Search PubMed⌕ Search

Biomedical subjects

H Bartsch

Publications and source records attributed to H Bartsch.

At least 397 records · Page 22Linked to original sources
PubMed1981

[Breaking-out of osteosynthesis plate following femoral osteotomy near the hip joint (author's transl)].

Despite the progress in arthroplasty (TEP, double-cup plasty, ceramic prosthesis), adjustment osteotomy at the femur for prevention and treatment of osteoarthrosis of the hip is still an important procedure. It aims at reducing or removing pre-arthrotic deformity or at utilising remaining cartilaginous zones for taking part of the load. A wedge-shaped excision is usually performed in the intratrochanteric area. The fragments are then osteosynthesized under pressure by means of a blade plate (1, 2, 3, 4). If the osseous bridge between the blade and the osteotomy surface is too narrow, the blade may break out from its position. In such cases reosteosynthesis with a 90 degrees plate will not produce a stable result. The article describes three possibilities of saving the situation in such emergencies.

Adult↗
PubMed1981

Metabolic activation of aromatic amines and azo dyes.

Aromatic amines, amides and nitro compounds are a class of chemicals that produce tumors in a wide variety of tissues in experimental animals, including liver, urinary bladder, forestomach, small intestine, Zymbal's gland, subcutaneous tissue or skin. In man, exposure to some aromatic amines is associated with tumours of the urinary bladder and carcinoma of the renal pelvis. Their biological activity as carcinogens or genotoxic agents is, in all the cases that have been studied in detail, dependent on metabolic activation in vivo, occurring by multiple pathways. Differences in these metabolic pathways may largely account for the differences in tissues and species susceptibilities to cancer induction. Carcinogenicity of aromatic amines or amides is dependent on their oxidation to N-hydroxy derivatives, whilst the carcinogenicity of aromatic nitro compounds is linked to their reduction to hydroxylamines. Further conversion of the N-hydroxylamine or N-hydroxyamide to reactive intermediates can occur in several ways, which include (i) esterification of the N-hydroxy group, (ii) non-enzymic protonation of the nitrogen of the hydroxylamine and (iii) oxidation to a free radical of arylhydroxamic acids. Following generation of such reactive electrophilic intermediates in tissues or cells, macromolecular binding has been observed to nucleic acids and proteins. In many cases, arylamidated and arylaminated products are formed with nucleic acid bases; in the case of the well-studied 2-acetylaminofluorene, nucleophilic atoms of guanine are the predominant site of reaction. Relatively little is known of the structure and biological consequences of DNA adducts formed from other aromatic amines, amides or nitro compounds; more research in these directions is warranted.

1-Naphthylamine↗
PubMed1981

Mutagenicity of extracts of pickled vegetables collected in Linhsien County, a high-incidence area for esophageal cancer in Northern China.

Extracts of pickled vegetables commonly consumed in Linhsien County, a high-incidence area for esophageal cancer in Northern China, were studied for mutagenicity. The liquid residue from ethereal extracts produced a dose-dependent increase of mutants in Salmonella typhimurium TA98 and TA100 strains; mutagenicity required the presence of a fortified liver microsomal activation system induced by Aroclor 1254 in adult male BD VI inbred rats. An amount of extract equivalent to 2.8 g fresh pickled vegetables produced sixfold (75 revertants/g) and twofold (45 revertants/g) increases in revertant frequencies in strains TA98 and TA100, respectively. Roussin's red methyl ester, a tetranitroso compound, [(NO)2Fe(CH3S)]2, not previously reported to occur in nature, was isolated and identified from the ethereal extracts. The synthetic compound was mutagenic in strain TA100 in the presence of a liver activation system, producing 25 revertants/mumol. Findings on the presence of mutagenic compounds in pickled vegetables were discussed in relation to their possible etiologic role in cancer of the esophagus in Linhsien County.

China↗
PubMed1981

Mutagenicity studies in Salmonella typhimurium on some carcinogenic N-nitramines in vitro and in the host-mediated assay in rats.

N-Nitrodimethylamine, N-nitrodiethylamine, N-nitromorpholine and their N-nitroso analogs, N-nitrosodimethylamine, N-nitrosodiethylamine, and N-nitrosomorpholine, were tested in Salmonella typhimurium strains TA100 and TA1530. The mutagenicity of all compounds, except N-nitrodiethylamine, was demonstrated in liquid incubation assays in at least one of the tester strains; it required the presence of a postmitochondrial supernatant from the liver of Aroclor-treated rats, reduced nicotinamide adenine dinucleotide phosphate-generating system, and oxygen. When compared on a molar basis with their N-nitroso analogs, N-nitromorpholine was about 10 times less mutagenic and N-nitrodimethylamine about 70 times less mutagenic. Addition of disulfiram to the assays at a final concentration of 0.1 mM efficiently inhibited mutagenesis by all nitro and nitroso compounds; ascorbic acid at a 7.4 mM concentration produced less inhibition. Mutagenic activity of the three nitramines was also determined in the host-mediated assay in rats. After p.o. administration of each of the N-nitramines, cells of S. typhimurium strains TA1530 and TA100 that had been injected i.p. were isolated from the peritoneal liquid after 1, 3, and 6 hr. All three nitramines were found to be mutagenic for strain TA1530 but not for TA100. Mutation frequencies (number of histidine revertants per 10(6) surviving cells) were in the descending order N-nitromorpholine greater than N-nitrodiemethylamine greater than N-nitrodiethylamine. After a p.o. dose of N-nitrodiethylamine to rats, bacteria were also isolated from liver, lungs, and kidneys. Mutation frequency was highest in bacteria recovered from the liver but was not increased in those obtained from lungs and kidneys. The data suggest that carcinogenic nitramines exert their mutagenic effects through the formation of alkylating intermediates.

Animals↗
PubMed1981

[Metabolic activation and the mutagenic properties of carcinogenic N-nitramines in a liquid incubation test].

The study established the mutagenicity of carcinogenic dimethylnitramine and nitromorpholine in a liquid-incubation system using Salmonella typhimurium TA 100 and TA 1530 as indicator, in the presence of hepatic postmitochondrial supernatant obtained from 1254 aroclor-treated rats, oxygen and NADP+--generating system. Synthesis of mutagenic metabolites of nitramines was in correlation with the level of N-dimethylase activity. Ascorbic acid and disulfiram efficiently inhibited intramune-induced mutagenesis. Metabolic activation of nitramines involves (a) conversion of nitramines to nitrosoamines due to reduction of a nitro group, (b) hydroxylation by means of multi-function oxydases, and (c) heterolysis resulting in the formation of an end metabolite which is actually responsible for carcinogenicity and mutagenicity.

Aniline Compounds↗
PubMed1981

Quantitative estimation of endogenous nitrosation in humans by monitoring N-nitrosoproline excreted in the urine.

Endogenous formation of N-nitrosoproline (NPRO) was demonstrated by monitoring its excretion in the urine of a male volunteer who had ingested vegetable juice, as a source of nitrate, and proline. The resulting NPRO was analyzed after derivatization by combined gas-liquid chromatography thermal energy analysis. The amount of total NPRO excreted in the urine was found to be proportional to the proline dose and increased exponentially with the nitrate dose ingested. Neither nitrate nor proline, when taken alone, led to a detectable increase in NPRO in urine. The amounts of NPRO formed (as estimated from the amounts excreted within 24 hr) after dosing 325 mg nitrate (NO3-) followed by 500 mg proline, ranged from 16.6 to 30.0 (mean, 23.3) micrograms per person. The simultaneous intake of ascorbic acid or alpha-tocopherol inhibited nitrosation of proline in vivo. Monitoring of NPRO or other N-nitroso compounds excreted in the urine thus appears to be a suitable procedure for estimating daily human exposure to endogenously formed N-nitroso compounds.

Ascorbic Acid↗
PubMed1980

Mutagenicity of benzo[a]pyrene 7,8-dihydrodiol and 7,12-dimethylbenz[a]anthracene 3,4-dihydrodiol in S. typhimurium mediated by microsomes from rat liver and mouse skin.

The mutagenic activities of trans-7,8-dihydro-7,8-dihydroxybenzo[a]-pyrene (BP 7,8-diol) and of trans-3,4-dihydroxy-7,12-dimethylbenz[a]-anthracene (DMBA 3,4-diol) towards S. typhimurium TA100 were measured in assays that were carried out on a micro-scale in liquid medium in the presence of microsomal fractions prepared from mouse skin or rat liver. In the presence of an NADPH-generating system, microsomal enzymes converted both diols into mutagens that were probably the respective 'bay-region' diol-epoxides. The rate of the enzyme-catalysed conversion of the BP 7,8-diol into mutagens by microsomal preparations from mouse epidermis was similar to that occurring with microsomes from rat liver. Pretreatment of mice by the topical application of benz[a]anthracene (BA) or 7,12-dimethylbenz[a]-anthracene (DMBA) increased the mutagenic activity of BP 7,8-diol mediated by mouse skin microsomal preparations by 2-fold and this was paralleled by a 4-fold increase in epidermal aryl hydrocarbon (benzo[a]pyrene) hydroxylase (AHH) activity. The results are discussed in relation to the high susceptibility of mouse skin to polycyclic aromatic hydrocarbon (PAH) carcinogenesis.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1980

Mutagenicity in Salmonella typhimurium of N-3-methylbutyl-N-1-methyl-acetonyl-nitrosamine and N-methyl-N-benzylnitrosamine, N-nitrosation products isolated from corn-bread contaminated with commonly occurring moulds in linshien county, a high incidence area for oesophageal cancer in Northern China.

Two synthetic N-nitrosamines (N-3-methylbutyl-N-1-methyl acetonylnitrosamine and N-methyl-N-benzylnitrosamine), previously isolated from corn-bread which had been inoculated with moulds occurring in Linshien county, Northern China and subsequent nitrosation by sodium nitrite, were tested in Salmonella typhimurium strains TA1535 and TA100 in the presence of a liver postmitochondrial supernatant from Aroclor-treated rats. A concentration-dependent increase in the number of mutant colonies in both bacterial strains was observed when N-3-methylbutyl-N-1-methylacetonyl-nitrosamine was assayed in liquid suspension and N-methyl-N-benzylnitrosamine in plate incorporation assays. Our finding that mutagenic N-nitrosamines are present in foodstuffs that may be consumed in Linshien county are discussed in relation to the possible etiological role of these compounds in cancer of the oesophagus in that area.

Animals↗
PubMed1980

Carcinogenicity of chloroethylene oxide, an ultimate reactive metabolite of vinyl chloride, and bis(chloromethyl)ether after subcutaneous administration and in initiation-promotion experiments in mice.

Repeated s.c. administration of chloroethylene oxide, a reactive metabolite of the carcinogen vinyl chloride, induced local tumors in mice, with an incidence comparable to that of bis(chloromethyl)ether, a structurally related human and animal carcinogen, when both compounds were applied at maximum tolerated chronically toxic doses; no tumors distant from the injection site were produced. Bis(chloromethyl)ether, chloroethylene oxide, and its rearrangement product chloroacetaldehyde, a highly toxic compound, were further tested in an initiation-promotion experiment. Application to the skin of a single dose of either bis(chloromethyl)ether or chloroethylene oxide, followed by 3-times-weekly applications of 12-O-n-tetradecanoylphorbol-13-acetate for 42 weeks, produced skin tumors in mice; chloroacetaldehyde under comparable conditions produced no increase in benign or malignant tumors. A good correlation between the chemical reactivity, on the basis of hydrolysis constants in aqueous media, and the carcinogenicity of the three compounds was noted. Our results support the hypothesis that epoxidation of the thylenic double bond in vinyl chloride yields an ultimate carcinogenic metabolite, chloroethylene oxide, a highly reactive compound which appears also to be largely responsible for the known genetic changes caused by the parent compound.

Animals↗
PubMed1979

The association of bacterial mutagenicity of hydrocarbon-derived 'bay-region' dihydrodiols with the Iball indices for carcinogenicity and with the extents of DNA-binding on mouse skin of the parent hydrocarbons.

The mutagenic activities of benz[alpha]anthracene, 7-methylbenz[alpha]anthracene, 7,12-dimethylbenz[alpha]anthracene, 3-methylcholanthrene and benzo[alpha]pyrene, together with those of the trans-dihydrodiols derived from these hydrocarbons that would be expected to yield 'bay-region' vicinal diolepoxides on further metabolism have been examined in assays with S. typhimurium TA100 using post-mitochondrial supernatant fractions prepared from the livers of 3-methylcholanthrene-treated rats. Mutagenic activities obtained have been compared with: (a) the extents of reaction with DNA that occur in mouse skin following treatment with these hydrocarbons; (b) the carcinogenicities of the hydrocarbons expressed as Iball indices; (c) their activities as tumour-initiating agents on mouse skin. Close positive associations were found between the microsome-mediated mutagenicities of the dihydrodiols that could yield "bay-region" diol-epoxides and: (a) the extents of reaction with DNA in hydrocarbon-treated mouse skin; (b) the carcinogenic potencies of the parent hydrocarbons; although these correlations are not perfect, the mutagenic activities of the hydrocarbons themselves in microsome-mediated assays with S. typhimurium show no correlation with their extents of DNA binding on mouse skin and a poor correlation with their activities as initiating agents. These comparisons also indicated a statistically-significant positive correlation between carcinogenicity and the in vivo DNA binding on mouse skin treated with the hydrocarbons. Differences in the metabolic pathways by which polycyclic hydrocarbons are activated in vivo and in vitro are discussed in relation to the improved correlations found with the dihydrodiols.

9,10-Dimethyl-1,2-benzanthracene↗