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H Dürk

Publications and source records attributed to H Dürk.

26 records · Page 2Linked to original sources

Fatty acids in liver microsomal lipids of rats exposed to hypoxia, tetrachloromethane, or both.

Arachidonic and docosahexaenoic acid in hepatic microsomal lipids from male Sprague-Dawley rats are greatly lowered when the animals have been exposed to tetrachloromethane; at the same time, palmitic, oleic and linoleic acid are significantly increased. Hypoxia alone causes similar derangements, but to a lesser extent. These are largely corrected 18 h after exposure; the effects induced by tetrachloromethane are persistent. The increases in 16:0, 18:1 and 18:2 suggest that in both cases microsomal enzymes involved in fatty acid metabolism are inhibited, either reversibly or irreversibly. Reduction of oxygen partial pressure during tetrachloromethane exposure has little effect upon hepatotoxicity as judged by hepatic enzymes in serum; only the onset of their release into the bloodstream is earlier.

Animals↗

Tetrachloromethane metabolism in vivo under normoxia and hypoxia. Biochemical and histopathological effects relative to alkane exhalation.

About 250 mumol/kg tetrachloromethane is metabolized by male Sprague-Dawley rats receiving a dose of 500 mumol/kg by inhalation. Determination of enzyme activities and histopathological assessment show that various parameters reflecting cellular injury do not differ for the same amount of tetrachloromethane metabolized under different oxygen partial pressures. On the other hand, the amounts of ethane and pentane exhaled under hypoxic conditions are greater than under normoxia. The previously reported differences in the toxicity of tetrachloromethane upon exposure under normoxia or hypoxia seem to be mainly due to the different amounts of tetrachloromethane metabolized under both conditions.

Alkanes↗

Binding of trichloromethyl radicals to lipids of the hepatic endoplasmic reticulum during tetrachloromethane metabolism.

Metabolism of tetrachloromethane (carbon tetrachloride) by liver microsomal fraction under anaerobic conditions and in vivo leads to covalent binding of trichloromethyl radicals to lipids. The resulting covalently modified lipids contain two different types of fatty acids: a group of monomeric trichloromethyl fatty acid residues, usually with one double bond less than the precursor fatty acids, and a group of fatty acids that are not sufficiently volatile for gas chromatography. The liquid-chromatographic properties of the latter indicate high molecular mass, presumably due to cross-linking. The chemical structures of the monomeric fatty acids were elucidated, and these support the view that the most significant reactive metabolite of tetrachloromethane is the trichloromethyl radical. The isomer patterns of the monomeric trichloromethyl fatty acids in vitro and in vivo are almost identical, which shows that anaerobic incubation of tetrachloromethane with microsomal fraction very well reflects the processes involved in hepatotoxicity of tetrachloromethane in vivo.

Animals↗

Carbon tetrachloride metabolism in vivo and exhalation of volatile alkanes: dependence upon oxygen partial pressure.

Metabolism of carbon tetrachloride in rats at atmospheric and reduced oxygen pressure has been determined indirectly by its disappearance from the inhaled air; it is inversely related to oxygen concentration and increases with decreasing partial pressure, as expected for reductive dehalogenation; oxygen partial pressure has been reduced to about a third of normobaric conditions. Concurrently exhalation of ethane and pentane as indication of lipid peroxidation has been monitored, showing a drastic increase when the oxygen partial pressure is reduced in the presence of carbon tetrachloride. Time course and duration of these processes indicate that the total metabolism of carbon tetrachloride is limited by the concomitant destruction of cytochrome P-450; also, oxidative destruction of polyunsaturated fatty acids apparently does not proceed beyond the end of metabolic activation of carbon tetrachloride. The molar ratios of the amount of metabolized carbon tetrachloride to the amounts of exhaled hydrocarbons lead to the same conclusion, namely that "lipid peroxidation" in this case does not proceed as an autocatalytic, self-propagating chain reaction.

Animals↗

Determination of alkanes in breath to monitor lipid peroxidation in the presence of volatile toxicants and metabolites. An optimized, automatic method.

Determination of alkanes in breath of laboratory animals and humans has become a standard-method for monitoring lipid peroxidation in vivo. Isothermal gas chromatography on Porasil C enables sensitive, rapid and repetitive determination of all C2-C5-hydrocarbons in breath. Volatile toxicants and metabolites, which would coelute with the alkanes of later injected samples, are deviated by using a precolumn. An automatic switching unit controls withdrawal and injection of samples and backflush of the precolumn in a repetitive manner at fixed intervals. This increases accuracy and sensitivity of analysis and enables virtually unattended operation. The system has been applied for a study on the oxygen-dependence of CCl4-metabolism in the rat.

Alkanes↗

[Keratomalacia in rheumatoid arthritis: immunohistologic and enzyme histochemical studies].

Corneal and conjunctival biopsies of 13 patients with rheumatoid arthritis and corneal ulceration (RA-keratomalacia) have been characterized by immunohistological and histochemical analysis. Biopsies from 13 patients with bacterial conjunctivitis, 7 patients with allergic conjunctivitis, 15 patients with senile cataract and 15 patients with keratokonus served as controls. The phenotypic composition of the conjunctival inflammatory infiltration of rheumatoid corneal ulceration was not significantly different from the other inflammatory eye diseases studied. However, conjunctival epithelial cells of all RA-patients showed strong de novo expression of HLA-DR- and DP-antigens. HLA-DQ-antigens were only weakly expressed in a minority of patients. In bacterial conjunctivitis a less intense HLA-class-II-expression was found to be restricted to HLA-DR-antigens. Furthermore, in RA patients stromal fibroblasts of the cornea expressed lysosomal elastase. Both observations could be explained by paracrine action of interleukins produced by infiltrating T-lymphocytes and macrophages. Thus, it might be tempting to speculate that immunologically induced, elastase mediated autodegradation of corneal stroma may be an important factor in the pathogenesis of rheumatoid corneal ulceration.

Antigens, Differentiation, T-Lymphocyte↗