It is well known
that Cd is a widespread heavy metal and is released into the environment by
power stations, heating systems, metal-working industries, waste incinerators, urban
traffic, and cement factories and as a by-product of phosphate fertilizers
(Sanità and Gabbrielli 1999). Cd has been considered as an extremely
significant pollutant affecting all life forms because of its high toxicity and
great solubility in soil and water. It has been demonstrated that the level of
Cd in the soil appears to be increasing over time (Jones et al 1992). Cd accumulation in soil
and water now poses a major environmental and human health problem (Schützrndübel
et al 2001). It was reported
that Cd is accumulated by many cereals, potatoes, vegetables and fruits and
that humans take up at least 70% of the Cd which originates from plant food
(Wagner 1993). Studies on Cd toxicity in plants are well documented. Cd can
induce low mitotic index and pycnosis, inhibit cell division and cell proliferation,
and has toxic effects on chromosome morphology including c-mitosis, anaphase
bridges, chromosome stickiness (Liu et
al 1992). Cd has toxic effect on nucleoli in the root tip cells of Allium cepa L. (Liu et al 1995) and alters the synthesis
of RNA and impedes ribonuclease activity in rice (Shah and Dubey 1995).
Although the toxicity and tolerance mechanisms of Cd in plants have been widely
discussed at the biochemical and cell physiology levels over the last decade
(Zenk 1996; Sanità and Gabbrielli 1999; Rauser 1999; Kamnev and Lelie 2000),
only a few investigations have been carried out using electron energy loss spectroscopy
(EELS) and cytochemical tests to localize intracellular Cd. The objectives of
this investigation were to increase our understanding of the effects on root
ultrastructure and Cd accumulation sites at subcellular level in the root cells
of A. cepa grown in different
concentrations of Cd solutions, using EELS and cytochemical tests.
Ø Heavy metal toxicity
The toxicity produced by transition metals generally involves
neurotoxicity, hepatotoxicity and nephrotoxicity (stohs and
Bagchi,1995).Differences in solubility, absorbability, transport and chemical
reactivity in these metals will lead to specific difference in toxicity within the body (stohs
and Bagchi,
1995). The chemical from of heavy metals in soil solution is dependant of the
metal concerned, pH and the presence of other ions (Das et al., 1997). The
toxicity symptoms observed in plants in the presence of excessive amount of
heavy metals may be due to a range of interaction at the cellular level (Hall,
2002). Toxicity may result from the binding of metals to sulphydryl groups in
proteins, leading to an inhibition of activity or disruption of structure (Vaan
Assche and Clijter,1990).Enzymes are one of the main targets of heavy metal
results in marked decreases in soil enzymes
activity (Tyler et al.,1989).Metal interaction with ligand group of
enzymes largely defines their toxicity, and the inhibition of enzymes may be
due to masking of catalytically active group or protein denaturation (das et
al., 1997). In addition ,heavy metal excess may stimulate the formation of free
radicals and reactive oxygen species (Dietz et al.,1999; Gallego et al.,1996;
Groppa et al., 2001; sandolio et
al.,2001; Fornazier et al.,2002). In order to cope with highly toxic metals, or
to maintain the level of essential metal with in physiological ranges, plants
have evolved complex mechanisms that serve to control the uptake, accumulation
and detoxification of metals.
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