Essential Roles and Hazardous Effects of Nickel in Plants - Reviews of Environmental Contamination and Toxicology - page 141

Excessive amounts of reactive oxygen species (ROS) are produced from exposure
to Ni in plants (Gajewska et al. 2006 ; Gajewska and Skłodowska 2007 ). ROS pro-
duce oxidative damage to membrane lipids and proteins from lipid peroxidation and
membrane degradation (Dat et al. 2000 ; Verma and Dubey 2003 ). Plants defend
themselves from such oxidative attacks by enzymatic means. Examples of such
defense enzymes are catalase (CAT), peroxidase (POD), superoxide dismutase
(SOD), glutathione reductase, and others. In addition, plants use nonenzymatic
means to defend themselves, most notably by exuding compounds that are antioxi-
dants, to wit, ascorbic acid (AsA), phenolics, tocopherols, and reduced glutathione
(GSH) antioxidants. These natural entities help plants to alleviate the toxic effects of
ROS by removing, neutralizing, or scavenging them (Pandolini et al. 1992 ; Noctor
and Foyer 1998 ; Alscher et al. 2002 ; Verma and Dubey 2003 ; Freeman et al. 2004 ;
Maheshwari and Dubey 2009 ). However, when high exposure levels to metals occur,
these defenses often fail to suficiently scavenge excess ROS; the result is enhanced
lipid peroxidation and electrolyte leakage (Howlett and Avery 1997 ; Zhang et al.
2007 ; Wang et al. 2008 ). Because Ni is a redoxically inactive metal, it does not
directly generate ROS (Boominathan and Doran 2002 ). However, in some previous
studies, it has been reported that excessive ROS generation takes place under high
Ni application that causes membrane lipid peroxidation (Baccouch et al. 1998b ; Rao
and Sresty 2000 ; Gajewska and Skłodowska 2005 ) and decreased protein thiolation,
in many plant species (Maheshwari and Dubey 2009 ). Therefore, such changes in
sterol and phospholipid composition of the plasma membranes may occur at high Ni
levels that might alter plant membrane permeability functions (Ros et al. 1990 ).
As mentioned previously, Ni is known to compete with several other essential metal
nutrients (e.g., Mg, Mn, Fe, Zn, and Ca; Heale and Ormrod 1982 ; Marschner 1995 ;
Cataldo et al. 1978 ; Körner et al. 1987 ; Kochian 1991 ; Küpper et al. 1996 ). Therefore,
when Ni is present in plant tissues, the concentration of these other nutrients tend to
decrease (Gabbrielli et al. 1990 ; Rubio et al. 1994 ; Rahman et al. 2005 ; Ahmad et al.
2007 ). Ca and Zn are required for membrane stability (Valko et al. 2005 ; Taiz and
Zeiger 2006 ) and Fe is a constituent (cofactor) of many antioxidative enzymes (e.g.,
catalase and peroxidase; Ranieri et al. 2003 ). Therefore, a Ni-induced Fe-deiciency
may decrease the activities of antioxidant enzymes, and hence, increase lipid peroxi-
dation, with a consequential membrane permeability loss (Baccouch et al. 1998b,
2001 ; Boominathan and Doran 2002 ).

9.3 Photosynthetic Pigments

High Ni levels in plants may alter the concentrations of photosynthetic pigments,
such as chlorophyll a , b and carotenoids (McIlveen and Negusanti 1994 ; Balaguer
et al. 1998 ; Seregin and Kozhevnikova 2006 ). These changes commonly induce leaf
chlorosis and necrosis, which are common symptoms of Ni toxicity in plants
(Gajewska et al. 2006 ). Excess Ni concentrations may directly damage the photo-
synthetic apparatus of leaves in several ways. Excess Ni may destroy mesophyll and