PubMed Health⌕ Search

Biomedical subjects

J Bastin

Publications and source records attributed to J Bastin.

47 records · Page 3Linked to original sources
PubMed1987

Change in energy reserves in different segments of the nephron during brief ischemia.

Rat kidneys were made ischemic for 5 to 120 seconds. Segments of individual nephrons were dissected from freeze dried sections and analyzed for ATP, phosphocreatine, glycogen, glucose, glucose-6-phosphate, lactate and creatine kinase. ATP fell most rapidly in proximal convoluted and straight tubules (PCT, PST) and distal convoluted tubules (DCT), and most slowly in glomerulus and papilla. Phosphocreatine levels ranged fivefold and was highest in DCT, where it approached that of brain. Creatine kinase ranged 100-fold with lowest level in PCT, where the ischemic fall in phosphocreatine was so slow as to suggest a function other than that of an energy reserve. Glycogen varied tenfold from modest levels in distal segments to very low levels in PST, and was not used rapidly in any segment. Glucose consumption and lactate production were most rapid in distal portions. High-energy phosphate consumption for the first 7.5 seconds of ischemia, calculated from these data, indicates roughly-equal energy metabolism in proximal and distal segments, with lower levels in papilla, and especially in glomerulus. The absolute values suggest that the in vivo metabolic rate of the nephron continued almost unabated for 5 or 10 seconds of ischemia.

Adenosine Triphosphate↗
PubMed1987

Role of catecholamines in the control of newborn kidney adenine nucleotide content.

During the 1st h of extrauterine life, the adenine nucleotide content of the rat kidney is modified: the ATP level increases (+30%) while ADP and AMP are lowered (-30 and -50%, respectively). This leads to a high value of energy charge in the newborn kidney (0.89 vs. 0.80 in the fetus). It was possible to obtain in utero a similar modification of ATP, ADP, AMP concentrations by injections to the fetuses of cAMP, dibutyryl cAMP, or isoprenaline. Conversely, the postnatal changes in adenine nucleotide content could be prevented by administration to the fetus, just before birth, of beta- or beta 1-adrenoreceptor antagonists. Therefore the rise of kidney energy charge following parturition appears to be under hormonal control. Glucagon had no effect on kidney adenine nucleotide content. It is strongly suggested that the catecholamines released at the time of parturition are the triggering factor of this evolution.

Adenine Nucleotides↗
PubMed1987

[Mitochondrial oxidative phosphorylation in the rat kidney during the perinatal period].

Oxidative metabolism in the developing rat kidney has been studied on isolated mitochondria. An increase of about 50% in state 3 respiration has been observed at birth, using succinate, glutamate, or palmitoyl-L-carnitine as a substrate. The rate of respiration in the presence of 2,4-dinitrophenol was found identical to state 3 respiration in all cases. Cytochrome oxidase activity did not change between the fetal and newborn stages. The increase of mitochondrial respiration revealed here, which is not linked to a modification of the respiratory chain, could be involved in the rise of kidney ATP level and energy charge observed at birth.

Aging↗
PubMed1986

Perinatal changes in adenine nucleotide content of developing rat kidney.

Adenine nucleotides have been measured in fetal and newborn kidneys of rat using the luciferine-luciferase method. In fetuses, between days 18 and 21 of gestation there is a drop of the relative amount of ATP in the renal nucleotide pool. Consequently, the kidneys of 21 days-old fetuses have lowered ATP/ADP ratio (3.6) and energy charge (0.80) compared with values found on day 18 (6.9 and 0.91, respectively); this relative energy deficit is heightened in progesterone induced postmaturity. One hour after delivery whether the gestational stage is 21, 22 or 23 days, there is a rise in ATP and a decrease in AMP content which restore a high energy level in kidney of the newborn and a 30% increase in the total adenine nucleotide pool.

Adenine Nucleotides↗
PubMed1985

Changes in carnitine-palmitoyl-transferase and carnitine-acetyl-transferase activity in rat kidney during development; effects of fasting.

Developmental changes in the activities of two enzymes catalysing transfer of fatty acid across the mitochondrial membrane (carnitine-palmitoyl-transferase and carnitine-acetyl-transferase) were studied in the kidneys of developing rats from late fetal life to 10 days post-partum and were compared to cortical adult value. The activities of carnitine-palmitoyl-transferase and carnitine-acetyl-transferase increased after birth to reach a maximal value on day 5. Thereafter both activities decreased to reach adult cortical value. The cytochrome c oxidase activity (index of mitochondrial activity) increases continuously from late fetal age to adult. In kidneys of fetuses from starved mothers the carnitine-palmitoyl-transferase activity is higher than that of controls while carnitine-acetyl-transferase activity is not changed. In postmature fetuses (23 days post-coïtum) carnitine-palmitoyl-transferase activity is the same as in 21 days post-coïtum old fetuses. These results are discussed in relation to variations in nutritional and hormonal changes occurring during the perinatal period.

Acetyltransferases↗
PubMed1981

Mallory bodies in alcoholic liver disease: identification of cytoplasmic filament/cell membrane and unique antigenic determinants by monoclonal antibodies.

Polyclonal and monoclonal antibodies have been produced to Mallory body protein (MBP) extracted from isolated Mallory bodies (MBs). The polyclonal antibodies reveal a unique determinant in MBs. The first monoclonal antibody (anti-JMB1) detects a second unique determinant (JMB1) in MBs which is not detectable in normal hepatocytes. The second monoclonal antibody (anti-JMB2) shows that MBs contain another determinant which is associated with the cell and nuclear membranes and a cytoplasmic filament system of normal hepatocytes and bile duct epithelium; this antigen is not detectable in the cell membranes or cytoplasmic filament systems of hepatocytes which contain MBs. The third monoclonal antibody (anti-JMB3) reacts only with an antigen (JMB3) in mesenchymal cells of alcoholic cirrhotic liver and its significance, at this time, is unclear. It is suggested that the metabolism of JMB1, JMB2, and JMB3 antigens is deranged in hepatocytes damaged by alcohol. It is concluded that the antigenic structure of MBs is more complex than hitherto realised and that all of these antigens are distinct from prekeratin (a component of epidermal cell intermediate filaments).

Cell Membrane↗
PubMedDate not supplied

Cytotoxic T lymphocytes recognize influenza haemagglutinin that lacks a signal sequence.

A surprising feature of most cytotoxic T lymphocytes (CTL) responding to influenza infection is that they recognize the unglycosylated (non-transmembrane) proteins of the virus, including the nucleoprotein. Recognition of cells that express nucleoprotein by CTL does not depend on a definite signal sequence within the protein, and the epitopes recognized can be defined with short synthetic peptides in vitro. Haemagglutinin (HA), the major transmembrane protein of the virus, is recognized by a minor population of CTL from infected mice. We have deleted the sequence coding for the N-terminal signal peptide from a complementary DNA encoding HA of the H1 subtype. The signal-deleted HA is detected with antibodies as a short-lived, unglycosylated, intracellular protein. However, CTL raised to the complete molecule recognize cells expressing the signal-deleted HA and vice versa. These results cast doubts on the assumption that CTL recognize the HA molecule only after its insertion into the plasma membrane.

Animals↗
PubMedDate not supplied

Restoration of antigen presentation to the mutant cell line RMA-S by an MHC-linked transporter.

In mammalian cells, short peptides derived from intracellular proteins are displayed on the cell membrane associated with class I molecules of the major histocompatibility complex (MHC). The surface presentation of class I-peptide complexes presumably alerts the immune system to intracellular viral protein synthesis. Peptides derived from the cytosol must reach the cisternae of the endoplasmic reticulum where they are required for the assembly of stable class I molecules, and it has been proposed that the products of the two MHC-encoded ATP-binding cassette (ABC) transporter genes function to deliver the peptides across the membrane of the endoplasmic reticulum. This idea is supported by experiments in which transfection of a human cell line defective in class I expression with a complementary DNA of one of these genes restored cell surface expression levels. Here we show that the complete phenotype of the mouse mutant cell line RMA-S, in which lack of surface expression of stable class I molecules correlates with an inability to present viral peptides originating in the cytosol, is repaired by the cDNA of the other transporter gene. These results are consistent with the possibility that the two transporter polypeptides form a heterodimer.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMedDate not supplied

Effect of glucocorticoids on mitochondrial oxidative enzyme and Na-K-ATPase activities in the rat proximal tubule and thick ascending limb of Henle.

The activities of three mitochondrial oxidative enzymes (citrate synthase, 3-ketoacid-CoA transferase, beta-hydroxyacyl-CoA dehydrogenase) and Na-K-ATPase were microassayed in isolated segments of the rat proximal convoluted tubule (PCT) and medullary thick ascending limb of the loop of Henle (mTAL). The effects of adrenalectomy (ADX) and ADX plus exogenous glucocorticoids were analyzed. The hormonal replacement was daily injections of dexamethasone (10 micrograms/100 g body weight/24 h) for 5 days. ADX lowered the activity of all oxidative enzymes studies in the mTAL, but not in the PCT and led to a decrease in Na-K-ATPase in both nephron segments. Dexamethasone restored the normal level of oxidative enzymes and Na-K-ATPase in the mTAL and of Na-K-ATPase in the PCT. We conclude that the activities of citrate synthase, 3-ketoacid-CoA transferase and beta-hydroxyacyl-CoA dehydrogenase and of Na-K-ATPase are coordinately regulated in the mTAL and that glucocorticoids are essential for the long-term regulation of these enzyme activities in this nephron segment. In contrast, the activities of mitochondrial oxidative enzymes are not influenced by glucocorticoids in the PCT. This study presents the first evidence for a cell-specific regulation by glucocorticoids of oxidative metabolism in the nephron of adult rat kidney.

3-Hydroxyacyl CoA Dehydrogenases↗