Liver Respiration Research Articles

Control of the citric acid cycle by glyoxylate. 2. Mechanism of the inhibition of respiration in liver and kidney particles.

Research Article| December 01 1962 Control of the citric acid cycle by glyoxylate. 2. Mechanism of the inhibition of respiration in liver and kidney particles A RUFFO; A RUFFO Search for other works by this author on: This Site PubMed Google Scholar A ADINOLFI; A ADINOLFI Search for other works by this author on: This Site PubMed Google Scholar G BUDILLON; G BUDILLON Search for other works by this author on: This Site PubMed Google Scholar G CAPOBIANCO G CAPOBIANCO Search for other works by this author on: This Site PubMed Google Scholar Biochem J (1962) 85 (3): 593–600. https://doi.org/10.1042/bj0850593 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation A RUFFO, A ADINOLFI, G BUDILLON, G CAPOBIANCO; Control of the citric acid cycle by glyoxylate. 2. Mechanism of the inhibition of respiration in liver and kidney particles. Biochem J 1 December 1962; 85 (3): 593–600. doi: https://doi.org/10.1042/bj0850593 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Journal Search Advanced Search This content is only available as a PDF. © 1962 The Biochemical Society1962 Article PDF first page preview Close Modal You do not currently have access to this content.

Respiration and phosphorylation in liver and heart mitochondria from altitude-exposed rats.

Studies were made of respiration and oxidative phosphorylation in heart and liver mitochondria isolated from adult rats continuously exposed to simulated altitudes of 17,000, 20,000, or 21,000 ft for 2–7 weeks. Hypoxia had no effect on the P:O ratios in either heart or liver mitochondria, but some other aspects of mitochondrial respiration were altered in altitude-exposed rats. Liver mitochondrial respiration of rats maintained at 21,000 ft was lower than that of controls (succinate respiration, –30%; agr-ketoglutarate, –10%; β–hydroxybutyrate, –20%). In mitochondria from the hearts of rats exposed for 6 weeks to 17,000 ft, respiratory stimulation with ADP was greater than in mitochondria from the hearts of control animals. Submitted on March 13, 1961

DER EINFLUSS VON RESERPIN AUF DIE ANTITHYREOIDALE WIRKUNG VON KALIUMPERCHLORAT

ABSTRACT 1. Reserpine does not inhibit the tissue respiration of liver in normal male rats (in vitro). 2. The decrease of tissue respiration of the liver with simultaneous morphological stimulation of the thyroid gland after long administration of reserpine is due to a minute inhibition of the hormone synthesis in the thyroid gland. 3. The morphological alterations of the thyroid in experimental hypothyroidism due to perchlorate can not be prevented with reserpine.

Fat deficiency and the calorigenic action of L-thyroxine.

The influence of a fat-deficient diet on the calorigenic action of l-thyroxine was investigated. The BMR, endogenous and substrate respiration (succinate) of liver slices and hemidiaphragms were determined. The increase of BMR in fat-deficient animals was confirmed. Furthermore, both endogenous and ‘substrate’ respiration of liver and diaphragm were higher than in controls. When thyroxine was administered, the fat-deficient animals demonstrated a greater BMR response than did controls. Substrate respiration of liver and diaphragm indicated that both fat deficiency and thyroxine treatment increase succinate utilization and that these effects are additive in these tissues.

THE EFFECT OF 2-AMINOETHYLISOTHIOURONIUM (AET) ON THE RESPIRATION OF MOUSE LIVER AND SPLEEN SLICES

The effect of AET injected in vivo on the respiration of liver and spleen slices from non-irradiated and X-irradiated mice was studied. The mice were killed 4 or 24 hours after the injection of a protective dose of AET and the livers and spleens were removed, sliced, and incubated for 3 hours in Krebs–Henseleit bicarbonate buffer containing uniformly labelled C14 glucose. In both non-irradiated and X-irradiated mice, initially, AET depressed the respiration of C14O2 from incubated liver slices but this depressing effect appeared to be overcome with time. Whole body X irradiation increased the total C14O2 respired by liver slices from mice injected with saline or AET prior to X irradiation and killed 4 or 24 hours after X irradiation. Whole body X irradiation decreased the total C14O2 respired by the spleen slices and the 24-hour samples showed the greatest decrease. In both the non-irradiated and X-irradiated mice AET did not appear to affect the total C14O2 respired by spleen slices.

Influence of Excess Dietary Molybdenum on Rat and Calf Liver and Heart Enzymes

Experiments were designed to study the effect of excess dietary molybdenum on various enzymes of the liver and cytochrome oxidase of the heart of a monogastric and a ruminant animal in an attempt to gain information as to the mechanism of molybdenosis in animals. Rats fed diets containing added molybdenum at 500 and 800 ppm showed molybdenum toxicity symptoms, including diarrhea and decreased rate of growth. These diets did not affect tyrosine oxidase activity or concentration of copper in the liver, but caused an increase in the concentration of molybdenum in this organ and a reduction in liver respiration and liver xanthine oxidase. A second group of rats was fed highmolybdenum diets which raised the concentration of molybdenum in the liver but did not cause diarrhea. These rats also showed a reduction in liver xanthine oxidase activity. Thus, it appears that possible decreased utilization of protein, resulting from diarrhea as exhibited by the first group of rats, was not solely responsible for the reduced xanthine oxidase activity noted. Also, increased liver molybdenum concentration per se can influence the level of the enzyme. A slight lowering in blood uric acid concentration was observed in these rats. The cytochrome oxidase activity in the heart was not affected. The concentration of molybdenum found in the liver upon feeding 500 ppm molybdenum in the diet was not exceeded when 800 ppm was fed. It appears that there may be a liver “threshold” for molybdenum of 500 ppm or less; above this dietary level, liver storage is not increased. Calves maintained on diets containing 200 and 400 ppm molybdenum were observed to have increased concentrations of molybdenum in the livers, but no decrease in liver respiration or xanthine oxidase or in heart cytochrome oxidase.

THE EFFECT OF 2-AMINOETHYLISOTHIOURONIUM (AET) ON THE RESPIRATION OF MOUSE LIVER AND SPLEEN SLICES

The effect of AET injected in vivo on the respiration of liver and spleen slices from non-irradiated and X-irradiated mice was studied. The mice were killed 4 or 24 hours after the injection of a protective dose of AET and the livers and spleens were removed, sliced, and incubated for 3 hours in Krebs–Henseleit bicarbonate buffer containing uniformly labelled C14 glucose. In both non-irradiated and X-irradiated mice, initially, AET depressed the respiration of C14O2 from incubated liver slices but this depressing effect appeared to be overcome with time. Whole body X irradiation increased the total C14O2 respired by liver slices from mice injected with saline or AET prior to X irradiation and killed 4 or 24 hours after X irradiation. Whole body X irradiation decreased the total C14O2 respired by the spleen slices and the 24-hour samples showed the greatest decrease. In both the non-irradiated and X-irradiated mice AET did not appear to affect the total C14O2 respired by spleen slices.

Oxidative processes in hypervitaminosis A in albino rats.

Albino rats were made hypervitaminotic A by feeding 30,000 iu of vitamin A daily by mouth; the effect of this hypervitaminosis was compared with a similar pair-fed group. Food consumption and body weight gain were reduced. Study of liver and kidney slices shows that the latter manifest no significant increase in oxygen consumption in presence of succinate or acetate. There is slight increase in O2 consumption in brain homogenates. Liver homogenate shows 15.2% inhibition with succinate and 5.6% with ascorbate oxidation. Liver homogenate shows 19.3% inhibition of succinate dehydrogenase activity by Thunberg technique with methylene blue indicator. It is concluded that hypervitaminosis A inhibits liver respiration by affecting the dehydrogenase, or any immediate step following it, and the cytochrome c-cytochrome oxidase end of the succinoxidase system is little affected.

Liver respiration in normal and roentgen irradiated rats: the utilisation of a succinate.

Liver respiration in normal and roentgen irradiated rats: the utilisation of a succinate.

Liver Respiration in Normal and Roentgen Irradiated Rats; the Utilisation of a Succinate

Liver Respiration in Normal and Roentgen Irradiated Rats; the Utilisation of a Succinate

Zur Temperaturaktivierung der Substratatmung tierischer Gewebe

(1) The influence of temperature on tissue respiration of frog skin and rat liver, stimulated by succinate and pyruvate, was studied. The temperatures ranged from 17.5 to 47.5°C. (2) The activation-energy (μ) of the substrate-stimulated respiration was significantly lower than that of the endogeneous O2-uptake. Therefore, in the submaximal range of temperature, the relative activity of the stimulated respiration decreased with increasing temperatures.

Dependence of activation energy of tissue respiration on body size in mammals

(1) The activation energy of the liver respiration in an interval of temperature between 17.5 and 37.5°C was determined in mice, rats, and guinea pigs. (2) A systematic decrease with increasing body size was observed.

On the bioenergetics of bile secretion

Experiments were performed on animals with fistula of the common bile duct and on isolated liver with fistula of the gall bladder. It was established with the aid of enzyme poisons (sodium cyanide, sodium fluoride, monoiodacetic acid, 2,4-dinitrophenol, sodium arsenate) that tissue respiration of liver and oxidative phosphorylation connected with it are the main origins of energy in bile secretion.

Liver respiration in normal irradiated and synkavit-treated rats: endogenous respiration in phosphate buffer.

Liver respiration in normal irradiated and synkavit-treated rats: endogenous respiration in phosphate buffer.

Liver Respiration in Normal Irradiated and Synkavit-Treated Rats: Endogenous Respiration in Phosphate Buffer

Whole body roentgen irradiation of rats with 450 r is shown to increase the endogenous respiration of liver slices. Pretreatment with syekavit results in a similar but earlier effect, which becomes irreversible after larger doses. (auth)

Effect of prolonged cold exposure on in vitro respiration and anaerobic glycolysis of rat liver.

Liver slices were prepared from rats that had been exposed to cold (5 ± 1°C) for intervals of 2, 4, 6 or 9 weeks, and assays were made for respiratory rate and the rate of anaerobic glycolysis. The results of the respiration experiments indicated the first 4 weeks' cold exposure was associated with increasing qo2 values, whereas exposure longer than 4 weeks was associated with qo2 that returned toward the control value. The results indicated further that the exact nature of the substances being metabolized in the conventional tissue slice experiment was unknown. The results of the anaerobic experiments indicated the rate of anaerobic glycolysis decreased progressively as the duration of cold exposure was increased.

Oxygen consumption of liver following subtotal hepatectomy of normal and hypothyroid rats.

Respiration of regenerating liver was compared with the rate of regeneration at varying intervals after removal of the left lateral and median lobes of the liver of rats. This subtotal hepatectomy was found to remove 66% of the total liver of rats in a comparable weight range; control animals were laparotomized, the liver was exposed for the same length of time, and the viscera were manipulated in an analogous manner. At 1, 2, 3, 4, 7 and 14 days postoperative, the rats were killed by exsanguination, the liver remnant was weighed and slices prepared for manometric studies in Ringer-phosphate-glucose medium. At 3 days, when growth was most rapid, liver respiration was increased 40%. By 14 days, when the liver had reached its calculated preoperative weight and growth had slowed considerably, respiration was 14% higher than controls. Hypothyroid rats, prepared by previous thyroidectomy, had a lower rate of liver regeneration after hepatectomy, but respiration, although at a lower level, showed comparable stimulation.

Studies on the interaction between phagocytes and tubercle bacilli. III. Some metabolic effects in guinea pigs associated with infection with tubercle bacilli.

In continuing studies concerning the interactions between phagocytes and tubercle bacilli the effect of tuberculous infection on respiration and glucose utilization was investigated in guinea pigs. Peritoneal exudates rich in polymorphonuclear leucocytes, derived from guinea pigs infected with tubercle bacilli, had a significantly higher rate of respiration than the same cells from normal animals. The difference between cells from normal and infected animals was greater when the animals were infected with a virulent strain (Vallée) than when infected with an attenuated one (R1Rv or BCG). By the use of glucose labelled with C(14) at position 1 or 6, or uniformly labelled glucose, it was established that this difference in oxygen uptake between normal and infected cells was probably not caused by a difference in the pathway of glucose utilization. Similarly, the respiration of liver and kidney slices from normal and infected guinea pigs was compared and it was found that liver slices showed differences similar to those shown by leucocytes, but that the kidney slices did not. The possibility has not been ruled out that the difference in rate of respiration of liver slices due to infection might be caused by tuberculous lesions in the livers of infected animals. The mononuclear cells which invade the liver have a higher rate of oxygen uptake than liver cells. The rate of glucose utilization and the total amount of CO(2) produced was also determined in intact guinea pigs. Both functions were found not to differ significantly in normal and infected animals. The rate of production of CO(2) from C(1) and C(6) of glucose was the same in both groups of animals. The ratio of the rate of production of C(14)O(2) from C(1) and C(6) of glucose by the whole animal was found to be about 1.35. It was found to be much higher with polymorphonuclear leucocytes (C(1)/C(6) = 8 in the absence of serum). During the process of phagocytosis this ratio increased from about 25 to about 130 (in the presence of 2 per cent serum) indicating an increase in the direct oxidative pathway of glucose utilization during stimulated cellular activity.

Tissue respiration of rats acclimatized to low barometric pressure.

Rate of respiration of tissues of male albino rats acclimatized to 18,000 feet simulated altitude for periods averaging 11.2 weeks was determined by Warburg technique under 100% oxygen. Results from 12 experimental animals were compared with 7 controls simultaneously maintained at normal barometric pressure. Acclimatized animals showed no significant changes in growth rate, total metabolic rate or rectal temperature. Hemoglobin values and heart-body weight ratios were elevated. Tissue respiration of brain, small intestine, diaphragm, liver, skeletal muscle, atrium and ventricle was not significantly different from that of controls. Adrenal-body weight ratios were unchanged but increased adrenocortical activity is suggested by a significant increase in adrenal qO2. Respiration of acclimatized kidney slices was significantly reduced. It is concluded that generalized adaptation of cellular metabolism to hypoxia does not occur in acclimatization but that changes may be demonstrated in tissues specifically involved in the adaptation process. Submitted on February 29, 1956

Liver respiration, succinoxidase and DPN-cytochrome c reductase activity in vitamin K-deficiency and after treatment with long-acting anticoagulants.

Liver respiration, succinoxidase and DPN-cytochrome c reductase activity in vitamin K-deficiency and after treatment with long-acting anticoagulants.