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Biomedical subjects

A Hartwig

Publications and source records attributed to A Hartwig.

69 records · Page 4Linked to original sources
PubMed1981

[Effect of osmolarity and pH of the medium on the density of red blood cells of newborns and adults].

The influence of osmolarity and pH-value of a buffered saline glucose solution (BSG) on the density of red blood cells (RBC) of human newborns and adults were tested. The median density of RBC increases with increasing osmolarity by 1.2 mg/ml cells per 10 mosmol/l increase of osmolarity. This holds true for newborns and adults. The median density of RBC increases with increasing pH. The density of RBC of newborns increases by 5.7 mg/ml cells per one pH-unit increase, the density of RBC of adults increases by about 10.3 mg/ml cells per one pH-unit increase. These differences are probably caused by different physical-chemical properties of HbF and HbA.

Adult↗
PubMed1978

Successful cryopreservation of auricle fragments from rat hearts at -196 degrees C.

The influence of electrolyte composition and glucose concentration of a cryoprotective medium on the survival of auricle fragments from adult rat hearts after storage at -196 degrees C was investigated. Using a K+-, Mg++-, Ca++-rich solution with increased glucose concentration, a high rate of surviving fragments was found after cryopreservation.

Animals↗
PubMed1975

[Antimycin A-resistant oxygen consumption in rabbit reticulocytes].

In rabbit reticulocytes there exists an Antimycin A-resistent oxygen consumption. It amounts to about 20% of the total oxygen consumption, independently of the degree of maturation of the cells and of the presence of external substrates. The main substrate of the Antimycin A-resistent oxygen consumption is glucose, which is metabolized by the pentose phosphate pathway. NADP-dependent substrates provide more CO2 in the presence of Antimycin A. The 14CO2-formation from metabolites of the citric acid cycle and of metabolites directly connected with this cycle is decreased in the presence of Antimycin A, whereas no 14CO2 is formed from long-chain fatty acids. A H2O2-formation by a NADPH-oxygenase is postulated. The mitochondria contribute reducing equivalents to the cytosolic oxygen consumption. The postulated interactions include hydrogen transfer and the malate-shuttle.

Animals↗
PubMedDate not supplied

Comutagenicity and inhibition of DNA repair by metal ions in mammalian cells.

Mutagenic and/or carcinogenic metal compounds may act directly by interaction with DNA and/or indirectly by interference with genetic control and repair mechanisms. In a previous report, we investigated the mutagenicity and comutagenicity of nickel(II) in the V79 Chinese hamster HGPRT-assay. Our present findings demonstrate that like nickel(II), chromium(VI) and cadmium(II) are also comutagenic with UV. Furthermore, there is only a weak concordance with comutagenic effects observed in bacterial test systems. In the case of nickel(II), there is a good correlation between comutagenicity and inhibition of DNA repair, as determined by using the nucleoid sedimentation technique with HeLa cells. This inhibition may occur via replacement of other divalent ions essential in repair enzymes.

Animals↗
PubMedDate not supplied

Interaction of carcinogenic metal compounds with deoxyribonucleic acid repair processes.

The potentials of nickel(II) and cadmium(II) to interfere with the repair of different types of deoxyribonucleic acid (DNA) lesions was investigated. Concerning the nucleotide excision repair pathway, nickel(II) has been shown to reduce the incision and the ligation frequency after ultraviolet (UV)-irradiation. When applying a gel mobility shift assay and HeLa nuclear cell free extracts, nickel(II) diminishes the specific binding of a protein to UV-damaged DNA, suggesting that nickel(II) interferes with the DNA-protein interactions involved in the damage recognition after UV-irradiation. Similarly, the incision frequency is reduced in the presence of low concentrations of cadmium(II). Concerning the repair of oxidative DNA damage induced by visible light, non-cytotoxic concentrations of nickel(II) caused a complete repair inhibition of DNA base modifications like 7,8-dihydro-8-oxoguanine (8-hydroxyguanine) and of DNA strand breaks. Since the repair of DNA damage is essential for the prevention of cancer, its inhibition may account for the carcinogenic action of the respective metal compounds.

Arsenic↗