Betreff: Damage Producing Reactive Oxygen Species (RO...

Von: prd34

Datum: Sat, 21 Jul 2007 10:21:10 -0700 (PDT)



I was reading about the production of Free Radicals and about how, in particular, a Reactive Oxygen Species (ROS), called Singlet Oxygen is produced:

We mentioned above that some of the reactive oxygen species (ROS) were not actually free radicals. That is the case for singlet oxygen, 1O2, which although not a free radical, behaves like one, and is extremely injurious to cells in the body.

One way in which singlet oxygen is generated is by the action of sunlight, particularly the ultraviolet part, whereby it breaks the bonds of normal diatomic oxygen, O2. Normal oxygen is generally very stable. However, when sunlight strikes the skin, any diatomic oxygen that is present may be broken down into singlet oxygen.
(The Miracle of Antioxidants, 2002, pp. 44-45, McCleod & White)

Now, I was thinking that

"Well, if ultraviolet rays which only hit the skin can cause the production of the ROS Singlet Oxygen within the body, then what about microwaves which pass right through the body?"

So I decided to do a search and found that microwave discarges are indeed used for this specific purpose - the creation of Singlet Oxygen. Now, if this can happen outside the body then there should be no reason why it also cannot happen inside the body in producing this "extremely-injurious-to-cells" ROS. Microwave exposure has been shown to induce a depletion of a number of the body's antioxidants: SuperOxide Dismutase (S.O.D.), Glutathione, and CoEnzyme Q10, and this might just explain - in part - why.

J Phys Chem A. 2007 Apr 26;111(16):3010-5. Epub 2007 Apr 4.

Quenching of I(2P1/2) by O3 and O(3P).

Azyazov VN, Antonov IO, Heaven MC.

Department of Chemistry, Emory University, Atlanta, Georgia 30322, USA.

Oxygen-iodine lasers that utilize electrical or microwave discharges to produce singlet oxygen are currently being developed. The discharge generators differ from conventional chemical singlet oxygen generators in that they produce significant amounts of atomic oxygen. Post-discharge chemistry includes channels that lead to the formation of ozone. Consequently, removal of I(2P1/2) by O atoms and O3 may impact the efficiency of discharge driven iodine lasers. In the present study, we have measured the rate constants for quenching of I(2P1/2) by O(3P) atoms and O3 using pulsed laser photolysis techniques. The rate constant for quenching by O3, (1.8 +/- 0.4) x 10(-12) cm3 s-1, was found to be a factor of 5 smaller than the literature value. The rate constant for quenching by O(3P) was (1.2 +/- 0.2) x 10(-11) cm3 s-1.

PMID: 17407271 [PubMed]

Now, the following studies show very clearly how dangerous the ROS Singlet Oxygen truly is - in that it can halt biological activity of a cell by causing DNA breaks:

Biochim Biophys Acta. 1989 Mar 1;1007(2):151-7.

Singlet molecular oxygen causes loss of biological activity in plasmid and bacteriophage DNA and induces single-strand breaks.

Di Mascio P, Wefers H, Do-Thi HP, Lafleur MV, Sies H.
Institut für Physiologische Chemie I, Universität Düsseldorf, F.R.G.

Damage of plasmid and bacteriophage DNA inflicted by singlet molecular oxygen (1O2) includes loss of the biological activity measured as transforming capacity in E. coli and single-strand break formation. Three different sources of 1O2 were employed: (i) photosensitization with Rose bengal immobilized on a glass plate physically separated from the solution; (ii) thermal decomposition of the water-soluble endoperoxide 3,3'-(1,4-naphthylidene) dipropionate (NDPO2); and (iii) microwave discharge. Loss of transforming activity was documented after exposing bacteriophage M13 DNA to 1O2 generated by photosensitization employing immobilized Rose bengal, and with bacteriophage luminal diameter X174 DNA, using the thermodissociable endoperoxide (NDPO2) as a source of 1O2. These findings are in agreement with experiments in which plasmid DNA pBR322 was exposed to a gas stream of 1O2 generated by microwave discharge. The effects of 1O2 quenchers and of 2H2O indicate 1O2 to be the species responsible. Strand-break formation in pBR322 and luminal diameter X174, measured as an increase of the open circular form at the expense of the closed circular supercoiled form, was observed without alkaline treatment after exposing the DNA to 1O2, using either agarose gel electrophoresis or sucrose gradient separation. The effect of quenchers and 2H2O indicate the involvement of 1O2 in DNA damage. We conclude that singlet oxygen can cause loss of biological activity and DNA strand breakage.
PMID: 2920171 [PubMed - indexed for MEDLINE]

FEBS Lett. 1987 Jan 19;211(1):49-52.

Loss of transforming activity of plasmid DNA (pBR322) in E. coli caused by singlet molecular oxygen.

Wefers H, Schulte-Frohlinde D, Sies H.

Plasmid DNA pBR322 in aqueous solution was exposed to singlet molecular oxygen (1O2) generated by microwave discharge. DNA damage was detected as loss of transforming activity of pBR322 in E. coli (CMK) dependent on the time of exposure. DNA damage was effectively decreased by singlet-oxygen quenchers such as sodium azide and methionine. Replacement of water in the incubation buffer by D2O led to an increase in DNA damage. 9,10-Bis(2-ethylene)anthracene disulfate was used as a chemical trap for 1O2 quantitation by HPLC analysis of the endoperoxide formed.
PMID: 3026841 [PubMed - indexed for MEDLINE]

Now, the next study also indicates the protective effects of both quenchers and antioxidants carotenoids and tocopherols:

Mutat Res. 1992 Sep;275(3-6):367-75.

Singlet oxygen induced DNA damage.

Sies H, Menck CF.
Institut für Physiologische Chemie I, Universität Düsseldorf, Germany.

Singlet oxygen generated by photoexcitation and by chemiexcitation selectively reacts with the guanine moiety in nucleosides (kq + kr about 5 x 10(6) M-1s-1) and in DNA. The oxidation products include 8-oxo-7-hydro-deoxyguanosine (8-oxodG; also called 8-hydroxydeoxyguanosine) and 2,6-diamino-4-hydroxy-5-formamidopyrimidine (FapyGua). Singlet oxygen also causes alkali-labile sites and single-strand breaks in DNA. The biological consequences include a loss of transforming activity as studied with plasmids and bacteriophage DNA, and mutagenicity and genotoxicity. Employing shuttle vectors, it was shown that double-stranded vectors carrying singlet oxygen induced lesions seem to be processed in mammalian cells by DNA repair mechanisms efficient in preserving the biological activity of the plasmid but highly mutagenic in mammalian cells. Biological protection against singlet oxygen is afforded by quenchers, notably carotenoids and tocopherols. Major repair occurs by excision of the oxidized deoxyguanosine moieties by the Fpg protein, preventing mismatch of 8-oxodG with dA, which would generate G:C to T:A transversions.
PMID: 1383777 [PubMed - indexed for MEDLINE]

This final study shows that 50 Hz Extremely Low Frequency Electromagnetic Fields can induce both cell proliferation and DNA damage. It also indicates the production of 8-hydroxy-2'-deoxyguanosine (8-OHdG), a hallmarker of oxidative damage, and one believed to proceed through a singlet-oxygen-involvment mechanism.

Biochim Biophys Acta. 2005 Mar 22;1743(1-2):120-9. Links

50-Hz extremely low frequency electromagnetic fields enhance cell proliferation and DNA damage: possible involvement of a redox mechanism.

Wolf FI, Torsello A, Tedesco B, Fasanella S, Boninsegna A, D'Ascenzo M, Grassi C, Azzena GB, Cittadini A.
Institute of General Pathology and Giovanni XXIII Cancer Research Center, L.go F. Vito, 1-00168 Rome, Italy.

HL-60 leukemia cells, Rat-1 fibroblasts and WI-38 diploid fibroblasts were exposed for 24-72 h to 0.5-1.0-mT 50-Hz extremely low frequency electromagnetic field (ELF-EMF). This treatment induced a dose-dependent increase in the proliferation rate of all cell types, namely about 30% increase of cell proliferation after 72-h exposure to 1.0 mT. This was accompanied by increased percentage of cells in the S-phase after 12- and 48-h exposure. The ability of ELF-EMF to induce DNA damage was also investigated by measuring DNA strand breaks. A dose-dependent increase in DNA damage was observed in all cell lines, with two peaks occurring at 24 and 72 h. A similar pattern of DNA damage was observed by measuring formation of 8-OHdG adducts. The effects of ELF-EMF on cell proliferation and DNA damage were prevented by pretreatment of cells with an antioxidant like alpha-tocopherol, suggesting that redox reactions were involved. Accordingly, Rat-1 fibroblasts that had been exposed to ELF-EMF for 3 or 24 h exhibited a significant increase in dichlorofluorescein-detectable reactive oxygen species, which was blunted by alpha-tocopherol pretreatment. Cells exposed to ELF-EMF and examined as early as 6 h after treatment initiation also exhibited modifications of NF kappa B-related proteins (p65-p50 and I kappa B alpha), which were suggestive of increased formation of p65-p50 or p65-p65 active forms, a process usually attributed to redox reactions. These results suggest that ELF-EMF influence proliferation and DNA damage in both normal and tumor cells through the action of free radical species. This information may be of value for appraising the pathophysiologic consequences of an exposure to ELF-EMF.
PMID: 15777847 [PubMed - indexed for MEDLINE]

Posted By prd34 to Do You Have Microwave Illness? at 7/22/2007 12:13:00 AM