A detailed policy statement is available that describes the procedures used for unpublished proprietary data so that this information can be used in the evaluation without compromising its confidential nature (WHO (1990) Revised Guidelines for the Preparation of Environmental Health Criteria Monographs.
1.1.4 Effects on experimental animals and humans The data regarding developmental and reproductive toxicity show that lower fetal body weight in rats is the critical effect.
the cellular, metabolic, and chemical processes involved in different organs and to define rigorously how their interactions modulate the toxic response. Although research points to the importance of CYP2F2 in biomarker alterations (that is, BrdU labeling indices) that have been observed in styrene-exposed mice, the committee judged the studies to generally lack the scientific rigor necessary to ensure the validity of the conclusions. All the studies noted above relied on the intraperitoneal injection of styrene and its metabolites into the model species, the mouse, with the exception of Cruzan et al. (2012) study, which exposed mice via gavage. Consequently, the response of the candidate target organ, the lung, is based on the concentration of the compound delivered to it by the circulation. In none of the studies were the circulating concentrations determined. Other organ systems in the animal were exposed at the same time. When the response in another organ, the liver, was compared with that in the lung, it became clear that at least two organs are targets for cytotoxicity produced by styrene and its circulating metabolites. Studies of workers in the styrene industry found styrene or its metabolites in both blood and urine and identified a number of additional target organs in at least three other systems—the lymphohematopoietic system (bone marrow, lymph nodes, and spleen), gastrointestinal system (esophagus and pancreas), and urinary system (kidney and bladder)—that should be included in mechanistic studies that use animal models. The need to study other organs in addition to the lungs is especially true for studies in which metabolic capabilities of the model are altered by eliminating the genes for specific activation and detoxification enzymes in the animal as a whole. Additional studies that compare the kinetics of styrene metabolism using a range of recombinant P450 proteins, including CYP2F1 (the human orthologue of CYP2F2), are needed to establish the catalytic efficiency of these proteins with styrene. When both liver and lung were assessed in the studies evaluated in this section, the metabolic function and toxic response in both organs were altered. When gene manipulation was restricted to one organ, the liver, the toxic response in the other, the lung, was altered. Circulating concentrations of key compounds in the toxic response (when evaluated) were also altered. Taken as a whole, this evidence suggests that the activities and toxic responses of multiple organs may play a role in modulating the circulating concentrations of styrene, its metabolites, and other key compounds, such as glutathione, and in affecting the toxic response of other organs in the same individual.
Current talk about "a tremendous increase in cancer due to pollution and our unhealthy diet ofprocessed foods" merely reflects the facts that (1) we are not dying as childrenor young adults from violence, infection,malnutrition, or obstetrical catastrophes, but are living long enough to get cancer; (2) primitive societies do not always make the diagnosis of cancer when it strikes, and(3) people's fear of cancer makes them willing to believe obvious untruths.
On the basis of an assay of bronchiolar epithelial proliferation, bronchiolar toxicity, produced by both styrene-7,8-oxide enantiomers, was markedly lower in knockout than in wild-type mice and is equal to that of carrier-treated controls (Cruzan et al. 2012). Whether this was true for epithelium in other airways that were more proximal was not assessed. The study also found that the portion of bronchiolar epithelial cells, which contained BrdU labelling, actually decreased at higher doses of styrene, and this suggests that cells that have the potential for replication may be lost as part of the toxic response at higher doses. In CYP2F2-/mice in which a transgene for three human CYP450 mono-oxygenases (CYP2F1, 2A13, and 2B6) was inserted, lung toxicity, on the basis of the same proliferation assay, was observed with 4-vinylphenol but not styrene or the R- or S-styrene oxides (Cruzan et al. 2013). A major deficiency of these studies is that there were no quantitative measurements of the differences in metabolic capacity of the airways in wild-type and transgenic mice. How the presence of the CYP450 isozymes in the liver and other organs affected their response was not addressed. In knockout mice deficient in hepatic CYP450 reductase, which is critical for CYP450 function, lavage and serum markers of lung and liver toxicity were higher than in carrier-treated controls (Carlson 2012). Although the metabolism of styrene to the R- or S-styrene oxides was markedly reduced in the liver, production of the R-styrene oxide in the lungs doubled, and S-styrene oxide production was unchanged compared with controls.
The purpose of this report is to show proof - evidence - that microwave cooking is not natural, nor healthy, and is far more dangerous to the human body than anyone could imagine. However, the microwave oven manufacturers, Washington City politics, and plain old human nature are suppressing the facts and evidence. Because of this, people are continuing to microwave their food - in blissful ignorance - without knowing the effects and danger of doing so.
We have information that the primary difference between animal and plant proteins is their amino acid profiles and it is those profiles that direct the rates at which the absorbed amino acids are put to use within the body. Animal based proteins, of course, are much more similar to our proteins, thus are used more readily and rapidly than plant proteins. That is, ‘substrate’ amino acids derived from animal based proteins are more readily available for our own protein synthesizing reactions which allows them to operate at full tilt. Plant proteins are somewhat compromised by their limitation of one or more amino acids. When we restore the relatively deficient amino acid in a plant protein, we get a response rate equivalent to animal proteins. My own lab produced experimental data to support this view–and of course, similar observations of years past in other laboratories can also be interpreted in this way.
But my main thesis, insofar as my own work is concerned, is that our observations on protein and cancer, although studied in considerable detail, were signals of hypotheses that were more important and more global. Thus, I don’t especially like dwelling on the finer structural and functional characteristics of animal and plant proteins as being of great importance. Rather, my views are more along the lines of asking what are the consequences–both biologically and socioculturally–of our enormous reverence for protein, especially our unreasonable reverence for ‘high quality’ animal protein. It is on this path that I find some unusually significant gems.
The Bay Area Regional Health Inequities Initiative (BARHII) is a nationally recognized leader in transforming public health practice to advance health equity to create healthier communities. It is a collaborative of public health directors, officers, senior managers and staff from the 11 San Francisco Bay Area health departments and the California Department of Public Health. In 2017, BARHII transitioned its fiscal sponsorship to the Tides Foundation.
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Mismatch repair (MMR) has a central role in maintaining genomic stability by repairing DNA replication errors and inhibiting recombination between homologous sequences (Bellacosa, 2001). It is a post-replicative mechanism capable of eliminating base-base mismatches and insertion/deletion loops that arise during DNA synthesis. In the mammalian MMR system two heterodimeric complexes recognize mispaired bases; the hMSH2-hMSH3 (MutSs) complex, which preferentially recognizes insertion/ deletion loops; and the hMSH2-hMSH6 (MutSa) complex, which recognizes both base-base mispairs and insertion/ deletion loops. Two other proteins, and hPMS2, form a heterodimer (MutLa) that is then able to bind to the previously mentioned hMSH2 heterodimers. This complex is thought to interact with and recruit other proteins required for the repair process including Exo1, PCNA, RPA and Polg. In addition, a recent report demonstrated that MutLa is a latent endonuclease that is activated in the presence of a mismatch, MutSa, RFC, PCNA and ATP (Kadyrov et al., 2006). hMLH1 has been shown to form two other heterodimers, MutLs and MutLg, with the and hMLH3 proteins respectively. The roles of these two complexes in post-replicative error repair remains largely inconclusive, although it is believed that each could act as a "backup" for MutLa if the need arose. MMR improves the fidelity of DNA biosynthesis 100-1000 fold and reduces the error rate to one error per 1010 bases (Modrich and Lahue, 1996). Defective MMR results in mirosatellite instability (MSI), characterized by the expansion or contraction of the number of tandem repeats, due to polymerase slippage at the many microsatellite loci that occur throughout the genome.