{"id":{"repo_id":"mit","oai_identifier":"oai:dspace.mit.edu:1721.1/35699"},"canonical_url":"https://search.dev.ndltd.org/etd/mit/oai:dspace.mit.edu:1721.1/35699","repository":{"repo_id":"mit","name":"MIT","base_url":"https://dspace.mit.edu/oai/request"},"display":{"title":"The carcinogenicity, mutagenicity, and toxicity of arsenic and cadmium","abstract":"Recent epidemiological data has indicated that chronic exposure to metals such as arsenic and cadmium increases the risk of cancer and other diseases. These metals may have negative biological effects on cells by disrupting homeostatic cellular processes and altering normal signal transduction. One possible mechanism for many of these negative effects may involve overproduction of reactive oxygen species that damage proteins, lipids, carbohydrates, and nucleic acids. To compound this oxidative damage, there is evidence consistent with the inhibition of repair of damaged DNA by these metals. As a result, there is an increase in mutagenicity and toxicity in the organisms. This thesis reviews the current literature relevant to the biochemistry and biology of arsenic and cadmium.","abstract_html":"Recent epidemiological data has indicated that chronic exposure to metals such as arsenic and cadmium increases the risk of cancer and other diseases. These metals may have negative biological effects on cells by disrupting homeostatic cellular processes and altering normal signal transduction. One possible mechanism for many of these negative effects may involve overproduction of reactive oxygen species that damage proteins, lipids, carbohydrates, and nucleic acids. To compound this oxidative damage, there is evidence consistent with the inhibition of repair of damaged DNA by these metals. As a result, there is an increase in mutagenicity and toxicity in the organisms. 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