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Biomedical subjects

H Greim

Publications and source records attributed to H Greim.

At least 127 records · Page 7Linked to original sources
PubMed1976

Carcinogenic potential of chlorinated ethylenes tentative molecular rules.

Chlorinated ethylenes are activated in mammalian metabolism to oxiranes. Only those with asymmetric chlorine substitution are mutagenic (trichloroethylene, vinylidence chloride and vinyl chloride) whilst the symetric molecules (tetrachloroethylene, cis- and trans-1.2-dichloroethylene) are inactive in this respect. Thus, stability of the oxirances (higher in the symmetric molecules, lower in the asymmetric ones) seems to be the important feature for the mutagenic, and possibly carcinogenic potential.

Carcinogens↗
PubMed1975

Uptake of taurocholic acid into isolated rat-liver cells.

Binding and transport characteristics for uptake of taurocholic acid by isolated rat liver cells were studied. 1. An adsorption of taurocholate to the cell surface is terminated in less than 15 s. A Ks of 0.55 mM and a total binding capacity of 3.8 nmol/mg cell protein is determined. 2. The rate of uptake of taurocholate follows Michaelis-Menten kinetics with Km = 19 muM and V = 1.7 nmol/mg protein min. 3. There is a broad pH optimum for uptake between pH 6.5 -- 8.0. 4. The activation energy amounts to 29 kcal/mol. At high taurocholate concentration an unusual upward bend is observed in the Arrhenius plot. 5. Taurocholate uptake is competitively inhibited by taurochenodeoxycholate (Ki = 9 muM). It is noncompetitively inhibited by bromosulfophthalein (Ki = 3 muM). 6. At physiological taurocholate concentrations a 200-fold intracellular accumulation of taurocholate is observed. 7. Uptake is inhibited by about 75% by either antimycin A, carbonylcyanide m-chlorophenyl-hydrazone, ouabain. 8. Replacement of extracellular Na+ by either K+ or sucrose results in a 75% decrease of uptake. 9. It is concluded that taurocholate uptake is a carrier-mediated process, and suggested that the energy for intracellular accumulation is made available by cotransport of Na+.

Animals↗
PubMed1975

Cytochrome P-450 in the activation and inactivation of carcinogens.

The capacity of isolate mouse liver microsomes to alter the mutagenicity for bacteria of the primary carcinogen N-methyl-N'-nitro-N-nitrosoguanisine (MNNG) and the secondary one dimethylnitrosamine (DMN) was studied. Microsomal activation of DMN and inactivation of MNNG were decreased by protein- and protein-cholinedeficient diets and were increased by pretreatment with microsomal enzyme inducers. The decrease and increase paralleled the content of cytochrome P-450 present in the different microsomal preparations. With human liver microsomes of differing cytochrome P-450 contents similar correlation was obtained, whereas normal rat liver microsomes did not activate or inactivate DMN or MNNG. Oxidative demethylation of DMN by mouse liver microsomes and the activation of DMN to a mutagen followed similar kinetics. Both reactions were inhibited by carbon monoxide and the inhibition was maximally reversed by monochromatic light at 450 nm. These observations indicate that at least some carcinogens are activated or inactivated by the unspecific cytochrome P-450 dependent enzyme system, suggesting that the extent of this biotransformation may be one factor influencing human carcinogenesis.

Animals↗
PubMed1975

[Liver damage following intestinal by-pass surgery for weight reduction].

The jejuno-ileal bypass for weight reduction can hardly be considered a non-specific treatment: 3-4% of the patients develop chronic hepatic damage, 1-2% suffer hepatic failure due to massive fatty liver, rapidly progressing liver cirrhosis or hepatic fibrosis. Fatty liver is an invariable sequel of this operation. Once the above-mentioned symptoms set in or an incipient cirrhosis or fibrosis is diagnosed, immediate restoration of normal passage is required. The intestinal bypass syndrome observed in the patient (fem.) (viz. table 1) does not wholly coincide with the enteral bile acid loss syndrome occurring in extensive ileum resection (56) where usually there is no evidence of fatty liver, icterus, cholestasis or encephalopathy. Animal experiments seem to confirm that the blind loop in the broadest sense of the term is responsible for the sometimes fatal hepatic damage. Possibly we are confronted here with a pattern of hepatic damage due to toxic nutritive effects similar to cirrhosis as a sequel of low-protein and low-calorie intake or to the phenomenon observed in animal experiments. The cholestasis confirmed by biopsy and chemical methods is a manifestation of these hepatic disorders. The clinical aspects resemble the Reye syndrome that we know in pediatrics. Patients have to be carefully selected and informed about possible postoperative damage; a continuous clinical follow-up with biopsy of the hepatic tissue is also indicated.

Adult↗