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Present investigation was undertaken to study the frequency and spectrum of induced viable macromutations employing SA, EMS and gamma radiation in chickpea (Cicer arietinum L.) cultivar Vishwas (Phule G 5). The seeds of chickpea, cultivar Vishwas were treated with three different concentrations / doses of SA (2, 3 and 4 mM), EMS (8, 12 and 16 mM) and gamma radiations (400, 500 and 600 Gy). The mutagen administered seeds were sown in experimental fields to raise M1 progeny. Seeds of M1 plants and control were harvested separately and sown to raise M2 population. The M2 progeny were screened for viable macromutaions. A wide spectrum of viable macromutations was isolated in the M2 generation. In all twenty four different types of viable morphological macromutations were observed. These included 7 types of plant type mutations and 6 types of leaf mutations, 1 types of flower mutation, 5 types of pod mutation and 5 types of seed mutations. Results indicated that all mutagenic treatments were effective in inducing viable mutations in chickpea, during M2 generation. Differences in response to different mutagens were observed in the spectrum and frequency of viable mutations. Some mutation types occurred more frequently than others. The frequency and spectrum of viable mutations were relatively high with EMS followed by gamma radiation and SA. In the present investigation, an attempt has been made for increasing frequency and spectrum of locally important chickpea cultivar ‘Vishwas’ employing chemical and physical mutagens.
Genotoxic carcinogens, able to damage DNA by alkylation reactions, represent a very diverse class of agents which are capable of producing a wide range of DNA modifications. The mechanisms leading to genetic changes as a result of exposure to alkylating agents (AAs) have been studied in male germ cells of Drosophila using a structure-activity relationship approach (SAR). The analytical tools available concern both genetic and molecular assays. The genetic tests enable to quantify excision repair and clastogenic potency of the AA after treatment of post-meiotic male germ cells and to determine the degree of germ-cell specificity, i.e., the mutagenic effectiveness in post-versus premeiotic cell stages. For a selected group of alkylating agents the molecular spectra have been studied in post-meiotic cell stages. On the basis of these descriptors clear SAR's between genotoxic activity in germ cells and physico-chemical parameters (s-values and O6/N7-alkylguanine adducts) and carcinogenic potency in rodents became apparent, resulting in five distinct classes of alkylating agents so far. These classes are: 1) SN2-type monofunctional AAs, 2) SN1-type monofunctional AAs, 3) polyfunctional AAs, 4) agents able to form etheno-DNA adducts, and 5) aflatoxin B1 (AFB1) a bulky-adduct forming agent. The recent finding that the molecular data obtained with Drosophila and data of the specific locus tests in male mice show remarkable similarities for most genotoxic agents supports the view that Drosophila is a useful model system for the study of transgenerational damage.
Ethenobases are exocyclic adducts formed with DNA by some environmental carcinogens such as vinyl chloride or urethane. In the last few years, they have received a renewed interest due to the development of sensitive techniques of analysis that made it possible to measure their formation in vivo. This minireview summarizes the information gained recently from the work of several laboratories, including ours. Increased levels of DNA etheno adducts have been measured in target tissues from rodents exposed to vinyl chloride or urethane. Hepatic tumours caused by exposure to vinyl chloride in humans and in rats and lung tumours induced by urethane in mice exhibit base pair substitution mutations in the ras and p53 genes which seem to be exposure-specific and consistent with the promutagenic properties of ethenobases. Background levels of etheno adducts have been detected in DNA from non-exposed humans or animals, pointing to an alternative, endogenous pathway of formation. This background may be affected by dietary factors. It could arise from the reaction of trans-4-hydroxy-2-nonenal (or its epoxide 2,3-epoxy-4-hydroxynonanal), a lipid peroxidation product, with nucleic acid bases. Elevated levels of etheno adducts are found in hepatic DNA from humans and rodents with genetic predisposition to oxidative stress and lipid peroxidation in the liver, and with an associated increased risk of liver cancer. These data suggest that DNA ethenobases could serve as new biomarkers of oxidative stressłipid peroxidation.
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