Journal of Applied Science Studies - Ozean Publications

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Ozean Journal of Applied Sciences 1(1), 2008 various fungicides. When male and female rats were exposed to mancozeb, the liver showed centrilobular necrosis with extramedullary haemopoiesis and the kidney showed tubular dilation, necrosis and congestion of blood vessels (Szepvolgyi et al., 1989). Selmanoglu et al. (2001) revealed congestion of blood vessels, increase in number of Kupffer cells, cellular infiltration and hydropic degeneration in liver of male rats treated with carbendazim. Sakr et al. (2004) reported that benomyl induced marked histopathological and histochemical changes in the liver of mice. Metalaxyl induced apoptosis in the liver of mice. The morphological changes of apoptosis observed in mice hepatocytes, in the current study, were previously described by Saraste and Pulkki (2000) which involve contraction in cell volume,condensation of nucleus and the nucleus becomes fragmented .Finally, the cell itself fragmented to form apoptotic bodies that are engulfed nearby phagocytosis. Apoptosis was induced by some fungicides. Sakr et al. (2005) reported that mancozeb induced apoptosis in hepatocytes of mice. Stefan et al. (1995) observed that exposing rat thymocytes to pyrrolidine dithiocarbamate resulted in cell shrinkage, chromatin fragmentation, glutathion depletion and evenual cell lysis, which is typical of apoptosis in these cells. Greenlee et al. (2004) reported that incubating mice embryo with the fungicides chlorothalonil and mancozeb increased the percentage of apoptosis and reduced development to blastocyst and mean cell number per embryo. In addition to morphological evidence of apoptosis, the total cellular DNA fragmentation coupled with laddering observed in our results are associated with cells undergoing apoptosis. This result agrees with previous findings that cleavage of nuclear DNA into oligonucleosomal fragments can be induced in hepatocyte nuclei (Jones et al., 1989) or in isolated nuclei (Cohen et al., 1995). Many studies investigating apoptosis process demonstrated that deregulation of nuclear Ca ++ activated an endonuclease that fragments DNA (Ray et al., 1991). The molecular regulation of apoptosis has been a focus of numerous investigations in recent years. Key players at the genetic level Bax, expression of which presumbly favor the progression of apoptosis process (Ray et al., 1996). A significant higher numbers of Bax-positive hepatocytes was found in liver of metalaxyl-treated mice, indicating that these cells are susceptible to apoptosis. In agreement of this result , Masson et al. (2000) reported that the proapoptotic proteins Bad and Bax were significantly higher in liver cirrhosis induced by CCl 4 . They added that apoptosis takes place in liver during CCl 4 -induced cirrhosis. Gordon et al. (2000) found that levels of the proapoptotic protein Bax are increased in livers from retrorsine-exposed rats relative to the levels observed in control livers. Chen et al. (2004) observed that the proapoptotic proteins Fas, Fasl , Bax were highly expressed in chronic hepatitis. Rathmell and Thompson (2002) mentioned that apoptosis in chronic hepatitis may begin from the injuryed DNA which activates the p53 protein to translocate the proapoptotic protein Bax to the mitochondria and form pores at the outer mitochondrial membrane to release the cytochrome c to the cytosol leading to the complete death of the hepatocytes. It was reported that the oxidative stress is the principle manifestations of metalaxyl-induced toxicity (Kaloyanova et al., 1991). Also, the link between oxidative stress and apoptosis was recorded (Buttke & Sandstorm, 1994). Besides oxidative damage directly inflicted on DNA by free radical, there are other indirect mechanisms by which radicals can cause destruction of the genome. As already reported,lipid peroxides enter the nucleus where they react with Fe +2 to generate the aloxyl radical which attacks DNA (Farag & Tappel, 1988). Also,intracellular calcium levels increase as a result of oxidation damage to membranes,calcium then enters the nucleus where it can activate nucleases which lead to DNA strand breaks ( McConkey et al. 1989). Marked reduction in antioxidant enzymes activities and tissue glutathione contents resulted in oxidative damage of tissues (Sharma et al. 1991). The depletion of glutathione is sufficient for the onest of apoptosis in cellular systems,especially,in hepatocytes (Nakatani et al., 2000). One or more of this mechanism are responsible for hepatotoxicity of metalaxyl. The potential role of antioxidants to reduce the activity of free radical-induced reactions has drawn increasing attention. Treating animals wth both metalaxyl and antox revealed an improvement in histopathological alterations induced by metalaxyl alone. Moreover, antox treatment leads to a decrease in the percent of apoptotic cells. Antox is an antioxidant drug composed of selenium, vitamin A acetate, ascorbic acid and vitamin E. Antox was used in therapy of different liver diseases (Watson et al.,1999; Hamooda et al., 2003; Zhong & Lemasters 2004; Oz et al., 2004). Antox succeeded in minimize cadmiuminduced toxicity in albino rats and increase the activity of endogenous antioxidants including glutathione, 24
Ozean Journal of Applied Sciences 1(1), 2008 superoxide dismutase and catalase (Hamooda et al., 2003). Watson et al. (1999) reported that bio-antox have protective effect against primary biliary cirrhosis. A significant reduction in oxidative stress parameters as well as in blood and hepatic lead level and in hepatic 8-oxodeoxyguanisone phosphate were recorded after giving antox to Schistosoma-infected and chronic lead exposed hamsters (El-Gohary et al., 2003). Antox was found to maintain blood glutathione, plasma vitamin C and serum selenium levels towards the normal range (Heaney et al., 1999). Antox is a multivitamin compound (e.g. vitamines A, B, C). Many investigators reported that vitamins may act as antiapoptotic agents (Bagchi et al., 2001; Qin et al., 2001; Minako et al., 2002) The effect of antox components (vitamines A, B, C) rests with strong antioxidants, free radical scavenging activity and inhibition of lipid peroxidation (Upsani et al., 2001). Thus, the preventive effect of antox against metalaxyl-induced liver damage and apoptosis recorded in the present work may be attributed to its antioxidant properties. REFERENCES Adams, J.M. & Cory, S. (1998). The Bcl-2 protein family: arbiters of cell survival. Science 281,1322-1326. Bagchi, M., Kusznski, C.A., & Balmoori, J. (2001). Protective effects of antioxidants against smokeless tobacco-induced oxidative stress and modulation of Bcl-2 and p53 in human oral keratinocytes. Free Radic.Res. 35(2),181-194. Buttke , T. & Sandstorm, P. (1994). Oxidative stress as a mediator of apoptosis. Immunol. Today, 15, 7-10. Chandra , J., Samali , A., & Orrenius, S. (2000). Triggering and modulation of apoptosis by oxidative stress. Free Radic. Biol. Med., 29, 323-332. Chen , N., Bai, L., Li, L., Chen , P., Zhang, C., Liu, C., Deng, T., Chen , H., Jai, K., & Zhou, Z. (2004) . Apoptosis pathway of liver cells in chronic hepatitis. World J. Gastroenterology., 10(21), 3201- 3204. Cohen , G., Macfarlane , M., Fearnhead , H., Sun , X., & Dinsdale , D. (1995). Mechanisms of cell death , with particular reference to apoptosis. In Molecular and Cellular Mechanisms of toxicity, ed. By F. D. Matteis and L. L. Smith , CRC Press , Boca Raton , FL. El-Gohary, M., Yassin, A.E., & Shalaby, M.A. (2003). The effect of chronic lead exposure on the effect of schistosomasis in hamsters and the protective effect of the antioxidant preparation "Antox". Hum.Exp.Toxicol., 22(9), 481-490. Farag , C. & Tappel, A. (1988). Damage to DNA concurrently with lipid peroxidation in rat liver slices. Biochem. J., 252, 893-896. Gordon, G.J., Coleman, W.B., & Grisham, J.W. (2000). Bax-mediated apoptosis in the livers of rats after partial hepatectomy in the retrorsine model of hepatocellular injury. Hepatology 32(2), 312-320. Greenlee, R., Ellis, M., & Berg, L. (2004). Low-dose agrochemicals and lawn –care pesticides induce developmental toxicity in murine preimplantation embryos. Environmental health perspectives, 112(6) , 703-709. Griffiths, G.J., Dubrez, L., Morgan, C.P., Jones, N.A., Whitehouse, J., Corfe, B.M., Drive, C., & Hickman, J.A. (1999). Cell damage-induced conformationonal changes of the pro-apoptotic protein Bak in vivo precede the onset of apoptosis. J.Cell Biol. 144, 903-914. Hamooda, H., Baalash, A., Saad, K., & Emara, A. (2003). Oxidative stress: A hallmark of cadmium induced toxicity in different tissues. Drug Metabolism Rev. 35(1), 231-237. Heaney, A.P., Sharer, N., Rameh B., Bregnza, J.M., & Durrington, P.N. (1999). Prevention of recurrent pancreatitis in familial lipoprotein lipase deficiency with high-dose antioxidant therapy. J.Clinic.Endocrinol.Metabol., 84(4),1203-1205. Hrelia, P., Maffei, F., Fimognari, C., Vigagni, F., & Cantelli-Forti, G. (1996). Cytogenetic effects of Metalaxyl on human and animal chromosomes. Mutat Res., 369(1-2), 81-86. Jones , D., McConkey, D., Nicotera, P., & Orrenius, S. (1989). Calcium activated DNA fragmentation in rat liver nuclei. J. Biol. Chem., 264, 6398-6403. Kaloyanova , F., Ivanova-Chemishanska , L., Zaykov , H. , Baynova , A. , Mihaylova , A. , Mircheva , V. , Anton , G., Shumkov, N., Vergieva, T., & Hal, Z. (1991). Toxicological evaluation of agromet (Metalaxyl) preparation . J. Hyg Epidemiol Microbilo Immunol., 35(4) , 375-382. 25
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Location & Geology of the Study Are
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ACKNOWLEDGEMENT The authors are gra
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Fig. 7 CMOS test chip layout design
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Wolf, S. (1995). The Submicron MOSF
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