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Biomedical subjects

C Richter

Publications and source records attributed to C Richter.

At least 181 records · Page 10Linked to original sources
PubMed1989

[The intermamillary index of newborn infants].

Using 500 healthy newly born babies age specific standard for intermamillary index was defined in order to improve objective criteria for the clinical features of 'widely spaced nipples' as it is to realize in connection with a variety of complex morphogenetic disturbances. Independent of sex and of post natalage the mean value is y mean = 23.31 and the standard deviation s = +/- 1.24. Consequently, the normal +/- 2s range is to be appraised between 21.0 and 26.0. In small-for-gestational-age infants and in babies born by breech presentation the + 2s limit is reduced to 25.0.

Anthropometry↗
PubMed1988

Do mitochondrial DNA fragments promote cancer and aging?

Reactive oxygen species are important in carcinogenesis, diseases, and aging, probably through oxidative damage of DNA. Our understanding of this relationship at the molecular level is very sketchy. It has recently been found that in mitochondria oxidative DNA damage is particularly high and may not be repaired efficiently. I propose that oxidatively generated DNA fragments escape from mitochondria and become integrated into the nuclear genome. This may transform cells to a cancerous state. Time-dependent nuclear accumulation of mitochondrial DNA fragments may progressively change the nuclear information content and thereby cause aging. This proposal can be tested experimentally.

Aging↗
PubMed1988

Mono(ADP-ribosylation) in rat liver mitochondria.

This paper investigates protein mono(ADP-ribosylation) in rat liver mitochondria. In isolated inner mitochondrial membranes, in the presence of both ADP-ribose and NAD+, a protein is mono-(ADP-ribosylated) with high specificity. The reaction apparently consists of enzymatic NAD+ glycohydrolysis and subsequent binding of free ADP-ribose to the acceptor protein. In terms of chemical stability, the resulting bond is unique among the ADP-ribose linkages thus far characterized. Formation of a Schiff base adduct between free ADP-ribose and the acceptor protein is excluded. In intact mitochondria at least three classes of proteins are ADP-ribosylated in vivo. One ADP-ribose-protein linkage is of the carboxylate ester type as indicated by its lability in neutral buffer. Another class of ADP-ribosylated proteins requires hydroxylamine for release of ADP-ribose. The third class is stable in hydroxylamine but labile to alkali, similar to the ADP-ribose-cysteine linkage in transducin formed by pertussis toxin.

Adenosine Diphosphate Ribose↗
PubMed1988

Ca2+ release from mitochondria induced by prooxidants.

A variety of chemically different prooxidants causes Ca2+ release from mitochondria. The prooxidant-induced Ca2+ release occurs from intact mitochondria via a route which is physiologically relevant and may be regulated by protein ADP-ribosylation. When the released Ca2+ is excessively cycled by mitochondria they are damaged. This leads to uncoupling, a decreased ATP supply, and a decreased ability of mitochondria to retain Ca2+. Excessive Ca2+ cycling by mitochondria will deprive cells of ATP. As a result, Ca2+ ATPases of the endoplasmic (sarcoplasmic) reticulum and the plasma membrane are stopped. The rising cytosolic Ca2+ level cannot be counterbalanced due to damage of mitochondria which, under normoxic conditions, act as safety device against increased cytosolic Ca2+. It is proposed that prooxidants are toxic because they impair the ability of mitochondria to retain Ca2+.

Animals↗
PubMed1988

Normal oxidative damage to mitochondrial and nuclear DNA is extensive.

Oxidative damage to DNA can be caused by excited oxygen species, which are produced by radiation or are by-products of aerobic metabolism. The oxidized base, 8-hydroxydeoxyguanosine (oh8dG), 1 of approximately 20 known radiation damage products, has been assayed in the DNA of rat liver. oh8dG is present at a level of 1 per 130,000 bases in nuclear DNA and 1 per 8000 bases in mtDNA. Mitochondria treated with various prooxidants have an increased level of oh8dG. The high level of oh8dG in mtDNA may be caused by the immense oxygen metabolism, relatively inefficient DNA repair, and the absence of histones in mitochondria. It may be responsible for the observed high mutation rate of mtDNA.

Alloxan↗
PubMed1987

NADP+ phosphatase: a novel mitochondrial enzyme.

Mitochondria contain a NADP+ phosphatase in the matrix space. This is shown by both incubation of mitochondria and subfractions derived thereof with added NADP+ and by analysis of endogenous pyridine nucleotides after enzymatic oxidation in Ca2+-loaded mitochondria. The apparent KM for NADP+ is about 1.2 mM. NADPH is not a substrate. The enzyme may be important for modulation of posttranslational modification of macromolecules in mitochondria.

Animals↗
PubMed1987

Mobilization of mitochondrial Ca2+ by hydroperoxy-eicosatetraenoic acid.

Hydroperoxy-eicosatetraenoic acids (HPETEs) and less effectively, also hydroxy-eicosatetraenoic acids (HETEs) stimulated Ca2+ release from rat liver mitochondria. Ca2+ release is accompanied by intramitochondrial pyridine nucleotide oxidation and hydrolysis. Both Ca2+ release and pyridine nucleotide oxidation are impeded when the flow of electrons between pyridine nucleotides and HPETE is impaired. Measurements of the mitochondrial membrane potential indicate that HPETE-stimulated Ca2+ release is not due to uncoupling of mitochondria. It is suggested that HPETEs and HETEs may act as mobilizers of mitochondrial Ca2+ during signal transduction related to proliferation and tumor promotion.

Animals↗
PubMed1987

[Roentgenologic data patterns and hemodynamics in biopsy-proven dilated myocardial diseases].

The chest plain images of 63 patients suffering from histologically proved dilated myocardial diseases: primary cardiomyopathy (27), active and residual myocarditis (23), toxic cardiomyopathy (3), endomyocardial fibrosis (2), thesaurismotic cardiomyopathy (2), obstructive intramural fine vessel diseases (6) were analysed and correlated with invasively determined parameters: end-diastolic volume index, wall mass index, left ventricular end-diastolic pressure, pulmonary artery mean pressure, ejection fraction. The x-ray findings proved to occur in four different patterns which were defined as left heart involvement and three different patterns of bilateral left and right heart involvement representing various stages of left heart failure. This kind of image evaluation with functional classification is characterized by increased sensitivity, accuracy and information in detail in comparison with the heart lung index or other usual procedures.

Adult↗
PubMed1987

[Choriocarcinoma: neutropenia--acute emergency].

A patient aged 21 with metastatic choriocarcinoma was treated with Methotrexate. After twice application a severe neutropenia developed. The treatment of the febrile granulocytopenic cancer patient receiving antineoplastic therapy was performed by human gammaglobulin, transfer factor, leucocyte transfusion and selective antimicrobial modulation.

Adult↗
PubMed1986

Menadione- (2-methyl-1,4-naphthoquinone-) dependent enzymatic redox cycling and calcium release by mitochondria.

The results presented in this paper reveal the existence of three distinct menadione (2-methyl-1,4-naphthoquinone) reductases in mitochondria: NAD(P)H:(quinone-acceptor) oxidoreductase (D,T-diaphorase), NADPH:(quinone-acceptor) oxidoreductase, and NADH:(quinone-acceptor) oxidoreductase. All three enzymes reduce menadione in a two-electron step directly to the hydroquinone form. NADH-ubiquinone oxidoreductase (NADH dehydrogenase) and NAD(P)H azoreductase do not participate significantly in menadione reduction. In mitochondrial extracts, the menadione-induced NAD(P)H oxidation occurs beyond stoichiometric reduction of the quinone and is accompanied by O2 consumption. Benzoquinone is reduced more rapidly than menadione but does not undergo redox cycling. In intact mitochondria, menadione triggers oxidation of intramitochondrial pyridine nucleotides, cyanide-insensitive O2 consumption, and a transient decrease of delta psi. In the presence of intramitochondrial Ca2+, the menadione-induced oxidation of pyridine nucleotides is accompanied by their hydrolysis, and Ca2+ is released from mitochondria. The menadione-induced Ca2+ release leaves mitochondria intact, provided excessive Ca2+ cycling is prevented. In both selenium-deficient and selenium-adequate mitochondria, menadione is equally effective in inducing oxidation of pyridine nucleotides and Ca2+ release. Thus, menadione-induced Ca2+ release is mediated predominantly by enzymatic two-electron reduction of menadione, and not by H2O2 generated by menadione-dependent redox cycling. Our findings argue against D,T-diaphorase being a control device that prevents quinone-dependent oxygen toxicity in mitochondria.

2,4-Dinitrophenol↗
PubMed1986

N-methyl-4-phenylpyridine (MMP+) together with 6-hydroxydopamine or dopamine stimulates Ca2+ release from mitochondria.

The nigrostriatal neurotoxin N-methyl-1,2,3,6-tetrahydropyridine (MPTP) causes Parkinsonism in humans and laboratory animals. MPTP neurotoxicity is dependent on its oxidation to N-methyl-4-phenylpyridine (MPP+). The mechanism by which MPP+ causes destruction of dopamine-containing nigrostriatal cells is unknown. Here we show that MPP+ but not MPTP is taken up by energized mitochondria. MPP+ in the presence of dopamine and particularly of 6-hydroxydopamine stimulates Ca2+ release from mitochondria. Ca2+ release is accompanied by hydrolysis of intramitochondrial pyridine nucleotides. Our findings suggest that the MPTP-induced model of Parkinson's disease may be due to a disturbed Ca2+ homeostasis in dopamine neurons.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1986

[Are thoracic radiographs in the recumbent position useful in the diagnosis of chronic left heart insufficiency? Comparison of x-ray findings with left ventricular hemodynamics].

108 patients (88 male, mean age 50 years, 20 female, mean age 49) having coronary heart disease (40), cardiomyopathy (39), hypertension (9), valvular disease (9), pulmonary diseases (5) and without cardiac diseases (6) underwent chest plain radiographs in standing and recumbent position immediately before being investigated invasively by left and right heart catheterisation, angiocardiography and coronary angiography. Two experienced radiologists evaluated the plain films with special reference to the findings of the heart and lung vessels, particularly the pulmonary veins. Dilatated veins of the upper lobes were observed more often if the radiograph was obtained from the recumbent patient. A significant close correlation with increased LVEDP was, however, revealed in both positions. A possible simulation of pathological dilatation of the venous trunci of the upper lobes merely due to the redistribution of the blood flow in the horizontal position was excluded. The results show that reliable conclusions can be drawn concerning chronic left ventricular failure if the characteristic pulmonary vein findings are visualised in patients both in the standing and in the recumbent position.

Adult↗
PubMed1985

Lipid peroxidation decreases the rotational mobility of cytochrome P-450 in rat liver microsomes.

Phenobarbital-induced rat liver microsomes were subjected to NADPH- and Fe2+-catalyzed lipid peroxidation. The formation of approx. 95 nmol malondialdehyde/mg protein during 18 min peroxidation at 37 degrees C was observed. Membrane rigidity measured by means of the steady-state fluorescence anisotropy rs of diphenylhexatriene increased in parallel with the malondialdehyde formation. Both the amount of malondialdehyde and rs remained constant thereafter during incubation of the peroxidized membranes for 2 h. The aminopyrine demethylase activity decreased by about 60% upon lipid peroxidation for 18 min, whereas no significant loss of benzphetamine demethylase activity within the same time range was observed. A time-dependent formation of protein complexes of high molecular weight, comprising most of the microsomal polypeptides, upon lipid peroxidation was observed in SDS-polyacrylamide gel electrophoresis. The effect of microsomal lipid peroxidation on protein-protein interactions was examined by measuring the rotational mobility of intact cytochrome P-450. Rotational diffusion was measured by observing the decay of flash-induced absorption anisotropy r(t) of the P-450 X CO complex. Analysis was based on a 'rotation-about-membrane normal' model with the equation r(t) = r1exp(-t/phi 1) + r2exp(-t/phi 2). In control microsomes, two classes (rapid and slow) of rotating populations of cytochrome P-450 were observed with phi 1 approximately equal to 150 microseconds, fraction r1/(r1 + r2) approximately equal to 40% and phi 2 approximately equal to 2 ms, fraction r2/(r1 + r2) approximately equal to 60%. A relatively small decrease in the rotational mobility of P-450 was observed by a 18-min lipid peroxidation, while a subsequent incubation of peroxidized microsomes for 2 h at 37 degrees C resulted in a dramatic immobilization of P-450 by the increase of both r2/(r1 + r2) approximately equal to 75% and phi 2 approximately equal to 10-25 ms. The decrease in the P-450 mobility during 18-min lipid peroxidation would be due to the rigidification of the lipid bilayer. However, because the lipid fluidity remained unchanged thereafter, the significant immobilization of P-450 by the subsequent 2-h incubation is deduced to be due to formation of protein aggregates.

Animals↗