ARI Volume 2 Number 1.pdf - Zoo-unn.org

Superoxide dismutase (sod) activity and serum calcium level in rats 265Serum Calcium (mg\ml)10.90.80.70.60.50.40.30.20.10Newly Weaned RatMiddle Aged RatAged RatControl 1% 5% 10%Concentrations of Insecticide in DietFigure 1: Serum calcium levels (mg\ml) of rats exposed to insecticidecontaminated dietsThe group with high SOD activity possessed verylow level of serum Ca 2+ . This may be as a result ofthe scavenging ability of SOD on the superoxideradicals generated by the increase in cytosolic Ca 2+level. The elevated Ca 2+ level can cause severaltissue injuries and subsequently affect membranepotential and mitochondrial uncoupling (Marklundand Marklund, 1974). Several studies withxenobiotics demonstrated mitochondrial energyuncouplers (Deuterman, 1980), which suggestdisruption of energy supply as a common principalcause of cellular cytotoxicity.Acute pesticide poisoning, particularly indeveloping countries, is frequent and thus of greatimportance in public health. The magnitude of theproblems depends on a number of contributingfactors, such as types of pesticide regulations,awareness of the degree of danger, training tominimized exposure and availability of medicaltreatment facilities. The use of pesticide indeveloping countries is often characterized by lackof vital knowledge of its toxicity and proceduresfor safe use. This plays a critical role in obtainingdirect exposure by both target and non-targetorganisms.The action of “Rambo” insecticide on nontargetgroups may vary widely in comparison tothe other insecticides like paraquat (Palmeira,1999); deltamethrin, zeta–cypermethrin anddimethoate (Moreby et al., 2001). It has becomeapparent that both SOD and Ca 2+ are important toboth toxicological and physiological processes. Therelative importance of the various Ca 2+ dependentprocesses in cells needs to be further clarified andthe toxicity of “Rambo” insecticide with otherpyrethroid could be further compared usingbiochemical markers.REFERENCESBOWLER, C., MONTAGU, M. V. and IRIZE, D.(1992). Superoxide dismutase and stresstolerance. Analytical Review PlantPhysiology and Molecular Biology, 43: 83– 116.BRIDGES, J. W., BENFORD D. J. and HUBBARD S.A. (1983). Mechanisms of toxic Injury.Annals of New York Academy of Sciences,83: 42 – 63.CARAFOLI, E. (1987). Intracellular calciumhomeostasis. Analytical Review inBiochemistry, 56: 395 – 433.CERIOTI, G. (1974). Inorganic substances. Pages1566 – 1572. In: H. C. CUTINS (ed).Clinical Biochemistry. Principles andMethods, Volume 2, Blackwell ScientificPublications, Oxford.COMPORTI, M. (1993). Lipid peroxidation, anoverview. Pages 65 – 87. In: POLI, G.,ALBANO, E. and DIANZANI, M. U. (Eds.).Free radicals: from basic science tomedicine. Birkhauser Verlag Basell,Switzerland.CUNHA-BASTOS, V. L. T., CUNHA-BASTOS, J.,LIMA J. S. and CASTRO-FAIRA, M. V.(1991). Brain acetylcholinesterase as an“in-vitro” detector of organophosphorusand carbamate insecticide in water. WaterResources, 25: 835 – 840.DEUTERMAN, W. C. (1980). Metabolism oftoxicants: phase II reactions. Pages 92 –104. In: Hodgson E. and Guthrie, F. E.(Eds.). Introduction to BiochemicalToxicology. Blackwell ScientificPublications, Oxford.DUNCAN, D. (1955). Multiple range test andmultiple F-tests. Biometrics, 11: 1 – 42.