Journal of Stress Physiology &
Biochemistry, Vol.
8 No. 4
2012, pp. 55-61 ISSN 1997-0838
Original Text Copyright (cc) 2012 by Ghasemi, Heidari, Jameii, Purakbar
ORIGINAL
ARTICLE
Data source : Google Scholar
QueryDate : 2016-12-24
Cites : 11
Effects of Ni2+
toxicity on Hill reaction and membrane functionality in maize
Fatemeh Ghasemi, Reza Heidari,
Rashid Jameii and Latifeh Purakbar
Department
of Biology, Faculty of Science, Urmia University, Urmia, Iran
Telephone No.: +989149380292
*E-Mail: ayda1355@yahoo.com
Received July 4, 2012
Soil contamination with heavy
metals has become a worldwide problem, leading to losses in
agricultural yield and hazardous health effects as they enter the food
chain . Nickel as an essential trace element, affect a number of
biochemical and physiological processes in plants in toxic
levels. The most common symptoms are chlorosis, and inhibited
photosynthesis and respiration. Zea mays seeds were germinated
and cultured on nutrient solution with nickel concentrations of 50-200
μmol for a period of two weeks. Studied physiological makers
included photosynthetic pigments content, the rate of Hill reaction, K+
efflux and carbohydrate leakage from the roots to the external
solution and cell death as a Ni-induced membrane damage. By increasing
Ni concentration up to 100 μmol, the content of chlorophyll a
increased, but decreased at 200 μmol Ni. No significant changes in
chlorophyll b and carotinoids content observed.The rate of Hill
reaction as an ability of chlorophyll a in the reaction center of
PSII680 to split water, decreased by increasing Ni concentration.
Different concentrations of nickel increased the K+ efflux and sugar
leakage from roots to the culture and the cell death of root tips. The
present results suggested that the disruption of photosynthesis by Ni
cannot be attributed to any single factor and appears to result from
its combined effects on chloroplast structure, chlorophyll content and
photosynthetic protein complexes and treatment with different levels of
nickel may induce structural damage and alterations in membrane
properties by generation of reactive oxygen species.
