Abbreviations
As
Arsenic
As III Arsenite
As V Arsenate
1 Introduction
Arsenic (As) pollution causes a high ecological risk that impends the well-being of
human health. Industrialization, overexploitation, and urbanization have worsened
the natural resources, and it is estimated that water quality would further worsen with
the increased rate of arsenic contamination in the coming years. In some regions of
China, India, Pakistan, and Bangladesh, numerous “cancer villages” are recorded
(Alka et al. 2020). The water quality has become a serious threat (Mohapatra et al.
2013) in the past two decades. Intrusion of saline water and indiscreet use of
fertilizers and pesticides are the foremost factors which worsened the quality of
groundwater with high arsenic (As), iron (Fe), and fluoride (F) content. As is one of
the most predominant lethal metalloid in the environment, restricted not only to
geochemical (minerals and rocks) origin in an insoluble form but also from anthropogenic sources (Ji and Silver 1992, 1995). Trivalent arsenite (As III) and pentavalent arsenate (As V) are insoluble forms of As. According to the Comprehensive
Environmental Response (Compensation and Liability Act) As is categorized as the
No. 1 carcinogenic substance; it is ranked No. 5 among the potentially toxic
elements (PTEs). Arsenic has been called “essential toxins” because it is required
in trace amounts for growth and metabolism but is toxic at high concentration (Stolz
et al. 2002). Being the 33rd atomic number, this heavy metal is the twentieth highest
ubiquitous and naturally occurring metalloid in the earth’s crust. Arsenite is reportedly more toxic than arsenate (nearly 100 times) and can be oxidized to arsenate
microbiologically or chemically (Ehrlich 1996; Muller et al. 2003). Nearly one-third
of the periodic table elements are responsible for the transformation, degradation, or
adsorption mediated by microbial activity (Stolz et al. 2002). Microbes have developed a diverse and distinct mechanisms to avoid the toxicity of arsenic: (A) by
membrane lipids – peroxidation reactions (Ahmann et al. 1994; Ji and Silver 1995),
(B) reducing the uptake of As V by phosphate uptake channel (Holt 1994; Ji and
Silver 1995), and (C) through the ars operon that regulates arsenic detoxification
pathway (Ji and Silver 1995; Mukhopadhyay et al. 2002). In recent years, the
understanding on arsenic degradation or transformation has been significantly
advanced. A steady progress in recent researches on the physiological processes of
degradation or transformation delineating some of the biochemical mechanisms has
paved the way for better understanding of pathway. The understanding of Arsenic as
an inducer of oxidative stress is a good example of such a biochemical mechanism.
Numerous intuitions have been gained on identifying the gene expression changes
240
P. Narayanasamy and R. K. Subramanian
As
Arsenic
As III Arsenite
As V Arsenate
1 Introduction
Arsenic (As) pollution causes a high ecological risk that impends the well-being of
human health. Industrialization, overexploitation, and urbanization have worsened
the natural resources, and it is estimated that water quality would further worsen with
the increased rate of arsenic contamination in the coming years. In some regions of
China, India, Pakistan, and Bangladesh, numerous “cancer villages” are recorded
(Alka et al. 2020). The water quality has become a serious threat (Mohapatra et al.
2013) in the past two decades. Intrusion of saline water and indiscreet use of
fertilizers and pesticides are the foremost factors which worsened the quality of
groundwater with high arsenic (As), iron (Fe), and fluoride (F) content. As is one of
the most predominant lethal metalloid in the environment, restricted not only to
geochemical (minerals and rocks) origin in an insoluble form but also from anthropogenic sources (Ji and Silver 1992, 1995). Trivalent arsenite (As III) and pentavalent arsenate (As V) are insoluble forms of As. According to the Comprehensive
Environmental Response (Compensation and Liability Act) As is categorized as the
No. 1 carcinogenic substance; it is ranked No. 5 among the potentially toxic
elements (PTEs). Arsenic has been called “essential toxins” because it is required
in trace amounts for growth and metabolism but is toxic at high concentration (Stolz
et al. 2002). Being the 33rd atomic number, this heavy metal is the twentieth highest
ubiquitous and naturally occurring metalloid in the earth’s crust. Arsenite is reportedly more toxic than arsenate (nearly 100 times) and can be oxidized to arsenate
microbiologically or chemically (Ehrlich 1996; Muller et al. 2003). Nearly one-third
of the periodic table elements are responsible for the transformation, degradation, or
adsorption mediated by microbial activity (Stolz et al. 2002). Microbes have developed a diverse and distinct mechanisms to avoid the toxicity of arsenic: (A) by
membrane lipids – peroxidation reactions (Ahmann et al. 1994; Ji and Silver 1995),
(B) reducing the uptake of As V by phosphate uptake channel (Holt 1994; Ji and
Silver 1995), and (C) through the ars operon that regulates arsenic detoxification
pathway (Ji and Silver 1995; Mukhopadhyay et al. 2002). In recent years, the
understanding on arsenic degradation or transformation has been significantly
advanced. A steady progress in recent researches on the physiological processes of
degradation or transformation delineating some of the biochemical mechanisms has
paved the way for better understanding of pathway. The understanding of Arsenic as
an inducer of oxidative stress is a good example of such a biochemical mechanism.
Numerous intuitions have been gained on identifying the gene expression changes
240
P. Narayanasamy and R. K. Subramanian