الفهرس 
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Abstract
A diminished amount of antioxidant enzyme coupled with superoxide production in appears to be general characteristic of the tumor cells. This character can be used in cancer treatment. Thus the present study attempted to investigate the effect of 4-Azomalanonitrileantipyrine copper complex which have SOD like activity on tumor development using HepG2 and Vero cell lines.
Accordingly, the HepG2 and Vero cell lines were classified into six groups as follows: G1:HepG2 (Hepatocellular carcinoma cells) untreated, G2: Vero (Kidney monkey cells) untreated, G3: HepG2 cells treated with DMSO solvent, G4: Vero cells treated with DMSO solvent, G5: HepG2 cells treated with copper complex and G6: Vero cells treated with copper complex.
The following parameters were determined:
1. Life span prolongation of HepG2 and Vero cell lines which would evidence the antitumor activity of these complex.
2. Creatinine, Hb, GPT, and GOT were carried out as parameter to drug toxicity and follow the clinical status of the treated cells as well as its extent of responsiveness to treatment.
3. The Nitric oxide, MDA and the activities of antioxidant and glutathione related enzyme activity as well as the reduced glutathione content which would partly highlight the mode of action of the tested complex.
The results showed that:
1- Life span prolongation of HepG2 and Vero cells viability, which would evidence the antitumor activity of this complex.
2- Serum activity of glutamic pyruvic transaminase (GPT) and glutamic oxaloacetic transaminase (GOT) exhibited a significant increase in HepG2 and Vero cells treated with copper complex group compared to normal control group.
3- Serum level of creatinine showed no alteration but Hb exhibited a significant decrease in HepG2 and Vero cells treated with copper complex group compared to normal control group.
4- Nitric oxide level in liver homogenate exhibited a significant increase in HepG2 and Vero cells treated with copper complex group compared to compared to normal control group.
5- Malondialdehyde levels in both liver homogenate and erythrocyte cell lysate exhibited a significant decrease in HepG2 and Vero cells treated with copper complex compared to normal control group.
6- SOD and GPX activity in both liver homogenate and erythrocyte cell lysate exhibited a significant decrease in HepG2 and Vero cells treated with copper complex group compared to normal control group.
7- Reduced GSH level in both liver homogenate and erythrocyte cell lysate exhibited a significant decrease in HepG2 and Vero cells treated with copper complex group compared to normal control group.
The metal complex increase intracellular H2O2 either by acting artificial superoxide dismutase or by undergoing a redox-cycling reaction, possibly causing depletion of intracellular glutathione. Thus H2O2 generated by this complex seems to be involved in killing of cancer cells, which might be particularly susceptible to oxidative insult because of their low content of glutathione peroxidase. On contrary, the normal cell contain sufficient peroxidase to degrade H2O2 to H2O and O2 and incur less damage or incorporating the metal complexes into the cytoplasm. Thus this metal complex is suggested to bind to DNA and clear it with the formation of OH radicals when H2O2 is present from either dismutation of superoxide radicals or change in redox-cycling in the tumor cells.