1 Plant Archives Vol. 19, Supplement 1, 2019 pp. 299-308 e-ISSN:2581-6063 (online), ISSN:0972-5210 TOXICO PATHOLOGICAL STUDY OF COPPER SULFATE MODULATE BY ZINC OXIDE AND CORIANDRUM SATIVUM PLANT TREATMENT IN MICE Eman Hashimyousif, Hashim M. Obaid, Abdulkarim Jafar Karim, Muna Sachit Hashim and Rajiha A. Al.Naimi *Department of Pathology, College of Veterinary Medicine, University of Baghdad, Iraq. Abstract This experiment was designed in order to study the degree of toxic pathological effects of copper sulfate associated with zinc oxide and extract of Coriandrum sativum treatment in mice. We used 110 mice conducted on eleven groups of 10 mice 1 st group treated with distilled water as control negative, 2nd group treated with copper sulfate and then treated with distilled water as control positive, 3rd group treated with copper sulfate only, 4th group treated with low concentration copper sulfate with zinc oxide, 5th group treated with high concentration of copper sulfate with zinc oxide, 6th group traded with low concentration of copper sulfate and Coriandrum sativum,7 th group treated with high concentration of copper sulfate and zinc oxide and Coriandrum sativum, 8 th group treated with copper sulfate and Coriandrum sativum, 9 th group treated with copper sulfate at high concentration and Coriandrum sativum, 10 th group treated with zinc oxide only, 11 th group treated with Coriandrum sativum only. Each treated period for each groups were 8 weeks. Early patho-toxicological changes were: Congestion, edema, degenerations followed by necrosis in brain, atrophy and paleness of liver and kidneys. Hyperkeratosis within stomach wall. Suppurative broncho-pneumonia. increased of apoptosis for hepatocyte with increase of inclusion bodies in epithelial layer of renal tubules, present for renal cast, splenic white pulp depletion. These finding prefill toxicity by copper sulfate in mice but at the same time, treatment of zinc oxide and Coriandrum sativum or both acts as protection against toxicity of copper sulfate . Key words: Copper, toxicity, Coriandrum sativum. Introduction Copper is an essential trace element that is widely distributed in tissues of animal and plant (US.AF., 1990 and Institute of Medicine, 2001). Copper is very important for iron metabolism, collagen and elastin system, numerous metalloproteinase enzymes and non- metalloproteinase enzymes in animal which require copper to be biological active, recently it has been shown that cu is one of the key trace mineral required for an effective immune response (Harrison et al., 2000) Copper is absorbed, transported, distributed, stored, and excreted in the body according to complex homeostatic processes which ensure a constant and sufficient supply of the micronutrient while simultaneously avoiding excess levels (Stern, (2007, 2010). The recommended dietary intake for copper is 1.5-3.0 mg/day for adults; 0.7-2.5 mg/day for children; 0.4-0.7 mg/day for infants (US.AF., 1990). But Ingestion large doses less than one gram (637 mg/kg copper) cause's copper poisoning (Chuttani et al., 1965). Copper exposure, liver and other organ meats, seafood, nuts and seeds (including whole grains) are good sources of dietary copper (Institute of Medicine, 2001 and Harrison, 2000) Copper is released into the environment by mining, farming, and manufacturing operations and through waste water releases into rivers and lakes. Also released from natural sources, like volcanoes, wind blown dusts, decaying vegetation, and forest fires (ATSDR, 2004). Another source of copper is found in surface water, ground water, sea water and drinking water (ATSDR, 2004). The suggested safe level of copper in drinking water for humans varies depending on the source, but tends to be pegged at 2.0 mg/L (Nauja et al., 2008). In humans acute copper poisoning has occurred through contamination of beverage through storage in containers copper containing as well as contamination water (ATSDR, 2004). While ingested or cutaneous absorption of adequate amount of copper salt is able to produce acute gastro enteric poisoning, the usual poisoning in domestic animal is a chronic disorder, when copper stored in the liver reaches a critical level (Expert Group, 2002). Copper sulfate is the most common copper salt; it is used chief for agriculture purposes as a pesticide and in leather industry (ACGIH, 1986). A dose response effect to following ingestion is difficult to define but approximately 10 grams may be fatal in an adult (Akintonwa et al., 1989). The main brunt of copper sulfate is borne in the order by erythrocytes liver and then kidney leading to methanoglobinemia, hepatotoxicity and renal failure (Blundell et al., 2003). Uptake of copper from the intestines is susceptible to competitive inhibition by other transition metals (particularly zinc or iron). The presence of dietary proteins and amino acids,