7 edition of Biological Reactive Intermediates II:Chemical Mechanisms and Biological Effects found in the catalog.
April 1, 1982 by Springer .
Written in English
Advances in Experimental Medicine and Biology
|The Physical Object|
|Number of Pages||1476|
Suzanne M. Rodgers, and Jennifer L. Those symptoms are consistent with clinical studies in which exposures to carbon tetrachloride at approximatelyppm for periods of min resulted in headache, nausea and dizziness, but no deaths Davis Norling, Interaction of ethanol oxidation with glucuronidation in isolated hepatocytes, Biochem.
This causes the disruption of mitochondrial functions in the various parts of the body and hence ATP formation [24,34]. Davis also provided anecdotal data regarding compromised renal function in a worker experimentally exposed to carbon tetrachloride during an 8-h work day. However, changes in the methylation status of gene expression by xenobiotics such as aflatoxins, provides a mechanism by which its potential for expression can be altered in an epigenetic heritable manner, and it is expected that modifications in DNA methylation may result from threshold-exhibition events [51,52]. Measurement of the carbon tetrachloride concentrations up to 30 ppm were made at various breathing zone vicinities around the truck at the discharge end of the trip but these were made during periods of high wind and unlikely to be representative of the actual accident. ACS Central Science5 1
Inorganic Chemistry58 22 David Britt, Theodor Agapie. The DNA adducts are fairly resistant to DNA repair processes and this causes gene mutation and hence the development of cancers especially the hepatocellular carcinomas. Langmuir35 1 Preventive actions against proteolysis.
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The carcinogenic potency of AFB1 has been highly correlated to the extent of the covalent binding of AFBO, the metabolite of AFB1 to the cellular DNA, its capability of activating epigenetic mechanisms and the suppression of P53 genes tumor suppressor genes .
A number of xenobiotics are known to be inducers or inhibitors of CYPs. Molecular Pharmacology, 62, Diaz, David A. In these populations, individuals are exposed to aflatoxin contaminated foods as their daily meals with no choice of alternative foods especially people living in camps.
The second subject became nervous, nauseated, and listless, and the third subject experienced nausea, vomiting, dizziness, and became sleepy.
Aflatoxin Biological Reactive Intermediates II:Chemical Mechanisms and Biological Effects book and cyclochlorotine, a secondary metabolite of the fungus Penicillium islandicum that causes hepatic necrosis and has carcinogenic properties have been reported to have an effect on oxidative phosphorylation pathways.
The poor methods of harvesting of grains, storage and processing of the various foods; leads to food contamination with aflatoxin-producing fungi. No adverse effects were reported by any of the subjects and no changes in blood pressure or timed vital capacities were detected.
Journal of the American Chemical Society1 Cancer Research, 38, Simulation of the procedure resulted in carbon tetrachloride concentrations of in excess of ppm.
Evidence for hormesis is reviewed, and the hormesis model is contrasted with more widely accepted dose-response models in toxicology: a linear nonthreshold LNT model for mutagenesis and carcinogenesis, and a threshold model for most other toxicologic effects.
Colosi, Shixiang Gao, and Qingguo Huang. GSH is used as a cofactor by 1 multiple peroxidase enzymes involved in detoxification of peroxides generated from oxygen free radical attack on biological molecules; 2 transhydrogenases that reduce oxidized centers on DNA, proteins, and other biomolecules; and 3 glutathione S-transferases GST that conjugate GSH with endogenous substances like estrogens, exogenous electrophiles like aflatoxins and its metabolites, and other various xenobiotics.
Some of these include:. Relationship between pH and electrode potential as a function of temperature. GST in the alpha and pi classes are abundant in hepatocytes and are inducible by exogenous chemical substances and carcinogens like the aflatoxins [14,24].
There is scarce knowledge in the global population and various communities about the source, exposure risks of mycotoxins especially aflatoxins and their associated health problems. AFB activates these nuclear receptors to produce the metabolizing enzymes.
Kim, G. The concentration was estimated at 0. Hizukuri and J. Kalf,James J. The carbon tetrachloride concentrations were determined on the basis of the room volume and the amount of carbon tetrachloride necessary to achieve the desired concentration; there was no mention of air-flow rate or ventilation in the test room.
DOI: Cell Biochemistry, 9, Nitromethylene Insecticides Chapter They also cause genotoxicty and affect many various biochemical pathways where they cause metabolic activation, interact directly with DNA and causes mutations with eventual tumor formation [65,67].
Serum enzyme activities were monitored up to 7 days postexposure and remained within normal ranges.
Most human case reports were lack information on exposure concentrations and durations.iologicd Weractkxv ELSEVIER SCIENCE IRELAND Chemico-Biological Interactions 90 () Interaction of trichloromethyl free radicals with thymine in a model system: a mass spectrometric study Gerardo D.
Castro*a, John T. Simpsonb, Jos6 A. Castroa °Centro de Investigac/ones Toxicológicas CITEFAl CONICET Zufriategui - () Villa Martelli, Prov.
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