Respiring rat heart mitochondria were loaded with Ca2+ and then treated with Ruthenium Red. The factors affecting the subsequent Ca2+-efflux were studied. Addition of rotenone or antimycin led to a decline of efflux except at pH values above 7.2, provided the load was less than about 80 nmol per mg of protein. Oligomycin reversed the effect of the respiratory inhibitors. Independently of respiration, efflux was stimulated by the uncoupler trifluoromethyltetrachlorbenzimadazole, by mersalyl and by thyroid hormones. The stimulated efflux could be diminished by ADP, with Mg2+ as cofactor if efflux was rapid. With respiration in progress, efflux could be stimulated by N-ethylmaleimide and 5,5′-dithiobis-(2-nitrobenzoate). The effects of mersalyl and of thyroid hormones could be diminished with dithiothreitol. In the absence of stimulating agents, the Ca2+ efflux was proportional to the load up to some critical amount, this critical amount was decreased by the agents. Thyroxine and mersalyl caused ...
Literature References: Prepn: Diels, Beccard, Ber. 39, 4125 (1906); Bockmühl, Schwarz, DE 423031 (1925 to Hoechst); Frdl. 15, 1609. Use as diuretic: F. Brunn, Wien. Klin. Wochenschr. 37, 901 (1924). Toxicity data: E. B. Robbins, K. K. Chen, J. Am. Pharm. Assoc. 40, 249 (1951). Use of acid as physiological sulfhydryl inhibitor: P. Mavier, J. Hanoune, Eur. J. Biochem. 59, 593 (1975). ...
A latent ATP-dependent Ca storage system is enriched in preparations of pinched-off presynaptic nerve terminals (synaptosomes), and is exposed when the terminals are disrupted by osmotic shock or saponin treatment. The data indicate that a fraction of the Ca uptake (measured with 45Ca) is associated with the intraterminal mitochondria; it is blocked by ruthenium red, by FCCP, and by azide + dinitrophenol + oligomycin. There is, however, a residual ATP-dependent Ca uptake that is insensitive to the aforementioned poisons; this (nonmitochondrial) Ca uptake is blocked by tetracaine, mersalyl and A-23187. Moreover, A-23187 rapidly releases previously accumulated Ca from these (nonmitochondrial) storage sites, whereas the Ca chelator, EGTA, does not. The proteolytic enzyme, trypsin, spares the mitochondria but inactivates the nonmitochondrial Ca uptake mechanism. Chemical measurements of total Ca indicate that the ATP-dependent Ca uptake at the nonmitochondrial sites involves the net transfer of Ca ...
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TY - JOUR. T1 - Kinetics of Pi-Pi exchange in rat liver mitochondria. Rapid filtration experiments in the millisecond time range. AU - Ligeti, E.. AU - Brandolin, Gérard. AU - Dupont, Yves. AU - Vignais, Pierre V.. PY - 1985. Y1 - 1985. N2 - Phosphate-phosphate exchange through the inorganic phosphate (Pi) carrier of rat liver mitochondria was investigated by a new rapid filtration technique, which does not require the use of transport inhibitors to stop the reaction and offers high time resolution (starting from 10 ms), thus allowing kinetic measurements on a fine time scale even at room temperature. At approximately 22°C, isotopic equilibrium of [32P]Pi is achieved within 0.8-2.5 s - depending on the Pi concentration - and an initial linear phase, lasting for 400-500 ms, is observed. Complete inhibition of Pi exchange by an excess (33 nmol/mg) of mersalyl, a well-known organomercurial inhibitor, required 200 ms, pointing to the insufficiency of this reagent for effective inhibitor stop. On ...
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Transcriptional regulation of genes involved in fatty acid metabolism is considered the major long-term regulatory mechanism controlling lipid homeostasis. By means of this mechanism, transcription factors, nutrients, hormones and epigenetics control not only fatty acid metabolism, but also many metabolic pathways and cellular functions at the molecular level. The regulation of the expression of many genes at the level of their transcription has already been analyzed. This review focuses on the transcriptional control of two genes involved in fatty acid biosynthesis and oxidation: the citrate carrier (CIC) and the carnitine/ acylcarnitine/carrier (CAC), which are members of the mitochondrial carrier gene family, SLC25. The contribution of tissue-specific and less tissue-specific transcription factors in activating or repressing CIC and CAC gene expression is discussed. The interaction with drugs of some transcription factors, such as PPAR and FOXA1, and how this interaction can be an attractive
INTRODUCTION: The phosphate carrier (PiC) is a nuclear encoded protein that belongs to the mitochondrial carrier protein family. Its physiological role is to catalyze the transport of inorganic phosphate into the mitochondrial matrix (1). Uptake of phosphate into mitochondria is essential for the oxidative phosphorylation of ADP to ATP. Only one human gene for the PiC, that give rises to two alternatively spliced isoforms (A and B), has been detected.. The recombinant, reconstituted isoforms A and B exhibit similar substrate specificity and inhibitor sensitivity, but differ in their kinetic parameters and tissue distribution (2). We have analyzed the 5-flanking region of the human PiC gene and have identified a single transcriptional initiation site, an activation domain and an inhibition domain (3). MATERIALS AND METHODS: Materilas and methods employed are reported in ref. 3. RESULTS: Through deletion analysis of the 5 flanking regulatory region (-1213/-25 bp) and transient transfection of ...
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SWISS-MODEL Repository entry for P97521 (MCAT_RAT), Mitochondrial carnitine/acylcarnitine carrier protein. Rattus norvegicus (Rat)
Transcriptional regulation of genes involved in fatty acid metabolism is considered the major long-term regulatory mechanism controlling lipid homeostasis. By means of this mechanism, transcription factors, nutrients, hormones and epigenetics control not only fatty acid metabolism, but also many metabolic pathways and cellular functions at the molecular level. The regulation of the expression of many genes at the level of their transcription has already been analyzed. This review focuses on the transcriptional control of two genes involved in fatty acid biosynthesis and oxidation: the citrate carrier (CIC) and the carnitine/ acylcarnitine/carrier (CAC), which are members of the mitochondrial carrier gene family, SLC25. The contribution of tissue-specific and less tissue-specific transcription factors in activating or repressing CIC and CAC gene expression is discussed. The interaction with drugs of some transcription factors, such as PPAR and FOXA1, and how this interaction can be an attractive ...
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PreRX=pretreatment; ULN=upper limit of normal. Neutrophils, (absolute), low (10*3 c/uL): ,0.85*PreRx, if PreRx ,1.5; ,1.5 if PreRx ≥1.5. Alanine aminotransferase, high (U/L): ,1.25*PreRx if PreRx ,ULN; ,1.25*ULN if PreRx ≤ULN. Bilirubin, direct (mg/dL), high: ,1.1*ULN if PreRx ≤ULN;, 1.1*ULN if PreRx is missing; ,1.25*PreRx if PreRx ,ULN. Bilirubin, total (mg/dL), high: ,1.1*ULN if PreRx ≤ULN;, 1.1*ULN if PreRx is missing; ,1.25*PreRx if PreRx ,ULN ...
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Sixteen marine isolates from a NORPAX cruise, which were transferred once on medium after initial isolation, survived nutrient deprivation for at least 8 months (longest period test). All but one isolate remained cellularly intact, although their sizes and shapes changed greatly, and all became smaller, decreasing in size from 40 to 79%. Three starvation-survival patterns were demonstrated, namely (i) an initial increase in viable cells followed by a decrease until a constant number was reached, (ii) an increase in viable cells until a constant number was reached, and (iii) a decrease in viable cells until a constant number was reached. One isolate from each starvation-survival pattern was starved for 8 months and then was tested in comparison with 4-month-starved Ant-300 for [14C]glutamic acid uptake, respiration, and incorporation. The response to glutamic acid was rapid and linear in each case. The data indicate that the starvation-survival of Ant-300 is not an anomalous situation and that ...
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Of all diuretic drugs, the mercurial diuretics have the established advantage of combining effectiveness and safety when administered intramuscularly.1 They may on occasion cause local or generalized reactions of varying degree. Chemical modifications of these organic mercurial compounds have been employed in an effort to minimize such toxic effects.2, 3 Another mercurial compound, mercaptomerin sodium (Thiomerin) has recently been introduced. This preparation is an organic mercurial combined with a mercaptan (disodium salt of N-(gamma-carboxy-methyl-mercaptomercuri-beta-methoxy) propyl camphoramic acid). Formula: C(CH3), C(COONa) (CH3), CH2, CH2, CH(ONH CH2) CH (OCH2) CH2HgSCH2.. The stated clinical characteristics of mercaptomerin are:. 1. It is an effective ...
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