A the mechanisms of arsenic-induced toxicity have established

A study conducted by Tyler, C.R., et.al (2014) states that
arsenic can alter a multitude of systems in the brain.  HPA axis dysregulation that may underlie
behavioral deficits, particularly related to the hippocampus. Arsenic can
affect in the alterations of adult neurogensis and Ras-MAPK/ERK signaling.  It also have an impact on cholinergic and
monoaminergic signaling, though the mechanisms are not well understood at this
point. A study on Rodents have provided useful document  of the epidemiological evidence suggesting
that a number of mechanisms could cause cognitive deficits and mood disorders.
More research focused on the dynamics of epigenetics, particularly on
mechanisms of learning and memory and mood, will be important for understanding
the impact of arsenic on the brain.Studies on the mechanisms of arsenic-induced
toxicity have established that arsenic alters learning and memory in behavioral
assays and impacts multiple neurobiological processes including those of
neurogenesis and cholinergic, glutamatergic, and monoaminergic signaling
pathways. Work using animal models has revealed potent changes in hippocampal
function, morphology, and signaling leading to change in cognitive behavior
after arsenic exposure.


According to Hong, Y.-S., et.al (2014) Arsenic is the only
carcinogen known to cause cancer through respiratory exposure and
gastrointestinal exposure . The International Agency for Research on Cancer
(IARC) officially recognized it as carcinogenic
substance . Studies conducted in the United States, Taiwan, Bangladesh,
India, Argentina, and Chile further examined this association, and the results
supported those of previous reports . It states that inorganic arsenic
compounds can be categorized as clear carcinogens (group 1) or potential carcinogens
(group 2B) such as DMA and MMA, while arsenobetaine and other organoarsenicals
have not been categorized as carcinogens (group 3). Toxic mechanism behind
arsenic have been suggested, including induced chromosome abnormalities,
altered growth factors, altered DNA repair, oxidative stress, altered DNA
methylation patterns, enhanced cell proliferation, suppression of p53, and gene
amplification. International Agency for Research on Cancer has confirmed the
association of arsenic exposure with cancers of the skin, lungs, and bladder,
while reports on the relationship with the liver, kidney, and prostate cancer
remain limited. Key epidemiological evidence regarding the carcinogenicity of
arsenic stems from studies from those in Taiwan , Bangladesh , Chile , and
Argentina , who consume drinking water containing high concentrations of
arsenic (150 ?g/L). However, despite the well-established toxicity of
arsenic, studies regarding the association between chronic exposure to low
concentrations of arsenic and the development of cancer are lacking; further
study is needed to support effective public health management.

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A study conducted by Lin, H.J., et.al (2013) shows the results of
a 20-year retrospective cohort study on liver cancer patients (802 male and 301
female) from 138 communities in Taiwan found a significant increase in liver
cancer incidence in both genders at a arsenic concentration above 0.64 mg/L,
but no association was found at exposure levels lower than lower 0.64 mg/L.
Hopenhayn-Rich et al. observed a significant increase in lung cancer-related
deaths with arsenic intake. Moreover, numerous studies have investigated the
dose-dependent relationship between arsenic intake and lung cancer incidence,
making lung cancer the most well-known cancer associated with arsenic exposure.
In a recent study conducted in Taiwan, a high mortality rate and standardized
mortality ratio of lung cancer was observed among patients who consumed
high-arsenic concentrated drinking water for the past 50 years.


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