Essential Roles and Hazardous Effects of Nickel in Plants - Reviews of Environmental Contamination and Toxicology - page 142

epidermal cells (Heath et al. 1997 ; Hermle et al. 2007 ), deteriorate grana structure
and thylakoid membranes of chloroplasts (Szalontai et al. 1999 ; Molas 2002 ),
decrease grana size and increase the number of lamellae in nonappressed regions
(Molas 1997 ). Such modiications reduce chlorophyll ( a , b , total), xanthophylls,
and carotenoids (Krupa et al. 1993 ; Pandey and Sharma 2002 ; Gajewska et al. 2006 ;
Ahmad et al. 2007 ).
Nickel also competes with other essential nutrients in plants for uptake and trans-
location, and may reduce their concentrations to levels of deiciency. Therefore,
under Ni stress, the concentrations of Fe, Cu, Zn, Mg, Fe, and Mn may decrease
(Krupa and Baszynski 1995 ). This can produce secondary effects (Ewais 1997 ;
Gajewska et al. 2006 ; Shukla and Gopal 2009 ), because Mg is an integral part of the
chlorophyll and heme structures. Moreover, Fe and Mn are required for proper
chlorophyll metabolic functioning. When Ni toxicity is extreme, the chlorophyll
in chloroplasts may break down completely, producing leaf chlorosis and necrosis.

9.4 Photosynthesis

Nickel inhibits plant photosynthesis and alters gas exchange in plants (Nedhi et al.
1990 ; Bishnoi et al. 1993b ; Krupa et al. 1993 ). This may reduce the net photosyn-
thetic rate (Sheoran et al. 1990 ; Bishnoi et al. 1993b ; Krupa and Baszynski 1995 ),
stomatal conductance (Heath et al. 1997 ), transpiration rate (Bishnoi et al. 1993b ;
Pandey and Sharma 2002 ), and water-use eficiency (Bishnoi et al. 1993b ), when
toxic levels of Ni are present in plants. Toxic effects are also produced when Ni is
applied either directly to isolated chloroplasts of guard cells, or through roots
(Tripathy et al. 1981 ; Singh et al. 1989 ; Molas 2002 ; Boisvert et al. 2007 ). These
indings indicate that Ni may indirectly affect stomatal opening through alteration
in K + luxes across guard cell membranes. The reduced size of the stomatal aperture
results in decreased gaseous exchange across leaf surfaces that leads to reduced
photosynthetic rates (Nedhi et al. 1990 ; Bishnoi et al. 1993b ). However, in other
studies, a stable or increased transpiration rate and stomatal conductance, but a
decreased net photosynthetic rate, have been reported. In this case, the reduction in
photosynthetic rate appears to be a result of the toxic effects of Ni on metabolically
important phenomena, rather than on stomatal regulation (Moya 1995 ; Malkin and
Niyogi 2000 ; Papazogloua et al. 2007 ).
Excess Ni may also nonspeciically inhibit photosynthesis, and thereby damage
chloroplast structure (Heath et al. 1997 ; Hermle et al. 2007 ), reduce chlorophyll
synthesis or enhance its breakdown (Seregin and Kozhevnikova 2006 ), disorder
electron transport (Singh et al. 1989 ; Tripathy et al. 1981 ), inhibit Calvin cycle
enzymes, and affect stomatal closure, thereby inducing a CO 2 deicit in chloroplasts
(Sheoran et al. 1990 ). Molas ( 1997 ) reported that Ni-stressed Brassica oleracea
plants (10-20 mg L −1 ) suffered reduced chloroplast size, disorganized and deformed
grana and thylakoid membranes, and altered lipid composition of chloroplast mem-
branes. The authors suggested that these Ni-induced changes may arise from