gastrodermis of adult Schistosoma mansoni was examined by electron microscopy to determine the effects of starvation and the effects of hycanthone, administered in vitro. Special attention was focused on the relationship of the Golgi complexes with the process of autophagy. In general, autophagy was increased in the gastrodermis when it was exposed to stress conditions such as starvation and hycanthone. Acid phosphatase and thiamine pyrophosphatase activities were used as enzyme markers for the Golgi complexes and lysosomes. During the early stages of starvation, there was a 4-fold increase in the number of Golgi complexes per unit area in the gastrodermis. A progressive increase in the number of secondary lysosomes was evident as starvation time was increased. Hycanthone accelerated the effects of starvation. It was hypothesized that acid hydrolases are passed to the Golgi complexes via ER-derived vesicles. The enzymes are subsequently released as primary lysosomes from the Golgi complex to fuse with cytosegresomes and form secondary lysosomes (cytosomes).

Acid Phosphatase↗
PubMed2001

The relationship between neuropeptides and hormones in starvation.

OBJECTIVES: Some hormonal disturbances were demonstrated in starvation. Leptin, NPY and galanin play an important role in the control of appetite and in the mechanism of hormone release. METHODS: In order to evaluate the effect of starvation on the relationship between leptin, neuropeptide Y (NPY) galanin and pituitary and gonadal hormones release, plasma leptin, NPY and galanin as well as serum LH, FSH, prolactin (PRL), estradiol, progesterone levels in non-starved female rats (in diestrus) and after 72 hrs of starvation were measured with RIA methods. Effects of leptin, NPY and galanin administration on pituitary and gonadal hormones were investigated in vivo and in vitro experiments. RESULTS: Plasma leptin, NPY and galanin as well as serum estradiol and progesterone concentrations were significantly lower in starved rats as compared with non-starved rats. However serum prolactin level was significantly higher in starved rats. Opposite effects after leptin and NPY administration on hormone release in vivo and in vitro experiments were observed in non-starved rats. However, in starved rats we did not find changes in pituitary and gonadal hormones release after leptin, NPY and galanin injection or the hormonal response was blunted. CONCLUSIONS: 1) The disturbances in neuropeptides activity and in hormones release were observed in starvation. 2) Leptin, NPY and galanin have direct and indirect effects on pituitary and gonadal hormones release. 3) In starvation the hormonal response to leptin, NPY and galanin is impaired.

Animals↗
PubMed1975

Nutrition effect on liver and lysosomes. VIII. The undernourishment role in a following short-term starvation.

91 male, albino rats, Wistar strain, with body weight 150 +/- 10 g, subdivided into 2 series were investigated. The 1rst series animals (E) were fed on single daily meals in the course of 20 days, only 2 h in 24 h and after that period were subjected to complete starvation and investigated on the 24th, 48th, 72th and 96th h resp. after the ceasing of food supply. A 2nd animal series (C) serves as a control, which in the course of 20 days, were on a all-round diet and later put in identical conditions of complete starvation and also investigated on the 24th, 48th, 72th and 96th h. The liver histological, histo-enzymatical (AP, BG, AlkP and ATP) and electron microscopic changes followed up, as well as certain physiological, biochemical and morphometric indices. The dynamics of the alterations in complete starvation and the confrontation of the data between the 2 animal series with different preceding nutritional regimes show that: 1) single daily meals leads to real undernourishment; 2) the undernourishment predetermines a more severe course of the following period of complete starvation; 3) 3 phases are established during the complete starvation: adaptive, alterative-restorative and alterative. Each phase bears a definite subcellular characteristics where the lysosomes apparatus plays an essential role.

Acid Phosphatase↗
PubMedDate not supplied

[Effect of starvation and acetone on the enzyme systems of biotransformation and toxicity of xenobiotics--CYP2E1 substrates in rats].

In experiments on 205 rats it was fixed, that starvation during 2-3 days, as well as introduction of acetone (250 and 1000 mg/kg) considerably increases CYP2E1-dependent aniline and p-nitrophenol hydroxylase activity in the liver, kidneys, lungs and CYP3A dependent erythromycin N-demethylase activity, at the same time, suppress in a liver activity enzymes, dependent CYP2D, CYP1A2 and CYP2C as well as of activity UDP-glucuronosyl-transferase, sulfotransferase and glutathione-S-transferase. The starvation causes accumulation of KoA and increases activity of N-acetyltransferase in the liver. Starvation induces the change of enzymes activity and correlates with the intensifying of the processes of lipolysis, glycogenolysis, gluconeogenesis and, especially, ketogenesis which are appreciably initiated by introduction of acetone. The starvation and introduction of acetone increases metabolism of acetanilide and brombenzene, and, increasing the formation of toxic metabolites, raise its hepato-, nephro- and pulmotoxicity. The starvation attenuates elimination of indometacin from blood plasma, but intensifies conjugation of sulfadimidine with acetic acid.

Acetone↗
PubMed1986

The influence of starvation on some characteristics of the Ca2+ transport system and lipid content in rat liver mitochondria.

The effects of 48-hour starvation on some characteristics of the Ca2+ transport system as well as on lipid content and free fatty acids composition in rat liver mitochondria were determined. The ion fluxes in mitochondria in steady state and oscillations were measured using Ca2+, Sr2+ and H+ sensitive electrodes. The Ca2+ uptake in liver mitochondria was changed after starvation. In the case of equal amounts of endogenous mitochondrial Ca2+ the capability of liver mitochondria to accumulate and store exogenous Ca2+ was decreased after starvation. After inhibition of the energy dependent (active) Ca2+ transport by ruthenium-red (RR) the rate of the passive Ca2+ efflux was activated and this could be explained by the induction of the electroneutral 2H+/Me2+ exchange after starvation. The disproportion in the amounts of linoleic and docosahexaenoic acids in mitochondrial phospholipids after starvation is considered to be the possible cause of the changes in the structure and permeability of the mitochondrial membrane.

Animals↗
PubMed1979

Effects of cortisol or starvation on the activities of four enzymes in small intestine and liver of the rat during development.

The small intestine of the rat, like the liver, is a tissue with high activities of arginase, ornithine aminotransferase, and pyrroline-5-carbozylate reductase. These enzymes are thought to catalyse sequential steps in the synthesis of proline. We have compared the effect of cortisol or brief starvation on the activities of these enzymes and of soluble alanine aminotransrerase in the small intestine and liver during development. In the intestine, cortisol accelerated the increase in arginase activity, reversed the normal 2-week-long post-natal decline in that of pyrroline-5-carboxylate reductase, and delayed the normal decrease, in the third week, of ornithine aminotransferase activity. Starvation of neonates for 18 h raised the activity of arginase slightly, that of pyrroline-5-carboxylate reductase significantly, and had no effect on ornithine aminotransferase activity. Cortisol did not alter the hepatic activities of pyrroline-5-carboxylate reductase in neonates but induced premature rises in the activities of arginase and ornithine aminotransferase. Short starvation did not affect the hepatic activities of any of these enzymes. Alanine aminotransferase activity in both tissues was enhanced by cortisol but not by starvation. Thus in intestine, cortisol elicited some changes in the activity of three functionally related and one unrelated enzyme while starvation evoked changes only in pyrroline-5-carboxylate reductase. Neither stimulus appears to be specific for a metabolic pathway or to trigger a coordinated onset of proline synthesis from arginine.

Age Factors↗
PubMed1981

[Activities of 3-hydroxyl-3-methylglutaryl-CoA reductase and acetyl-CoA carboxylase and the rate of mevalonic acid, squalene, sterol and fatty acid biosynthesis from [1-14C]acetyl-CoA and [2-14C]malonyl-CoA in rat liver: effects of Triton WR 1339, starvation and cholesterol diet].

The effects of Triton WR 1339, starvation and cholesterol diet on the activities of 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoA reductase) and acetyl-CoA carboxylase and on the rates of mevalonic acid (MVA) biosynthesis from acetyl-CoA and malonyl-CoA in the soluble (140 000 g) and microsomal fractions of rat liver, on the rate of incorporation of these substrates into squalene, cholesterol and lanosterol in the rat liver postmitochondrial fraction and on the rate of fatty acid biosynthesis was studied. The administration of Triton WR 1339 (200 mg per 100 g of body weight twice) stimulated the activity of HMG-CoA reductase and MVA biosynthesis from acetyl-CoA and malonyl-CoA in the intact and solubilized microsomal fractions and had no effect on these parameters in the soluble fraction. Starvation for 36 hrs did not cause inhibition of the reductase activity or MVA biosynthesis from both substrates in the soluble fraction. Alimentary cholesterol significantly increased the activity of HMG-CoA reductase, had no effect on the rate of MVA biosynthesis from acetyl-CoA and stimulated the malonyl-CoA incorporation in to MVA in the soluble fraction. Starvation an alimentary cholesterol inhibited the HMG-CoA reductase activity and MVA biosynthesis from both substrates in the solubilized microsomal fraction. Triton WR 1339 stimulated 4--19-fold the lipid formation in the total unsaponified fraction and its components i.e. squalene, lanosterol, cholesterol, from acetyl-CoA and only insignificantly (1,2--1,7-fold) increased malonyl-CoA incorporation into these compounds. Starvation and alimentary cholesterol repressed lanosterol and cholesterol biosynthesis from acetyl-CoA, decreased malonyl-CoA incorporation into these sterols and had no influence on squalene biosynthesis from the two substrates. Triton WR 1339 and starvation inhibited the acetyl-CoA carboxylase activity, unaffected by alimentary cholesterol. No significant changes in the rate of fatty acid biosynthesis from the substrates were observed. The data obtained provide evidence for the existence of autonomic pathways of MVA biosynthesis localized in the soluble and microsomal fractions of rat liver. The pathway of MVA biosynthesis in the soluble fraction is less sensitive to regulatory factors. Sterol biosynthesis from malonyl-CoA is also more resistant to regulatory effects than sterol biosynthesis from acetyl-CoA. This suggests that HMG-CoA reductase localized in the soluble fraction takes part in MVA and sterol biosynthesis from malonyl-CoA.

Acetyl Coenzyme A↗
PubMed1984

The effects of intermittent starvation on lung development in suckling rats.

The effect of starvation on postnatal lung growth in rats was investigated. Litters were starved twice, each time for 24 hours, on Day 1 and Day 5 after birth. One group of littermates was sacrificed on Day 7, and another group, on Day 14 of postnatal life. Intermittent starvation diminished lung growth. This was accompanied by reduced somatic growth. On postnatal Day 7, lung volume, total number of alveoli, and internal surface area of the lung were decreased in starved rats, but structurally their lungs appeared similar to control lungs. On postnatal Day 14, a striking morphologic difference was observed between the lungs of control and starved pups. Following starvation, retardation of lung growth was manifested in all the parameters studied. One week of normal uninterrupted suckling could not overcome the starvation-induced initial effects on growing lungs. It is concluded that starvation, soon after birth, affects adversely the normal development of lung.

Animal Population Groups↗
PubMed1983

Muscle atrophy during starvation in a marine teleost.

The marine telost Pollachius virens undergoes a natural starvation during the winter, and provides a reversible, non-pathological model for studying muscle wasting. In the present study fish were kept without food under laboratory conditions for up to 12 weeks. The effects of starvation on muscle fibre size, volume fractions of mitochondria and myofibrils, and capillary supply were determined. Starvation results in a preferential atrophy and degradation of fast muscle myofibrillar proteins. For example, fibre cross-sectional area decreased from 1014 to 535 micrometers 2 (p less than 0.005) and myofibrillar volume fraction from 79.0% to 56.4% (p less than 0.001) in fast fibres following 12 weeks starvation. In contrast there was little change in these parameters in slow muscle fibres. Evidence is presented that M-line and Z-disc breakdown occur as an initial stage of myofibrillar degradation. Sarcoplasmic reticulum in atrophied fibres often appeared swollen and multi-membraned lysosome-like vesicles were common. The percentage of slow fibres (44 to 64%; p less than 0.025) and fast fibers (51 to 86%; p less than 0.01) without capillary contact increased and the percentage of fibre perimeter vascularised decreased during a 12 week starvation (6.3 to 3.3% in slow fibres and 2.8 to 1.1% fast fibres). The volume fractions of mitochondria in slow fibres decreased in parallel to the decrease in capillary supply (from 34.6 to 18.6%; p less than 0.001). Mechanisms of myofibrillar degradation during muscle wasting are discussed.

Animals↗
PubMed1977

Effect of starvation on muscle glucose metabolism: studies with the isolated perfused rat hindquarter.

Studies in man and experimental animals suggest that the metabolism of glucose by skeletal muscle is depressed during starvation. To investigate the basis for this, the effect of starvation on the uptake and disposition of glucose in skeletal muscle was studied in the isolated perfused rat hindquarter. In contrast to earlier work carried out in heart, neither glucose uptake, whether stimulated by insulin or exercise, nor glycolysis were depressed by 48 hr of starvation or by perfusion of the hindquarter with acetoacetate, palmitate, or octanoate. Glucose oxidation, assessed from the oxidation of 1-[14C]lactate, was depressed by approximately 75% in starved rats and by 30% in fed rats perfused with acetoacetate. Exercise increased lactate oxidation 10-fold in both fed and starved rats; however, the relative difference between the groups persisted. In general, changes in lactate oxidation were paralleled by changes in the activity of pyruvate dehycrogenase (active form). The data suggest that glucose metabolism in skeletal muscle is inhibited during starvation at the step of pyruvate oxidation and that this inhibition persists during exercise. The also suggest that the diminution of glucose uptake that occurs in skeletal muscle of intact organisms during starvation may not be related to the presence of high concentrations of free fatty acids and ketone bodies.

Acetyl Coenzyme A↗
PubMed1996

[The effect of prolonged starvation on changes in the activity of selected adaptive enzymes in rat liver].

Male rats of Wistar SPF stain (Velaz Prague) were used to investigate the influence of prolonged starvation on changes in the activity of selected adaptive enzymes in the liver and corticosterone in serum. Analyses were carried out on days 1,2,3,5 and 7 of starvation. The activity of tyrosine aminotransferase significantly increased in the period between days 2 and 5 of starvation, after which a decrease to the level of satiated animals was observed in the terminal period. Activities of tryptophane-2-3-dioxygenase and alanine aminotransferase increased in two phases reaching maximum values on days 2 and 7 of starvation. The activity of aspartate aminotransferase showed a progressive significant increase in dependence on the length of starvation. A more than threefold increase in corticosterone concentration was observed in the serum of starved animals in comparison with satiated rats.

Alanine Transaminase↗
PubMed1998

[Effect of starvation on the ultrastructure of hepatocytes of Hemidactylus frenatus (Lacertilia: Gekkonidae) with special emphasis on peroxisomes].

The influence of starvation on hepatocyte ultrastructure of Hemidactylus frenatus (Lacertilia: Gekkonidae) was investigated with special emphasis on peroxisomes. Wall lizards (Hemidactylus frenatus) were sacrificed after different periods of starvation and their livers were processed for standard transmission electron microscopy. Peroxisomes were demonstrated by means of the 3,3'-diaminobenzidine (DAB) cytochemical technique. A control group consisted of individuals which were fed "ad libitum" with Tenebrio molitor larvae. After a 7-day period of starvation the ultrastructural observation of hepatocytes disclosed a marked reduction of glycogen and lipid inclusions associated with fragmentation of the endoplasmic reticulum (ER). In later stages of starvation (14 and 25 days) ER proliferation and partial reconstruction of glycogen aggregations were observed. Increasing numbers of peroxisomes were arranged either in clusters (14 days) or in close association with mitochondria, lipid droplets and elongated crystalloid structures (25 days). Particularly noteworthy is the increasing cytochemical response of these organelles to the DAB reaction, suggesting greater metabolic activity of catalase. These data suggest that morphological and functional plasticity of hepatocytes may contribute to adaptation of Hemidactylus frenatus to prolonged starvation.

Animals↗
PubMed1987

Effect of starvation, malnutrition, and trauma on the gastrointestinal tract flora and bacterial translocation.

We have previously shown, in an animal model, that viable indigenous bacteria will cross the intact gastrointestinal (GI) mucosa and spread systemically, a process termed bacterial translocation, if the normal bacterial ecology of the gut was sufficiently disrupted to allow bacterial overgrowth or if the animals were severely immunosuppressed. Starvation or protein malnutrition disrupts the normal indigenous GI tract microflora and impairs host antibacterial defenses. Consequently, we tested the effect of the combination of starvation or protein malnutrition plus burn trauma in promoting bacterial translocation from the GI tract. Bacterial translocation was measured by quantitatively culturing the mesenteric lymph nodes, spleens, livers, blood, and peritoneal cavities of normal or burned (30% of total body surface area) CD1 mice deprived of food for three days or fed a low-protein (0.03%) diet. The effect of starvation or protein malnutrition on the gut microflora was determined by quantitatively measuring the levels of bacteria present in the ceca. Both starvation and protein malnutrition increased the cecal levels of gram-negative enteric bacilli and decreased the levels of lactobacilli and strict anaerobes. Surprisingly, neither starvation nor protein malnutrition promoted bacterial translocation, even though these animals lost over 20% of their body weight and the ecology of the gut microflora was disrupted. In fact, the protein-malnourished animals exhibited lower incidences of bacterial translocation than normally nourished animals when both groups were monoassociated with Escherichia coli C-25 or monoassociated and burned. Thus, it appears that protein malnutrition does not promote bacterial translocation, even when combined with burn trauma.

Animals↗
PubMed2001

Starvation-induced lysosomal degradation of aldolase B requires glutamine 111 in a signal sequence for chaperone-mediated transport.

Aldolase B is an abundant cytosolic protein found in all eukaryotic cells. Like many glycolytic enzymes, this protein was sequestered into lysosomes for degradation during nutrient starvation. We report here that the degradation of recombinant aldolase B was enhanced two-fold when rat and human hepatoma cells were starved for amino acid and serum. In addition, starvation-induced degradation of aldolase B was inhibited by chloroquine, an inhibitor of lysosomal proteinases and by 3-methyladenine, an inhibitor of autophagy. Aldolase B has three lysosomal targeting motifs (Q(12)KKEL, Q(58)FREL, and IKLDQ(111)) that have been proposed to interact with hsc73 thereby initiating its transport into lysosomes. In this study, we have mutated the essential glutamine residues in each of these hsc73-binding motifs in order to evaluate their roles in the lysosomal degradation of aldolase B during starvation. We have found that when glutamines 12 or 58 are mutated to asparagines enhanced degradation of aldolase B proceeded normally. However, when glutamine 111 was mutated to an asparagine or a threonine, starvation-induced degradation was completely suppressed. These mutations did not appear to alter the tertiary structure of aldolase B since enzymatic activity was not affected. Our results suggest that starvation-induced lysosomal degradation of aldolase B requires both autophagy and glutamine 111. We discuss the possible roles for autophagy and hsc73-mediated transport in the lysosomal sequestration of aldolase B.

Amino Acid Motifs↗
PubMed1979

Adenosine triphosphate pool levels and endogenous metabolism in Arthrobacter crystallopoietes during growth and starvation.

The adenosine triphosphate (ATP) content of Arthrobacter crystallopoietes was measured during growth, starvation and recovery from starvation. During exponential growth of the cells as spheres in a glucose slats medium, the level of ATP per cell remained constant at 8.0 x 10(-10) micrograms/cell. Morphogenesis to rodshaped cells and an increased growth rate following addition of casein hydrolysate was accompanied by an almost two-fold increase in the ATP level. As division of the rod-shaped cells proceeded, the level of ATP declined. After growing as rods for 12-14 h the cells underwent fragmentation to spheres during which time the ATP level again increased to the original value of 8.0 x 10(-10) micrograms/cell. As the spherical cells resumed growth on the residual glucose, their ATP content declined for a short period and then remained relatively constant. During starvation of sphere or rod-shaped cells for one week, the ATP level declined by approximately 70% during the first 40-50 h and then remained constant. The endogenous metabolism rate of spherical cells declined during the first 10-20 h of starvation and then remained constant at approximately 0.02% of the cell carbon being utilized per h. Addition of glucose to spherical cells which had been starved for one week increased both the ATP content per cell and their rate of endogenous metabolism. The ATP content fluctuated and then remained at a level higher than maintained during starvation while endogenous metabolism quickly declined.

Adenosine Triphosphate↗
PubMed1979

Adenylate nucleotide levels and energy charge in Arthrobacter crystallopoietes during growth and starvation.

The adenylate nucleotide concentrations, based on internal water space, were determined in cells of Arthrobacter crystallopoietes during growth and starvation and the energy charge of the cells was calculated. The energy charge of spherical cells rose during the first 10 h of growth, then remained nearly constant for as long as 20 h into the stationary phase. The energy charge of rod-shaped cells rose during the first 4 h of growth, then remained constant during subsequent growth and decreased in the stationary growth phase. Both spherical and rod-shaped cells excreted adenosine monophosphate but not adenosine triphosphate or adenosine diphosphate during starvation. The intracellular energy charge of spherical cells declined during the initial 10 h and then remained constant for 1 week of starvation at a value of 0.78. The intracellular energy charge of rod-shaped cells declined during the first 24 h of starvation, remained constant for the next 80 h, then decreased to a value of 0.73 after a total of 168 h starvation. Both cell forms remained more than 90% viable during this time. Addition of a carbon and energy source to starving cells resulted in an increase in the ATP concentration and as a result the energy charge increased to the smae levels as found during growth.

Adenine Nucleotides↗