The 3942-cm-1 optical band in irradiated silicon.
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Biomedical subjects
Publications and source records attributed to K Bergman.
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Whole-body autoradiography was used to study the tissue distribution of the plasticizer di-(2-ethylhexyl) adipate (DEHA), labelled in the acid [carbonyl-14C] or alcohol [2-ethylhexyl-1-14C]moiety, after iv or ig administration to male mice and rats and pregnant mice. With both DEHA preparations, during the first 24 hr after administration high levels of radioactivity were observed particularly in the body fat, liver and kidneys (after iv and ig administration) and in the intestinal contents (after ig administration) of both species. After administration of [carbonyl-14C]DEHA, radioactivity was also registered in the adrenal cortex, corpora lutea of the ovary, bone marrow, forestomach mucosa, salivary glands and Harder's gland in both species. [2-ethylhexyl-1-14C]DEHA derived radioactivity was found in the bronchi in male mice. Radioactivity was observed in the foetal liver, intestine and bone marrow during the first 24 hr after iv or ig administration of [carbonyl-14C]DEHA to pregnant mice. There was very little accumulation of [2-ethylhexyl-1-14C]DEHA in the mouse foetus but some was found in the urinary bladder, liver and intestinal contents as well as in the amniotic fluid. In an absorption/elimination study in rats of doses of 25 microCi/kg body weight of [14C]DEHA administered ig, dissolved in corn oil or dimethylsulphoxide, blood levels of radioactivity increased somewhat faster and were two or three times higher when DMSO was the vehicle indicating poor absorption of DEHA from the corn oil solution which more accurately reflects human contact with DEHA. Little radioactivity from [carbonyl-14C]DEHA was recovered in the bile, whereas [2-ethylhexyl-1-14C]DEHA was excreted in the bile in significant amounts particularly when DMSO was the vehicle. There was evidence of enterohepatic circulation of DEHA. Radioactivity was also excreted in the urine. As shown by autoradiograms obtained 4 days after the administration of [14C]DEHA there was no retention of DEHA and/or its metabolites in the tissues of mice.
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We constructed a genetic map of the fla-che region of the Rhizobium meliloti chromosome using cotransduction with bacteriophage phi M12. Several other chromosomal markers located in the general area are included in the map. We isolated plasmids carrying wild-type DNA inserts that complement the mapped mutations from a genomic library carried in the broad-host-range vector pLAFR1. The complementation data obtained from the clones confirmed the contransduction map and clarified the exact order of several of the behavioral genes. A restriction map of this area was developed by using the cloned DNA. One of the five individual EcoRI fragments subcloned from the original clones complemented two of the behavioral mutations.
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Vitamin A has been shown to affect the in vitro metabolism of 2AAF. At low concentrations of retinol or retinyl palmitate, a decreased production of ring-hydroxylated as well as deacetylated and N-hydroxylated metabolites was observed, measured by high performance liquid chromatography. The increased mutagenicity of 2AAF observed after addition of vitamin A in the Ames test cannot therefore be explained as a result of stimulated N-hydroxylation. However, the addition of retinol was found to enhance the mutagenicity of the metabolite N-OH-2AAF in the presence of an S-9 fraction of rat liver homogenate. No differences with regard to the covalent binding of 2AAF or its metabolites to rat liver DNA/RNA in vivo could be demonstrated in animals fed diets with normal or high vitamin A content.
The highly mutagenic heterocyclic amines, 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and 2-amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ), are formed during heating of protein-rich foods. In order to gain information about the distribution and fate of IQ and MeIQ in vivo, a whole-body autoradiographic study of i.v.-injected 14C-labeled IQ and MeIQ has been performed in male NMRI, pregnant NMRI, and female C3H mice. IQ and MeIQ showed similar distribution patterns. At short survival times, the autoradiograms were characterized by an accumulation of radioactivity in metabolic and excretory organs (liver, kidney, bile, urine, gastric and intestinal contents, salivary glands, nasal mucosa, and Harder's gland), as well as in lymphomyeloid tissues (bone marrow, thymus, spleen and lymph nodes) and in endocrine and reproductive tissues (adrenal medulla, pancreatic islets, thyroid, hypophysis, testis, epididymis, seminal vesicles, ampulla, and prostate). The liver and kidney cortex were identified as sites of retention of nonextractable radioactivity. IQ and MeIQ showed a strong affinity for melanin. IQ and MeIQ passed the placenta, but no radioactivity was retained in fetal tissues. The results pinpoint the liver as a site of IQ- and MeIQ-mediated toxicity. Future studies of IQ and MeIQ may be guided by and clarify the role of other tissue localizations in the toxicity of IQ and MeIQ.
Occupational exposure to carbon disulfide (CS2) is associated with several adverse effects such as neurotoxicity, atherosclerosis, liver injury and endocrinal disturbances. In the present study, the distribution of CS2 and its metabolites after inhalation of 35S- or 14C-labelled CS2 was studied in adult male mice with whole-body autoradiography. CS2 itself was registered in body fat and in well-perfused tissues at survival times up to 2 hours. Very little CS2 was taken up by the brain. The distribution patterns of CS2 metabolites were very different after administration of C35S2 or 14CS2. 35S-Labelled metabolites were initially concentrated in the liver and kidney, but were rapidly eliminated from the body. There was evidence of an extensive metabolic incorporation of sulfur split off from CS2 during its biotransformation. 14C-Labelled metabolites were likewise concentrated in the liver and kidney, but were also observed in large amounts in the nasal mucosa, bronchi, bone, pancreas, thyroid, adrenal cortex and testis. A marked retention of non-extractable 14C-labelled metabolites was seen in the liver and thyroid. The results point to several sites of specific CS2-induced toxicity due to the tissue disposition of metabolites of CS2.
Occupational exposure to carbon disulfide (CS2) has been associated with an increased rate of spontaneous abortions. Animal experiments have shown that CS2 is embryotoxic and teratogenic. In the present study, the embryonal and foetal distribution of CS2 and its metabolites was studied after administration of 35S- or 14C-labelled CS2 to pregnant mice in different stages of gestation. CS2 and its metabolites passed the placenta at all stages of gestation. High levels of metabolites of CS2 were registered in the embryonic neuroepithelium. In mid and late gestation CS2 itself accumulated in the cerebrospinal fluid (CSF) of the brain. 14C-labelled metabolites of CS2 showed affinity for bone and were retained in the liver even at long survival times (24 hours). These localizations may be of significance for some of the reported teratogenic effects of CS2, such as hydrocephalus, ossification defects and foetal liver injury, and support the idea that CS2 and/or its metabolites are embryotoxic and teratogenic by acting directly on embryonal and foetal structures.
Clouds of Rhizobium meliloti were attracted to localized sites on the surface of the infectible region of alfalfa roots. This behavior, which required active motility and chemotaxis, was not species specific. Correlation between the behavior of various mutants and their competitiveness for nodulation suggests that cloud formation has a role in the infection of host legume roots by rhizobia.
General transduction by phage phi M12 in Rhizobium meliloti SU47 and its derivatives is described. Cotransduction and selection for Tn5 insertions which are closely linked to specific loci were demonstrated. A derivative of SU47 carrying the recA::Tn5 allele of R. meliloti 102F34 could be transduced for plasmid R68.45 but not for chromosomally located alleles. Phage phi M12 is morphologically similar to Escherichia coli phage T4, and restriction endonuclease analysis indicated that the phage DNA was ca. 160 kilobases in size.
The covalent binding of 14C-1,1,2-trichloroethylene (14C-TRI) metabolites to calf thymus DNA in vitro and to RNA and DNA of mouse brain, lung, liver, kidney, spleen, pancreas, and testis after repeated i.p. injections has been studied. Hydrolysates of DNA reacted with 14C-TRI in vitro and hydrolysates of RNA and DNA from selected organs were separated on Aminex A6 for quantitation of alkylation products. The presence of 3,N4-etheno(deoxy)cytidine, 1,N6-etheno(deoxy)adenosine and 1,N6-ethenoadenine was investigated. No radioactivity could be registered in DNA incubated with 14C-TRI in the absence of liver microsomes. Covalent binding of 14C-TRI to DNA took place in the presence of liver microsomes from control mice. The binding was enhanced by 50% if liver microsomes from phenobarbital pretreated mice were used. The radioactivity in DNA reacted with 14C-TRI and microsomes from control mice was eluted in early fractions and together with thymidine. The same two peaks appeared on chromatography of DNA incubated with 14C-TRI and liver microsomes from phenobarbital pretreated mice. In addition, radioactivity was eluted together with 1,N6-ethenoadenine. Radioactivity was registered in RNA and DNA from all of the studied organs after i.p. injections of 14C-TRI. The radioactivity in RNA increased in the order brain less than testis less than pancreas less than kidney less than liver less than lung less than spleen. The radioactivity in DNA increased in the order brain less than kidney less than testis less than lung less than pancreas less than liver less than spleen. Aminex A6 chromatography revealed that the entire radioactivity in RNA from liver and kidney and in DNA from kidney, testis, lung, pancreas, and spleen was due to metabolic incorporation, particularly into guanine and adenine. This finding indicates that the C-C bond in TRI is split, with the formation of C1-fragments, during biotransformation in vivo. In liver DNA, the metabolic incorporation of radioactivity was insignificant. Instead, the dominant part of the radioactivity in liver DNA was eluted in early fractions. The elution profile of radioactivity in liver DNA gave no direct evidence of the formation of TRI-DNA adducts in vivo. No etheno-derivatives were identified as alkylation products of TRI in vivo, which is consistent with current theories of the metabolic fate of TRI.
The spreading of Rhizobium meliloti strains in various autoclaved soils was measured by using simple modifications of established techniques. Behavioral mutants were used to demonstrate that efficient spreading requires active motility and chemotaxis. The rate of spreading was affected by physical or chemical differences among soils and by changes in water content.
With the growing concern for the health hazards of occupational exposure to toxic substances attention has been focused on the organic solvents, which are associated with both deleterious nervous system effects and specific tissue injuries. Relatively little is known about the distribution of organic solvents and their metabolites in the living organism. Knowledge of the specific tissue localizations and retention of solvents and solvent metabolites is of great value in revealing and understanding the sites and mechanisms of organic solvent toxicity. Whole-body autoradiography has been modified and applied to distribution studies of benzene, toluene, m-xylene, styrene, methylene chloride, chloroform, carbon tetrachloride, trichloroethylene and carbon disulfide. The high volatility of these substances has led to the development of cryo-techniques. Whole-body autoradiographic techniques applicable to the study of volatile substances are reviewed. The localizations of nonvolatile solvent metabolites and firmly bound metabolites have also been examined. The obtained results are discussed in relation to toxic effects and evaluated by comparison with other techniques used in distribution studies of organic solvents and their metabolites.
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Current evidence suggests that a correlation exists between the capacity to perform excision repair of UV-induced DNA damage and maximum lifespan in different species. Preliminary evidence has also indicated differences of DNA repair capacities in lymphocytes of several strains of mice congenic at the H-2 locus. It is known that the H-2 system influences maximum lifespan potential in mice. In the present studies excision repair of UV-induced DNA damage, but not gamma-induced damage, was found to correlate the mean survival in the adult inbred mouse strains NZB and CBA, using PHA stimulated splenic lymphocytes. Furthermore, in (NZB X CBA)F2 hybrid with adult progeny the level of DNA repair of UV-induced damage corresponded to the H-2 allele (H-2d/2d from NZB or H-2b/2b from CBA) inherited from the parental strain. These studies suggest the possibility of a tricornered relationship between the main histocompatibility complex, one form of DNA repair, and lifespan within the species.