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From the causality of Nuclear transmutation to Genomic mutation
- 1. Jayakar Johnson Joseph FROM THE CAUSALITY OF NUCLEAR TRANSMUTATION TO GENOMIC MUTATION
- 2. INTRODUCTION Debating: Chronic intrinsic radiation from in-vivo radioactive decay is mutagenic, and not the direct effect of acute external radiation. In comparison with other industrial applications, radiation hazards from Healthcare, is negligible and easily manageable with safety standards
- 3. MUTAGENESIS Nuclear Transmutation Chronic Intrinsic Ionizing Radiation Food web & Food chain Radiation from Industry Point mutations Large-scale mutations CarcinogenicOncogenicMetabolicUsefulRepairable MANIFESTATION Evolution TumorsMetabolic disorders Manifestation Hierarchy
- 4. Nuclear transmutation Conversion of one chemical element or isotope into another eg. Potassium-40 Argon-40 Caused by: 1. Nuclear reaction: Chain reaction External particle reacts with a nucleus 2. Radioactive decay No external particle needed to trigger... ??
- 5. Food Chain from Food Web Radioactive Isotope reaches Humans through Food chain
- 6. Ionizing Radiation from Radioactive decay An ion is an atom or molecule in which the total number of electrons is not equal to the total number of protons, giving it a net positive or negative electrical charge. Ionization is the process of converting an atom or molecule into an ion by adding or removing charged particles such as electrons or other ions.
- 7. Mutagenesis Mutations are changes in a genomic sequence: the DNA molecular sequence Viral Cytosine, Guanine, Adenine, Thymine, Uracil MUTATION PHENOMENA Modification of bases Spontaneous hydrolysis Cross linking Dimerization Intercalation between bases Molecular Ionic variability Backbone damage Atomic Ionic variability Chronic Intrinsic Ionizing radiation Insertional mutagenesis
- 8. Pathological Manifestations of Mutations Change in Cellular Physiology Change in Cellular Architecture Change in Apoptosis Metabolic disorders Oncological disorders Carcinogenesis Excluding phenotypic manifestations If chronic intrinsic ionizing radiation persists
- 9. Conclusions: Supportive reference In biological systems, Chronic intrinsic ionizing radiation is mutagenic that is not the direct effect of acute external radiation. 1. All isotopes of an element have same in-vivo biochemical activity, whereas there biophysical activity differs. 2. Autofluorescent cell organelles: • Mitochondria • Lysosome 3. Photosynthesis Is Fusion and Fission are spontaneous and interrelated phenomenon … ??
- 10. Thank you Q & A
Editor's Notes
- Wilhelm Conrad Röntgen (27 March 1845 – 10 February 1923) was a German physicist, who, on 8 November 1895, produced and detected electromagnetic radiation in a wavelength range today known as X-rays or Röntgen rays, an achievement that earned him the first Nobel Prize in Physics in 1901
- Mutation ranges from Point mutations to Large-scale mutations
- Radioactive decays can be considered to be spontaneous nuclear reactions, as such a thing as a spontaneous chemical reaction.
- Spontaneous hydrolysis: DNA is not entirely stable in aqueous solution. Under physiological conditions the glycosidic bond may be hydrolyzed spontaneously and 10,000 purine sites in DNA are estimated to be depurinated each day in a cell. Numerous DNA repair pathway exist for the DNA, however, if the apurinic site failed to be repaired, misincorporation of nucleotide may occur during replication. Adenine is preferentially incorporated by DNA polymerases in an apurinic site. Cytidine may also become deaminated to uridine at one five-hundredth of the rate of depurination and can result in G to A transition. Eukaryotic cells also contains 5-methylcytosine, thought to be involved in the control of gene transcription, which can become deaminated into thymine. Modification of bases: Bases may be modified endogenously by normal cellular molecules. For example DNA may be methylated by S-adenosylmethionine, and glycosylated by reducing sugars. Many compounds, such as PAHs, aromatic amines, aflatoxin and pyrrolizidine alkaloids may form reactive oxygen species catalyzed by cytochrome P450. These metabolites form adducts with the DNA, which can cause errors in replication, and the bulky aromatic adducts may form stable intercalation between bases and block replication. The adducts may also induce conformational changes in the DNA. Some adducts may also result in the depurination of the DNA, it is however uncertain how significant the depurination as caused by the adducts is in generating mutation. Some alkylating agents such as N-Nitrosamines may also require the catalytic reaction of cytochrome-P450 for the formation of a reactive alkyl cation. Alkylation and arylation of bases can cause errors in replication. N7 and O6 of guanine and the N3 and N7 of adenine are most susceptible to attack; while N7-guanine adducts, which form the bulk of DNA adducts, appear to be non-mutagenic, alkylation at O6 of guanine is harmful because excision repair of O6-adduct of guanine may be poor in some tissues. The O6 methylation of guanine can result in G to A transition, while O4-methylthymine can be mispaired with guanine. The type of the mutation generated however may be dependent on the size and type of the adduct as well as the DNA sequence. Ionizing radiations and reactive oxygen species often oxidize guanine to produce 8-oxoguanine. Crosslinking: Some alkylating agents may produce crosslinking of DNA. Some natural occurring chemicals may also promotes crosslinking, such as psoralens after activation by UV radiation, and nitrous acid. Interstrand cross-linking blocks replication and transcription and can cause chromosomal breakages and rearrangements. Some crosslinkers such as cyclophosphamide, mitomycin C and cisplatin are used as anticancer chemotherapeutic because their high degree of toxicity to proliferating cells. Dimerization: UV radiation promotes the formation of a cyclobutyl ring between adjacent thymines, resulting in the formation of pyrimidine dimers. In human skin cells, thousands of dimers may be formed in a day due to normal exposure to sunlight. DNA polymerase η may help bypass these lesions in an error-free manner; however, individuals with defective DNA repair function, such as sufferers of Xeroderma pigmentosum, are sensitive to sunlight and may be prone to skin cancer. Intercalation between bases: Ethidium intercalated between two adenine-thymine base pairs. The planar structure of chemicals such as ethidium bromide and proflavine allows them to insert between bases in DNA, and cause frameshift mutation. The intercalation into DNA of anthracyclines such as daunorubicin and doxorubicin interferes with the functioning of the enzyme topoisomerase II, blocking replication as well as causing mitotic homologous recombination. Backbone damage: Arrows indicates chromosomal breakages due to DNA damage Ionizing radiations may produce highly reactive free radicals that can break the bonds in the DNA. Double-stranded breakages are especially damaging and hard to repair, producing translocation and deletion of part of a chromosomes. Alkylating agents like mustard gas may also cause breakages in the DNA backbone. Oxidative stress may also generate highly reactive oxygen species that can damage the DNA. Incorrect repair of other damages induced by the highly reactive species can also lead to mutations. The primary nucleobases are cytosine, guanine, adenine (DNA and RNA), thymine (DNA) and uracil (RNA), abbreviated as C, G, A, T, and U, respectively.