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Applied and Environmental Soil Science
Volume 2013 (2013), Article ID 642098, 7 pages
Research Article

Nickel in Soil Modifies Sensitivity to Diazinon Measured by the Activity of Acetylcholinesterase, Catalase, and Glutathione S-Transferase in Earthworm Eisenia fetida

Department of Animal Physiology and Ecotoxicology, Faculty of Biology and Environmental Protection, University of Silesia, Bankowa 9, 40007 Katowice, Poland

Received 16 July 2013; Accepted 24 September 2013

Academic Editor: Yongchao Liang

Copyright © 2013 Agnieszka Zawisza-Raszka and Bogdan Dolezych. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Nickel in typical soils is present in a very low concentration, but in the contaminated soils it occurs in locally elevated concentrations. The aim of this study was to examine the effect of nickel in the concentrations of 300 (very high, close to LOEC for reproduction) and 900 (extremely high, close to LOEC for mortality) mg/kg dry soil on the life history and acetylcholinesterase, catalase, and glutathione S-transferase activities in earthworm Eisenia fetida and to establish how nickel modifies the sensitivity to organophosphorous pesticide—diazinon. Cocoons production and juveniles’ number were significantly lower only in groups exposed to Ni in the concentration of 900 mg/kg dry soil for two months. Diazinon administration diminished the AChE activity in the GI tract and in the body wall. The interaction between diazinon and nickel was observed, and, in consequence, the AChE activity after the pesticide treatment was similar to controls in worms preexposed to nickel. Both pesticide administration and exposure to nickel caused an increase in the GST activity in examined organs and CAT activity in body wall. Both biometric and development data and simple enzymatic analysis, especially the AChE and GST, show a Ni pretreatment effect on the subsequent susceptibility to pesticide.