Essential Roles and Hazardous Effects of Nickel in Plants - Reviews of Environmental Contamination and Toxicology - page 140

of lateral roots may be inhibited by excess Ni in crops such as maize and rice (Seregin
et al. 2003 ). The reason for such growth inhibition may be that Ni easily crosses the
endodermal barrier and accumulates in pericycle cells, thereby affecting cell division
and proliferation (Seregin et al. 2003 ; Seregin and Kozhevnikova 2006 ).
The Ni-induced toxicity symptoms displayed in many aerial parts of certain plant
species start with foliar chlorosis; symptoms irst appear primarily in older leaves
and gradually move to younger ones (Pandey and Sharma 2002 ). Sometimes, chlo-
rosis starts at the leaf margins and slowly progresses to the interveinal areas. In
other cases, acute Ni toxicity causes necrotic spots to rapidly develop on leaf mar-
gins, and then these appear later in the interveinal areas of leaves (Baccouch et al.
1998a ). In severe cases, plants may develop necrotic lesions on younger as well as
older leaves and eventually cause death of entire leaves (Sun and Wu 1998 ). Since
Ni strongly competes with other essential elements, (such as Mg, Fe, Cu, Zn, and
Mn), the typical visual symptoms of Ni toxicity result from a deiciency of any of
these essential nutrients (Khalid and Tinsley 1980 ; Hasinur et al. 2005 ).
Many mechanisms have been proposed to explain how Ni produces its effects on
plant growth and development. Proposals for causative mechanisms include (1) a
general metabolic disorder (Mishra and Kar 1974 ; Baccouch et al. 1998a ; Murch
et al. 2003 ), (2) a decrease in cell wall plasticity (Pandolini et al. 1992 ), (3) impaired
cell division and elongation (Robertson and Meakin 1980 ; Demchenko et al. 2005 ),
(4) disorganization of nuclear structures (Sresty and Rao 1999 ), (5) chromosomal
aberrations (Liu et al. 1995 ), and/or nutritional imbalances (Ahmad et al. 2011 ).
The injury produced by treatment with 1.5-5.00 mM NiCl 2 caused mitotic tip arrest
of Vicia faba roots. Similarly, Demchenko et al. ( 2005 ) reported that treatment of
embryonic wheat ( Triticum aestivum ) roots with 0.1 mM NiSO 4 blocked cell divi-
sion in all except the distal ends of rhizodermal, exodermal, and middle curricular
areas, and in the peripheral cells of the caliptrogen. Sresty and Rao ( 1999 ) con-
cluded that inhibition of cell division often results from disruption of the nuclear
membrane, which causes nuclear structure disorganization (e.g., development of
two nucleoli in the nucleus and extensive condensation of chromatin). Regardless of
the exact mechanism by which Ni induces plant toxicity, ultimately, Ni-induced
stress reduces vegetative growth and decreases yield (Balaguer et al. 1998 ;
Tabatabaei 2009 ).

9.2 Membrane Permeability and Electrolyte Leakage

Compared to other known abiotic stresses, a few reports exist that address the effect
of metal ions on biological membrane permeability. However, it is known that ion
leakage is an important consequence of metal stress in plants from exposure to Cu
and Ni (Rao and Sresty 2000 ; Seregin and Kozhevnikova 2006 ). Membrane perme-
ability may be damaged due to high Cd and Ni exposure levels, and contact with
these metals induces loss of key osmolytes and turgor pressure (Wang et al. 2008 ;
Llamas et al. 2008 ).