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TOPIC: MCS ac Etiology: Redox and CYPs

MCS ac Etiology: Redox and CYPs 7 years 8 months ago #1

MCS usually originates from the airway epithelium and its sensory innervation - which has defects due to genetic disposition and environmental exposure.

A defective airway releases excessive inflammation subject to the detox enzyme chemical defense systems concerned with both xenobiotics and endogenous products such as aldehydes resulting from lipid peroxidation and the deactivation of reactive oxygen species (Yang 2008, Bolt 2006, Hayes 2005). It can be imagined they would be suppressed, inhibited, or overwhelmed in an extended chain reaction of oxidative stress (Deluca 2010).

Consumption of oxygen during normal cellular metabolism produces reactive oxygen and nitrogen species (RONS) most inactivated by antioxidant defenses including reduced glutathione, ascorbic acid, alpha tocopheral and enzymes superoxide dismutase, catalase, and glutathione peroxidase (Fisher-Wellman 2010, Datla 2007, Bains 1997, Halliwell 1994).

Balanced formation and inactivation of pro-oxidant species determine intracellular redox environment - represented by the ratios of interconvertable reduced (GSH) to oxidized (GSSG) form of glutathione - responsible for the initiation and regulation of many physiological processes within living systems.

Cellular functions that respond to shift in redox - favoring oxidizing or reducing conditions - include signal transduction, DNA and RNA synthesis, protein synthesis, enzyme activation, and regulation of the cell cycle (Shafer 2001).

A chronic oxidizing shift in redox - involving increased RONS production and decreased antioxidant defense - oxidative stress - has a role in many and varied disease conditions (Chung 2009, Dalle Donne 2006, Halliwell 1994).


"...NO...is formed on demand via the actions of NOS (nitric oxide synthase) on L-arginine...

...three distinct dimeric isoforms (Moncada 1997)...

...The form of NOS associated with immunological or infectious stimuli has been designated inducible NOS (iNOS), as its activation requires induction by cytokines and bacterially-derived lipopolysaccharides (Moncada 1991). Typically, a time lag of approximately 8 hrs is associated between induction of iNOS and detection of NO, in comparison to the extreme rapidity of the activation-response relationship of the constitutive isoforms...the amount of NO produced in the former instance is very high (micromolar range), as required for cytotoxity, whereas the biomodulatory nature of NO, produced via nNOS or eNOS activation, involves the synthesis of low (picomolar) quantities (Moncada 1997)...

...The assignment of the term 'constitutive' to the expression of the nNOS and eNOS isoforms highlights the fact that these enzymes are available for rapid activation in response to the appropriate intracellular signal (e.g. calcium), in contrast to iNOS, where the signal (e.g. cytokines) represents the initial trigger for de novo protein synthesis. However, the fact that nNOS and eNOS exist at a relatively constant expression level does not imply that these levels may not undergo long-term regulation...

...Changes in the regulation of expression of the constitutive isoforms of NOS have more often been associated with a variety of pathophysiological conditions..."


"...The NOS enzymes require optimal concentration of the cofactor BH4 and the substrate L-arginine for their function...

...BH4 induces a shift from O2- production by BH4 free iNOS to simultaneous NO and O2- production by BH4 repleted iNOS. When the antioxidant status of the microenvironment is insufficient to prevent the very rapid reaction between O2- and NO... peroxynitrite formation will occur...

...inhibition of iNOS retards the development of vascular injury in models characterized by oxyradical stress (e.g. atherosclerosis and transplantation) whereas in models with intact antioxidant capacity stimulation of iNOS mediates vasculoprotective effects...

...The importance of the endothelial isoform of NO synthase has been well established. Endothelium-derived NO has been shown to be essential for vascular homeostasis...

...Classically, iNOS has been regarded as an enzyme that produces nanomolar amounts of the NO radical, thereby causing cellular damage. The current study shows that iNOS can be a O2-, peroxynitrite as well as an NO-producing enzyme. The biological effects of iNOS not only depend on which radical species is released by the enzyme, but also on the antioxidant capacity of the cellular microenvironment of the enzyme..."


"...(i) LPS (bacterial lipopolysaccharides) induces the release of intermediary cytokines, which, in turn, induce NOS activity in Kupffer cells and hepatocytes;(ii) NO binds to heme iron in cytochromes P450 and prevents oxygen binding, thereby blocking enzyme activity; (iii) NO may also enhance degradation of cytochromes P450 by nitrosylation of heme or thiols in P450 apoprotein or impair transcriptional activation of P450...

...In summary, cytokine induced overproduction of NO could explain attenuation of activity, content, and transcription of cytochromes P450 by a diverse array of immunostimulants..."


"...the ubiquitous chemical defense network (phase I-II xenobiotic metabolizing and antioxidant enzymes) appears very early in the evolution and handles low molecular weight inorganic and organic xenobiotics, as well as endogenous non-protein signaling molecules, mediators of inflammation, degradation products, and toxic products of cellular metabolism (Goldstone 2006)..."

Phase I reactions form a new or modified functional group or a cleavage (oxidation, reduction, hydrolysis). These are non synthetic - the most important are cytochrome P450 isoenzymes (CYPs) that transfer electrons and catalyze oxidation.

Phase II reactions are synthetic - involving conjugation with an endogenous compound forming metabolites more polar and readily excreted by the kidneys and liver in urine and bile (Merck 1999).

Phase I and II enzymes apply to organic compounds including hydrocarbons of the ambient combustion aerosol.

A genetic finding among metabolizing enzymes is not necessary since the factor specific to MCS is the genetic propensity of sensory irritant receptors - their peptidenergic transmission - greater inflammatory release - furthering local tissue damage and setting forth the systemic reaction of oxidative stress.


Adamson A.W. Physical Chemistry of Surfaces. John Wiley, New York, NY 1982

Agopyan N et al. Negatively charged 2 and 10 micron particles activate vanilloid receptors, increase cAMP, and induce cytokine release. Tox and Appl Pharm 186(2): 63-76 2003

Andre E. et al. Cigarette smoke-induced neurogenic inflammation is mediated by alpha, beta-unsaturated aldehydes and the TRPA1 receptor in rodents. J Clin Invest 118:2574-82 2008

Baeza-Squiban A. et al. Diesel exhaust particles increase NFkB DNA binding activity and c-fos proto-oncogene expression in human bronchial epithelial cells. Tox In Vitro 13 817-22 1999

Bains J. & Shaw C. Neurodegenerative disorders in humans: the role of glutathione in oxidative stress-mediated neuronal death. Brain Res Rev 25:335-58 1997

Bandell M. et al. Noxious cold ion channel TRPA1 is activated by pungent compounds and bradykinin. Neuron 41:849-57 2004

Bang S. et al. Transient receptor potential A1 mediates acetaldehyde-evoked pain sensation . Eur J Neurosc 26:2516-23 2007

Baulig A. et al. Role of Paris PM2.5 components in the pro-inflammatory response induced in airway epithelial cells. Tox 261: 126-35 2009.

Baulig A. et al. Involvement of reactive oxygen species in the metabolic pathways triggered by diesel exhaust particles in human airway epithelial cells.Am J Physiol. Lung Cell mol Physiol 285 L671-679 2003a

Bautista D. et al. TRPA1 mediates the inflammatory actions of environmental irritants and proalgesic agents. Cell 124: 1269-82 2006

Bayram H. et al. The effect of diesel exhaust particles on cell function and release of inflammatory mediators from human bronchial epithelial cells in vitro. Am J Resp Cell Mol Biol 18:441-48 1998

Bedard A. and Parent A. Evidence of newly generated neurons in the human olfactory bulb. Dev Brain Res 151: 159-68 2004

Berg N.D. et al. Genetic susceptibility factors for multiple chemical sensitivity revisited. Int J Hyg Env H 213: 131-39 2010.

Bessac B. & Jordt S. Breathtaking TRP channels : TRPA1 and TRPV1 in airway chemosensation and reflex control. Phys 23:360-70 2008

Bessac B. et al. TRPA1 is a major oxidant sensor in murine airway sensory neurons. J Clin invest 118:1899-1910 2008a

Bessac B. et al. TRPA1 antagonists block the noxious effects of toxic industrial isocyanates and tear gases. FASEB J 23;4:1102-14 2009

Boland S. et al. Mechanisms of GSM-CSF release by diesel exhaust particles in human airway epithelial cells. Am J Phys 278: L25-32 2000

Boland S. et al. Diesel exhaust particles are taken up by human airway epithelial cells in vitro and after cytokine production. Am J Phys 276: L604-13 1999

Bolt H.M. & Their R. Relevance of the deletion polymorphisms of the glutathione-s-transferases GSTT1 and GSTM1 in pharmacology and toxicology. Curr Drug Metab 7:613-28 2006

Bolton J. et al. Role of quinones in toxicology. Chem Res Tox 13:135-60 2000

Bonvallot V. et al. Organic compounds from diesel exhaust particles elicit a pro-inflammatory response in human airway epithelial cells and induce cytochrome P450 1A1 expression. Am J Resp Cell Mol Biol 25: 515-21 2001

Bonvallot V. et al. Activation of transcription factors by diesel exhaust particles in human bronchial epithelial cells in vitro. Inhal Tox 12:359-64 2000

Brone B. et al. Tear gases CN, CR, and CS are potent activators of the human TRPA1 receptor. Tox Appl Pharm 231: 150-6 2008

Burtscher H. et al. Characterization of particles in combustion engine exhaust J Aerosol Sci 29:389-96 1998

Burtscher H. and Schmidt-Ott A. In situ measurement of adsorption and condensation of polyaromatic hydrocarbons on ultrafine c particles by means of photoemission. J Aerosol Sci 17:699-703

Cadle S.H et al. Composition of light duty motor vehicle particulat... in the Denver, Colorado area. Env Sc Tech 33;14: 2328-39 1999

Calderon-Garciduenas L. et al. Long-term air pollution exposure is associated with neuroinflammation, an altered innate immune response, disruption of the blood-brain barrier, ultrafine particulate deposition, and accumulationof amyloid beta-42 and alpha-synuclein in children and young adults. Tox Pathol 36: 289-310 2008

Calderon-Garciduenas L. et al. Brain inflammation and Alzheimer's-like pathology in individuals exposed to severe air pollution. Tox Pathol 32: 650-58 2004

Calderon-Garciduenas L. et al. Air pollution and brain damage. Tox Pathol 30: 373-89 2002

Calderon-Garciduenas L. et al. Respiratory tract pathology and cytokine imbalance in clinically healthy children chronically and sequentially exposed to air pollutants. Med hyp 55(5): 373-78 2000

Calderon-Garciduenas L., Maronpot R.R. et al. DNA damage in nasal and brain tissues of canines exposed to air pollutants is associated with evidence of chronic brain inflammation and neurodegeneration. Tox Pathol 31: 524-38 2003

Calderon-Garciduenas L., Mora-Tiscareno A. et al. Respiratory damage in children exposed to urban pollution. Pediatr Pulmonal 36: 148-61 2003

Calderon-Garciduenas L. et al. Respiratory tract pathology and cytokine imbalance in clinically healthy children chronically and sequentially exposed to air pollutants. Med Hyp 55(5): 373-378 2000

Christopoulos A. & El-Fakahany E. The generation of nitric oxide by G protein-coupled receptors. Life Sc 64;1:1-15 1999

Chung H. et al. Molecular inflammation: underpinnings of aging and age-related diseases. Ageing Res Rev 8:18-30 2009

Dai Y. et al. Sensitization of TRPA1 by PAR 2 contributes to the sensation of inflammatory pain. J Clin Invest 117:1979-87 2007

Dalle-Donne I. et al. Biomarkers of oxidative damage in human disease. Clin Chem 52:601-23 2006

Datla K.P. Short term supplementation with plant extracts rich in flavonoids protect nigrostriated dopaminergic neurons in a rat model of Parkinsons disease. Am Coll Nutr 26;4:341-49 2007

Deluca C. et al. Biological definition of multiple chemical sensiti... from redox state and cytokine profiling and not from polymorphisms of xenobiotic metabolizing enzymes. Tox and Appl Pharm 248: 285-92 2010

Deluca C. et al. The search for reliable biomarkers of disease in multiple chemical sensitivity and other environmental intolerances. Int J Env Res Pub H 8: 2770-97 2011.

Dinis P. Anandamide-evoked activation of vanilloid reeceptor I contributes to the development of bladder hyperreflexia and nociceptive transmission to spinal dorsal horn neurons in cystitis. J Neurosc 24:11253-263 2004

Escalera J. et al. TRPA1 mediates the noxious effects of natural sesquiterpene deterrents. J Biol Chem 283:24136-44 2008

Fisher-Wellman K.H. and Bloomer R.J. Exacerbated postprandial oxida...

stress induced by the acute intake of a lipid meal compared to isoenergetically administered carbohydrate, protein, and mixed meals in healthy young men. Am Coll Nutr 29;4:373-81 2010

Fung J. et al. Cytochrome P4501A1 in rat peripheral blood lymphocytes: inducibility in vivo and bioactivation of benzo[a]pyrene in the Salmonella typhimurium mutagenicity assay in vitro. Mutat Res 438:1-12 1999

Gavett S.H. et al. Capsaicin receptor antagonist and c-fiber depletion reduce pulmonary responses to particulate matter in BALB/c mice. The Toxicologists 18:405 1998

Gerde P. et al. The rapid alveolar absorption of diesel-soot adsorbed benzo[a]pyrene: bioavailability, metabolism, and dosimetry of an inhaled particle-borne carcinogen. Carcinogenesis 22;5:741-49 2001

Gerde P. et al. Benzo{a}pyrene at an environmentally relevant dose is slowly absorbed by, and extensively metabolized in, tracheal epithelium. Carcinogenesis 18:1825-32 1997

Gerde P. et al. Particle-associated polycyclic aromatic hydrocarbons - a reappraisal of their possible role in pulmonary carcinogenesis. Toxical Appl Pharmacol 108:1-13 1991

Goldstone J. et al. The chemical defensome: environmental sensing and response genes in the Strongylocentrotus purpuratus genome. Dev Biol 300:366-84 2006

Halliwell B. & Cross C. Oxygen derived species: their relation to human disease and environmental stress. EHP 102 (Suppl 10):5-12 1994

Harmsen A. et al. The role of macrophages in particle translocation from lungs to lymph nodes. Sci 230:1277-80 1985

Hayes J. et al. Glutathione transferases. Ann Rev Pharm Tox 45:51-88 2005

Hayes A. et al. Effects of neonatal administration of capsaicin on nociceptive thresholds in the mouse and rat. J Pharm Pharmacol 33;3:183-85 1981

Hinman A. et al.TRP channel activation by reversible covalent modification. Proc Nat Acad Sc USA 103:19564-568 2006

Holroyd K. et al. Genetic modeling of susceptibility to nitrogen dioxide-induced lung injury in mice. Am J Physiol 273;1-3:L595-602 1997

Huisman A. et al. Anti-inflammatory effects of tetrahydrobiopterin (BH4) on early rejection in renal allografts:modulation of inducible nitric oxide synthase. FASEB J 10.1096/FJ01-0890FJE 2002

Ichinose T. et al. Murine strain differences in allergic airway inflammation and immunoglobulin production by a combination of antigen and diesel exhaust particles. Tox 122;3:183-92 1997

Inoue K-i. et al. Effects of nanoparticles on antigen-related airway inflammation in mice. Resp Res 6:106 2005

Inoue T. & Bryant B. Multiple types of sensory neurons respond to irritating volatile organic compounds (VOCs): calcium fluorimetry of trigeminal ganglion neurons. Pain 117:193-203 2005

Jordt S. et al. Mustard oils and cannabinoids excite sensory nerve fibres through the TRP channel ANKTM1. Nature 427:260-65 2004

Jung C.G. Psychological Types. Princeton University Press and in the Portable Jung Viking Press 1921

Khatsenko O. et al. Nitric oxide is a mediator of the decrease in cytochrome P450-dependent metabolism caused by immunostimulants. Proc N Acad Sc USA 90:11147-51 1993

Kimata H. Effect of exposure to volatile organic compounds on plasma levels of neuropeptides, nerve growth factor, and histamine in patients with self reported multiple chemical sensitivity. Int J Hyg Env H 207:2 159-63 2004.

Kittelson D.B. Engines and nanoparticles: a review. J Aerosol Sci 29: 575-88 1998

Kleeberger S. Genetic susceptibility to ozone exposure. Tox Lett 82-83:295-300 1995

Kleeman M.J. et al. Size and composition distribution of fine particle matter emitted from woodburning, meat charbroiling, and cigarettes. Env Sc Tech 33;20: 3516-23 1999

Kumagai Y. et al. Generation of reactive oxygen species during interaction of diesel exhaust particle components with NADPH-cytochrome reductase and involvement of the bioactivation in the DNA damage. Free Rad Biol Med 222:479-87 1997

Kumagai Y. et al. Apparent inhibition of superoxide dismutase activity in vitro by diesel exhaust particles. Free Rad Biol Med 18:365-71 1995

Lewis J. et al. Trigeminal uptake and clearance of inhaled manganese chloride in rats and mice. Neurotox 26: 113-23 2005

Li N. et al. Induction of heme oxygenase-1 expression in macrophages by diesel exhaust particle chemicals and quinones via the antioxidant-responsive element. J Immunol 165: 3393-3401 2000

Lucchini R.G. et al. Neurological impacts from inhalation of pollutants and the nose-brain connection. Neurotox (2011) doi:10.1016/j.neuro.2011.12.001 in press

Lundborg M. et al. Ability of rabbit alveolar macrphages to dissolve metals. Exp Lung Res 7:11-22 1984

Macpherson L. et al. Noxious compounds activate TRPA1 ion channels through covalent modification of cysteines. Nature 445:541-45 2007

Matsui Y. et al. Tracking the pathway of diesel exhaust particles from the nose to the brain by x-ray florescense analysis. Spectrochimica Acta Part B 64: 796-801 2009

McNamara C. et al. TRPA1 mediates formalin-induced pain. Proc Nat Acad Sc USA 104:31525-30 2007

Meggs W.J. Hypothesis for induction and propagation of chemical sensitivity based on biopsy studies. Env H Perspect 105(2): 473-78 1997

Meggs W.J. et al. Nasal pathology and ultrastructure in patients with chronic airway inflammation (RADS and RUDS) following an irritant exposure. J Tox Clin Tox 34;4: 383 1996

Meggs W.J. and Cleveland Jr. C.H. Rhinolaryngoscopic examination of patients with multiple chemical sensitivity syndrome. Arch Env H 48: 1-14 1993

Merck Manual of Diagnosis and Therapy 17th Ed. Drug Input and Disposition; Metabolism. Chapter 298: pg 2563 Merck Research Laboratories 1999

Miyabara Y. et al. Murine strain differences in airway inflammation caused by diesel exhaust particles. Eur Resp J 11: 291-98 1998

Miyabara Y. et al. Diesel exhaust enhances allergic airway inflamma... and hyperesponsiveness in mice. Am J Resp Crit Care Med 157: 1138-44 1998a

Mohankumar S.M.J. et al. Particulate matter, oxidative stress and neurotoxicity. Neurotox 29: 479-88 2008

Molliere M.et al. Metabolism of benzo[a]pyrene in the combined rat liver-lung perfusion system. Tox 45:143-54 1987

Moncada S. et al. XIV. International Union of Pharmacology nomenclature in nitric oxide research. Pharmacol Rev 49:137-42 1997

Moncada S. et al. Nitric oxide: physiology, pathophysiology, and pharmacology. Pharmacol Rev 43:109-42 1991

Nassini R. et al. The 'headache tree' via umbellone and TRPA1 activates the trigeminovascular system. Brain doi:10 1093/brain/awr272 2011

Natusch D.F.S. and Tomkins P.A. Theoretical consideration of the adsorption of polynuclear aromatic hydrocarbon vapor onto fly ash in a coal-fired power plant. In Jones P.W. and Freudenthal R.I. (eds) Polynuclear Aromatic Hydrocarbons, Ravan Press, New York, NY 3:145-53 1978

Nielsen G.D. Mechanisms of activation of the sensory irritant receptor by airborne chemicals. Crit Rev Tox 21;3:183-208 1991

Nel A.E. et al. The role of particulate pollutants in pulmonary inflammation and asthma:evidence for the involvement of organic chemicals and oxidative stress. Curr Opin Pulm Med 7: 20-26 2001.

Nielsen G.D. Mechanisms of activation of the sensory irritant receptor by airborne chemicals. Crit Rev Tox 21:3:183-208 1991

Nyberg K. et al. Estimation of PH in individual alveolar macrophage phagolysosomes. Exp Lung Res 15:499-510 1989

Oortgiesen et al. Residual oil fly ash and charged polymers activate epithelial cells and nociceptive sensory neurons. Am J Physiol Lung Cell Mol Physiol 278: L683-95 2000

Pakkanen T.A. et al. Size distributions of mass and chemical compon... in street-level and rooftop PM1 particles in Helsinki. Atmosph Env 37: 1673-90 2003

Pereira W. Chlorination studies AM. II. The reaction of aqueous hypochlorous acid with alpha-amino acids and dipeptides. Biochem Biophys Acta 313:170-80 1973

Prior M. et al. Capsaicin pretreatment modifies hydrogen sulphide-induced pulmonary injury in rats. Tox Pathol 18;2:279-88 1990

Roy et al. Susceptibility to pollutant-induced airway inflammation is neurogenically mediated. EPA EIMS Metadata report 59754 2000

Satoh H. et al. Inhibitory effects of capsazepine and SR 48968 on citric acid-induced bronchoconstriction in guinea-pigs. Eur J Pharm 236;3:367-72 1993

Scheerens H. et al. The involvement of sensory neuropeptides in toluene diisocyanate-induced tracheal hyperreactivity in the mouse airways. Br J Pharm 119;8:1665-71 1996

Shafer F. & Buettner G. Redox environment of the cell as viewed through the redox state of the glutathione disulfide/glutathione couple. Free rad Biol Med 30:1191-1212 2001

Society of Automotive Engineers. Schematic of diesel particles and vapor phase compounds. SAE Paper no. 940233 1994

Steerenberg P.A. et al. Diesel exhaust particles induced release of interleukin 6 and 8 by (primed) human bronchial epithelial cells (BEAS 2B) in vitro. Exp Lung Res 24: 85-100 1998

Stone V. et al. The role of oxidative stressin the prolonged inhibitory effect of ultrafine carbon black on epithelial cell function. Tox in vitro 12:649-59 1998

Symanowicz P. et al. Lack of role for the vanilloid receptor in response to several inspired irritant air pollutants in the C57B1/6J mouse. Neurosc Lett 362:150-3 2004

Thomas R. et al. ETS1, NFkB and AP-1 synergistically transactivate the human GM-CSF promoter. Oncogene 14:Z845-55 1997

Thompson C.L et al. Relationships among benzo[a]pyrene metabolism benzo[a]pyrene-dial-epoxide DNA adduct formation and sister chromatid exchanges in human lymphocytes from smokers and nonsmokers. Cancer Res 49:6501-11 1989

Veronesi B. & Oortgiesen M. The TRPV1 receptor: target of toxicants and therapeutics. Tox Sc 89(1):1-3 2006

Veronesi B. et al. Effects of subchronic exposure to concentrated ambient particles VII Degeneration of dopaminergic neurons in APO E-1 mice. Inhal Tox 17; 4-5: 235-41 2005

Veronesi B. et al. Electrostatic charge activates inflammatory vanilloid (VR1) receptors. Neurotox 24: 463-73 2003

Veronesi B. et al. The surface charge of visible particulate matter predicts biological activation in human bronchial epithelial cells. Tox and Appl Pharm 178: 144-54 2002a

Veronesi B. et al. Particulate matter inflammation and receptor sensitivity are target cell specific. Inhal Tox 14(2): 159-83 2002b

Veronesi B. and Oortgiesen M. Neurogenic inflammation and particulate matter (PM) air pollutants. Neurotox 22: 795-810 2001

Veronesi B. et al. Vanilloid capsaicin receptors influence inflammatory sensitivity in response to particulate matter. Tox Appl Pharm 15;169(1): 66-76 2000

Veronesi B. et al. Particulate matter initiates inflammatory cytoki... by activation of capsaicin and acid receptors in a human bronchial epithelial cell line. Tox and Appl Pharm 154: 106-15 1999a

Veronesi B.et al. Neuropeptides and capsaicin stimulate the release of inflammatory cytokines in a human bronchial epithelial cell line. Neuropep 33;6: 447-56 1999b

Yang Y. et al. Endothelial glutathione-s-transferase A4-4 protects against oxidative stress and modulates iNOS expression through NF-kappa B translocation. Tox Appl Pharm 230:187-96 2008

Yeadon M. et al. Mechanisms contributing to ozone-induced bronchial hyperreactivity in guinea-pigs. Pulm Pharm 5;1:39-50 1992

Yeh H.C. et al. Comparisons of calculated respiratory tract deposition of particles based on the proposed NCRP model and the new ICRP66 MODEL. Aer Sci Tech 25:134-40 1996

Zhang L. Differential susceptibility to ozone-induced airways hyperreactivity in inbred strains of mice. Exp Lung Res 21;4:503-18 1995

Ziedinski H. et al. Modeling the interactions of particulates with epithelial lining fluid antioxidants. Am J Phys 277:L719-26 1999

Tags: CYPs, NO, NOS, P450, RONS, ROS, Redox, chemical, cytochrome, enzymes, More…
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MCS ac Etiology: Redox and CYPs 5 years 7 months ago #2

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That is a lot... I will not even try to pretend to understand it... I will however add this and hope somebody who has not been here in 2 years drops by to read it...


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