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This chapter will focus on recent progress on the mechanisms of metalloid uptake, metabolism, and detoxification in bacteria, archaea, and eukaryotic microbes. One of the initial challenges of the earliest cells would have been the ability to detoxify heavy metal ions, transition metal ions, and metalloids, including arsenic and antimony. The presence of arsenic resistance () genes in the genome of by far most living organisms sequenced to date illustrates firstly that genes must be ancient and secondly that arsenic is still ubiquitous in the environment, providing the selective pressure that maintains these genes in present-day organisms. Some early cells also probably could use arsenite as an electron acceptor, giving selective pressure for the evolution of respiratory arsenate reductase. As atmospheric O levels increased, arsenite was oxidized to arsenate abiotically. This provided an advantage for the evolution of arsenate reductases, some for arsenate respiration and energy production, and others for arsenate detoxification. Present-day selective pressure for metalloid resistance also comes from sources such as natural release of arsenic from volcanic activities, mining activities, the burning of coal, and other human activities. In addition is the use of arsenicals and antimonials as chemotherapeutic drugs for the treatment of parasitic diseases and cancer. Resistance to these drugs is becoming a major dilemma. Thus, an understanding of the molecular details of metalloid transport systems and detoxification enzymes is essential for the rational design of new drugs, and for treating drug-resistant microorganisms and tumor cells. Finally, this chapter will summarize recent identification of novel enzymes for arsenic reduction, oxidation, and methylation that expand the possibilities for metalloid metabolism and transformations.

This chapter will focus on recent progress on the mechanisms of metalloid uptake, metabolism, and detoxification in bacteria, archaea, and eukaryotic microbes. One of the initial challenges of the earliest cells would have been the ability to detoxify heavy metal ions, transition metal ions, and metalloids, including arsenic and antimony. The presence of arsenic resistance () genes in the genome of by far most living organisms sequenced to date illustrates firstly that genes must be ancient and secondly that arsenic is still ubiquitous in the environment, providing the selective pressure that maintains these genes in present-day organisms. Some early cells also probably could use arsenite as an electron acceptor, giving selective pressure for the evolution of respiratory arsenate reductase. As atmospheric O levels increased, arsenite was oxidized to arsenate abiotically. This provided an advantage for the evolution of arsenate reductases, some for arsenate respiration and energy production, and others for arsenate detoxification. Present-day selective pressure for metalloid resistance also comes from sources such as natural release of arsenic from volcanic activities, mining activities, the burning of coal, and other human activities. In addition is the use of arsenicals and antimonials as chemotherapeutic drugs for the treatment of parasitic diseases and cancer. Resistance to these drugs is becoming a major dilemma. Thus, an understanding of the molecular details of metalloid transport systems and detoxification enzymes is essential for the rational design of new drugs, and for treating drug-resistant microorganisms and tumor cells. Finally, this chapter will summarize recent identification of novel enzymes for arsenic reduction, oxidation, and methylation that expand the possibilities for metalloid metabolism and transformations.

This chapter will focus on recent progress on the mechanisms of metalloid uptake, metabolism, and detoxification in bacteria, archaea, and eukaryotic microbes. One of the initial challenges of the earliest cells would have been the ability to detoxify heavy metal ions, transition metal ions, and metalloids, including arsenic and antimony. The presence of arsenic resistance () genes in the genome of by far most living organisms sequenced to date illustrates firstly that genes must be ancient and secondly that arsenic is still ubiquitous in the environment, providing the selective pressure that maintains these genes in present-day organisms. Some early cells also probably could use arsenite as an electron acceptor, giving selective pressure for the evolution of respiratory arsenate reductase. As atmospheric O levels increased, arsenite was oxidized to arsenate abiotically. This provided an advantage for the evolution of arsenate reductases, some for arsenate respiration and energy production, and others for arsenate detoxification. Present-day selective pressure for metalloid resistance also comes from sources such as natural release of arsenic from volcanic activities, mining activities, the burning of coal, and other human activities. In addition is the use of arsenicals and antimonials as chemotherapeutic drugs for the treatment of parasitic diseases and cancer. Resistance to these drugs is becoming a major dilemma. Thus, an understanding of the molecular details of metalloid transport systems and detoxification enzymes is essential for the rational design of new drugs, and for treating drug-resistant microorganisms and tumor cells. Finally, this chapter will summarize recent identification of novel enzymes for arsenic reduction, oxidation, and methylation that expand the possibilities for metalloid metabolism and transformations.

This chapter will focus on recent progress on the mechanisms of metalloid uptake, metabolism, and detoxification in bacteria, archaea, and eukaryotic microbes. One of the initial challenges of the earliest cells would have been the ability to detoxify heavy metal ions, transition metal ions, and metalloids, including arsenic and antimony. The presence of arsenic resistance () genes in the genome of by far most living organisms sequenced to date illustrates firstly that genes must be ancient and secondly that arsenic is still ubiquitous in the environment, providing the selective pressure that maintains these genes in present-day organisms. Some early cells also probably could use arsenite as an electron acceptor, giving selective pressure for the evolution of respiratory arsenate reductase. As atmospheric O levels increased, arsenite was oxidized to arsenate abiotically. This provided an advantage for the evolution of arsenate reductases, some for arsenate respiration and energy production, and others for arsenate detoxification. Present-day selective pressure for metalloid resistance also comes from sources such as natural release of arsenic from volcanic activities, mining activities, the burning of coal, and other human activities. In addition is the use of arsenicals and antimonials as chemotherapeutic drugs for the treatment of parasitic diseases and cancer. Resistance to these drugs is becoming a major dilemma. Thus, an understanding of the molecular details of metalloid transport systems and detoxification enzymes is essential for the rational design of new drugs, and for treating drug-resistant microorganisms and tumor cells. Finally, this chapter will summarize recent identification of novel enzymes for arsenic reduction, oxidation, and methylation that expand the possibilities for metalloid metabolism and transformations.

This chapter will focus on recent progress on the mechanisms of metalloid uptake, metabolism, and detoxification in bacteria, archaea, and eukaryotic microbes. One of the initial challenges of the earliest cells would have been the ability to detoxify heavy metal ions, transition metal ions, and metalloids, including arsenic and antimony. The presence of arsenic resistance () genes in the genome of by far most living organisms sequenced to date illustrates firstly that genes must be ancient and secondly that arsenic is still ubiquitous in the environment, providing the selective pressure that maintains these genes in present-day organisms. Some early cells also probably could use arsenite as an electron acceptor, giving selective pressure for the evolution of respiratory arsenate reductase. As atmospheric O levels increased, arsenite was oxidized to arsenate abiotically. This provided an advantage for the evolution of arsenate reductases, some for arsenate respiration and energy production, and others for arsenate detoxification. Present-day selective pressure for metalloid resistance also comes from sources such as natural release of arsenic from volcanic activities, mining activities, the burning of coal, and other human activities. In addition is the use of arsenicals and antimonials as chemotherapeutic drugs for the treatment of parasitic diseases and cancer. Resistance to these drugs is becoming a major dilemma. Thus, an understanding of the molecular details of metalloid transport systems and detoxification enzymes is essential for the rational design of new drugs, and for treating drug-resistant microorganisms and tumor cells. Finally, this chapter will summarize recent identification of novel enzymes for arsenic reduction, oxidation, and methylation that expand the possibilities for metalloid metabolism and transformations.

This chapter will focus on recent progress on the mechanisms of metalloid uptake, metabolism, and detoxification in bacteria, archaea, and eukaryotic microbes. One of the initial challenges of the earliest cells would have been the ability to detoxify heavy metal ions, transition metal ions, and metalloids, including arsenic and antimony. The presence of arsenic resistance () genes in the genome of by far most living organisms sequenced to date illustrates firstly that genes must be ancient and secondly that arsenic is still ubiquitous in the environment, providing the selective pressure that maintains these genes in present-day organisms. Some early cells also probably could use arsenite as an electron acceptor, giving selective pressure for the evolution of respiratory arsenate reductase. As atmospheric O levels increased, arsenite was oxidized to arsenate abiotically. This provided an advantage for the evolution of arsenate reductases, some for arsenate respiration and energy production, and others for arsenate detoxification. Present-day selective pressure for metalloid resistance also comes from sources such as natural release of arsenic from volcanic activities, mining activities, the burning of coal, and other human activities. In addition is the use of arsenicals and antimonials as chemotherapeutic drugs for the treatment of parasitic diseases and cancer. Resistance to these drugs is becoming a major dilemma. Thus, an understanding of the molecular details of metalloid transport systems and detoxification enzymes is essential for the rational design of new drugs, and for treating drug-resistant microorganisms and tumor cells. Finally, this chapter will summarize recent identification of novel enzymes for arsenic reduction, oxidation, and methylation that expand the possibilities for metalloid metabolism and transformations.

This chapter will focus on recent progress on the mechanisms of metalloid uptake, metabolism, and detoxification in bacteria, archaea, and eukaryotic microbes. One of the initial challenges of the earliest cells would have been the ability to detoxify heavy metal ions, transition metal ions, and metalloids, including arsenic and antimony. The presence of arsenic resistance () genes in the genome of by far most living organisms sequenced to date illustrates firstly that genes must be ancient and secondly that arsenic is still ubiquitous in the environment, providing the selective pressure that maintains these genes in present-day organisms. Some early cells also probably could use arsenite as an electron acceptor, giving selective pressure for the evolution of respiratory arsenate reductase. As atmospheric O levels increased, arsenite was oxidized to arsenate abiotically. This provided an advantage for the evolution of arsenate reductases, some for arsenate respiration and energy production, and others for arsenate detoxification. Present-day selective pressure for metalloid resistance also comes from sources such as natural release of arsenic from volcanic activities, mining activities, the burning of coal, and other human activities. In addition is the use of arsenicals and antimonials as chemotherapeutic drugs for the treatment of parasitic diseases and cancer. Resistance to these drugs is becoming a major dilemma. Thus, an understanding of the molecular details of metalloid transport systems and detoxification enzymes is essential for the rational design of new drugs, and for treating drug-resistant microorganisms and tumor cells. Finally, this chapter will summarize recent identification of novel enzymes for arsenic reduction, oxidation, and methylation that expand the possibilities for metalloid metabolism and transformations.

This chapter will focus on recent progress on the mechanisms of metalloid uptake, metabolism, and detoxification in bacteria, archaea, and eukaryotic microbes. One of the initial challenges of the earliest cells would have been the ability to detoxify heavy metal ions, transition metal ions, and metalloids, including arsenic and antimony. The presence of arsenic resistance () genes in the genome of by far most living organisms sequenced to date illustrates firstly that genes must be ancient and secondly that arsenic is still ubiquitous in the environment, providing the selective pressure that maintains these genes in present-day organisms. Some early cells also probably could use arsenite as an electron acceptor, giving selective pressure for the evolution of respiratory arsenate reductase. As atmospheric O levels increased, arsenite was oxidized to arsenate abiotically. This provided an advantage for the evolution of arsenate reductases, some for arsenate respiration and energy production, and others for arsenate detoxification. Present-day selective pressure for metalloid resistance also comes from sources such as natural release of arsenic from volcanic activities, mining activities, the burning of coal, and other human activities. In addition is the use of arsenicals and antimonials as chemotherapeutic drugs for the treatment of parasitic diseases and cancer. Resistance to these drugs is becoming a major dilemma. Thus, an understanding of the molecular details of metalloid transport systems and detoxification enzymes is essential for the rational design of new drugs, and for treating drug-resistant microorganisms and tumor cells. Finally, this chapter will summarize recent identification of novel enzymes for arsenic reduction, oxidation, and methylation that expand the possibilities for metalloid metabolism and transformations.

This chapter will focus on recent progress on the mechanisms of metalloid uptake, metabolism, and detoxification in bacteria, archaea, and eukaryotic microbes. One of the initial challenges of the earliest cells would have been the ability to detoxify heavy metal ions, transition metal ions, and metalloids, including arsenic and antimony. The presence of arsenic resistance () genes in the genome of by far most living organisms sequenced to date illustrates firstly that genes must be ancient and secondly that arsenic is still ubiquitous in the environment, providing the selective pressure that maintains these genes in present-day organisms. Some early cells also probably could use arsenite as an electron acceptor, giving selective pressure for the evolution of respiratory arsenate reductase. As atmospheric O levels increased, arsenite was oxidized to arsenate abiotically. This provided an advantage for the evolution of arsenate reductases, some for arsenate respiration and energy production, and others for arsenate detoxification. Present-day selective pressure for metalloid resistance also comes from sources such as natural release of arsenic from volcanic activities, mining activities, the burning of coal, and other human activities. In addition is the use of arsenicals and antimonials as chemotherapeutic drugs for the treatment of parasitic diseases and cancer. Resistance to these drugs is becoming a major dilemma. Thus, an understanding of the molecular details of metalloid transport systems and detoxification enzymes is essential for the rational design of new drugs, and for treating drug-resistant microorganisms and tumor cells. Finally, this chapter will summarize recent identification of novel enzymes for arsenic reduction, oxidation, and methylation that expand the possibilities for metalloid metabolism and transformations.

This chapter will focus on recent progress on the mechanisms of metalloid uptake, metabolism, and detoxification in bacteria, archaea, and eukaryotic microbes. One of the initial challenges of the earliest cells would have been the ability to detoxify heavy metal ions, transition metal ions, and metalloids, including arsenic and antimony. The presence of arsenic resistance () genes in the genome of by far most living organisms sequenced to date illustrates firstly that genes must be ancient and secondly that arsenic is still ubiquitous in the environment, providing the selective pressure that maintains these genes in present-day organisms. Some early cells also probably could use arsenite as an electron acceptor, giving selective pressure for the evolution of respiratory arsenate reductase. As atmospheric O levels increased, arsenite was oxidized to arsenate abiotically. This provided an advantage for the evolution of arsenate reductases, some for arsenate respiration and energy production, and others for arsenate detoxification. Present-day selective pressure for metalloid resistance also comes from sources such as natural release of arsenic from volcanic activities, mining activities, the burning of coal, and other human activities. In addition is the use of arsenicals and antimonials as chemotherapeutic drugs for the treatment of parasitic diseases and cancer. Resistance to these drugs is becoming a major dilemma. Thus, an understanding of the molecular details of metalloid transport systems and detoxification enzymes is essential for the rational design of new drugs, and for treating drug-resistant microorganisms and tumor cells. Finally, this chapter will summarize recent identification of novel enzymes for arsenic reduction, oxidation, and methylation that expand the possibilities for metalloid metabolism and transformations.