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Vol. 20 No. 1 - January 2014

Arsenic: a toxicant

By: Saumya Srivastava and Yogesh Kumar Sharma*

Arsenic, a known carcinogen and a toxic metalloid, is slowly engulfing the entire world under its influence. At present, arsenic (As) has been taken into account as a dangerous environmental pollution and detected as a serious health risk in many countries of the world. Sometimes known as the King of Poisons, arsenic has been known to human kind for thousands of years, being used to harden bronze in the Middle East around 3000 BC, and prized as a dye by the Egyptians, Greeks and Romans. In the fifth century BC, Hippocrates suggested using arsenic compounds as an ulcer treatment, while in the 1st and 2nd centuries AD, the Roman Emperor Nero and Mithridates, King of Poutus, both used arsenic to murder their enemies. The first report of widespread environmental problems with As involved the leaching of the metal from mine tailings in Australia, Canada, Mexico, Thailand, the United Kingdom, and the United States. Later, As-contaminated aquifers were reported in Argentina, Bangladesh, Cambodia, Chile, China, Ghana, Hungary, Inner Mongolia, Mexico, Nepal, New Zealand, Philippines, Taiwan, the United States, and Vietnam. Consumption of water from these naturally contaminated aquifers led to chronic As poisoning in many of these locations, with perhaps the worst situation existing in Bangladesh.

Arsenic is a widely dispersed element in the Earth's crust and exists at an average concentration of approximately 5 mg/kg. Possible routes of human exposure to arsenic are from both natural and anthropogenic sources. In the environment, As can exist as inorganic or organic species. Of the two inorganic forms, the more highly oxidized arsenate (AsV) predominates in aerobic environments, while the more highly reduced arsenite (AsIII) is the predominant form in anaerobic environments, such as flooded rice paddy fields. AsV is an analog of inorganic phosphate (Pi) and is easily transported across the plasmalemma by Pi transporter (PHT) proteins while arsenite and undissociated methylated As species through the nodulin 26-like intrinsic (NIP) aquaporin channels. Arsenate is readily reduced to arsenite in plants, which is detoxified by complexation with thiol-rich peptides such as phytochelatins and/or vacuolar sequestration.

Arsenic occurs as a constituent in more than 200 minerals, although it primarily exists as arsenopyrite and as a constituent in several other sulfide minerals. Man made sources like smelting etc., insecticides, herbicides, dessicants and wood preservatives together with feed additives account for main anthropogenic sources of arsenic. Lastly, fossil fuel combustion also produces quantities of arsenic that may lead to long-term accumulation from the gases emitted to the surrounding areas. All of these factors release arsenic into the environment and can result in its accumulation in soils. Permissible limit of arsenic in agricultural soils is 20 mg/kg soil.

A large number of people are exposed to arsenic chronically throughout the world. Exposure occurs via the oral route (ingestion), inhalation, dermal contact etc. Several studies have indicated that the toxicity of arsenic on humans depends on the exposure dose, frequency, duration, the biological species, age and gender, as well as on individual susceptibilities and genetic and nutritional factors. The first symptoms of chronic long-term exposure to low levels of As result into arsenicosis which includes skin discolorations, chronic indigestion, and stomach cramps. Longer-term effects include skin, lung, kidney, and liver cancer as well as gangrene-like sores. Food and drinking water together account for 99% of the total human intake of As. Arsenic contamination of groundwater is often due to naturally occurring high concentrations of arsenic in deeper levels of groundwater. In the absence of an alternative source, people in acute arsenic problem areas are drinking arsenic-contaminated water without paying much attention to possible consequences and ill effects. Symptoms of arsenicosis are also seen in inhabitants of the contaminated area as brittle nails, deformity in hands and pigmentation. In soil the arsenic concentration from 5.40 to 15.43 ppm is quite toxic especially for sensitive crops (e.g. green beans, lima beans, spinach, cabbages, tomatoes etc.). In this way, not only humans, but plants too are suffering from its toxic effects. The soils of many regions of the world have become contaminated and unfit for cultivation of especially arsenic sensitive crops. Moreover, irrigation with arsenic laden water has exacerbated this problem by further adding arsenic to the soil. The added arsenic gradually accumulates in the soil, and reaches the toxic levels, and it is hazardous to crops in some soils that have been irrigated with highly contaminated water for 1020 years or more.

Arsenic is non-essential and generally toxic to plants. Roots are usually the first tissue to be exposed to As, where the metalloid inhibits root extension and proliferation. Upon translocation to the shoot, As can severely inhibit plant growth by slowing or arresting expansion and biomass accumulation, as well as compromising plant reproductive capacity through losses in fertility, yield, and fruit production. There is significant evidence that exposure to inorganic arsenic species results in the generation of reactive oxygen species (ROS). At sufficiently high concentrations, As interferes with critical metabolic processes, which can lead to death. Most plants possess mechanisms to retain much of their As burden in the root. However, a genotype-dependent proportion of the As is translocated to the shoot and other tissues of the plant.

AsV and AsIII both disturb plant metabolism, but through distinct mechanisms. AsV being a chemical analog of phosphate, disrupts at least some phosphate-dependent aspects of metabolism. It can compete with phosphate during phosphorylation reactions, leading to the formation of AsV adducts that are often unstable and short-lived. Like, the formation and rapid autohydrolysis of AsV-ADP sets in place a futile cycle that uncouples photophosphorylation and oxidative phosphorylation, decreasing the ability of cells to produce ATP and carry out normal metabolism. AsIII is able to enter root cells through nodulin 26-like intrinsic proteins. These proteins belong to the aquaporin family of major intrinsic proteins. In rice roots, the OsNIP2;1/OsLsi1 silicon transporter has been implicated as the major AsIII uptake protein, while AsIII efflux from rice root cells to the xylem is through the OsLsi2 silicon transporter. Other types of proteins may also facilitate the transport AsIII into cells.

Besides other remedial approaches being present like zinc and selenium fertilization, iron plaque formation, mycorrhizal association etc., and modern breeding and genetic engineering methods, phosphate application definitely proves to be one of the important remedial methods because of it being analogus to As, and sharing the same carriers for its uptake.

*Department of Botany, University of Lucknow, Lucknow e-mail: yogesh_s26@yahoo.com


This article has been reproduced from the archives of EnviroNews - Newsletter of ISEB India.


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