After a single intraperitoneal dose of 7.5 mg/kg of cisplatin [39].In a study by Ravindra et al, rats injected intraperitoneally with 0.4 mg/kg of cisplatin for a period of 8 weeks showed different alterations comprising marked proximal tubular dilation and 3-Bromopyruvic acid web desquamation along with acute tubular necrosis [40]. Other drugs like methrotrexate and cyclosporine have been reported to have a nephrotoxic effect culminating to cell death by direct tubular toxicity and intratubular precipitation [41,42] along with proximal tubular apoptosis and necrosis [43] respectively, but studies evaluating their dose dependent renal histopathological manifestations are not available.Nephrotoxicity is an integral and inherent accompaniment of multiple anti-neoplastic drugs [23,24,44?6] which usually have a narrow therapeutic index and the minimum dosage required to significantly decrease tumor burden is usually associated with substantial nephrotoxicity. The significantly diminished renal toxicity of N-substituted ethylenediamine complexes of gold could be attributed to their different anti-proliferative mechanism of action and selective sparing of the proximal tubular epithelial cells. Their mechanism although not precisely delineated, comprises a cumulative impact on induction of cell cycle blockage, interruption of the cell mitotic cycle, programmed cell death (apoptosis) or premature cell death (necrosis) [47]. Hepatotoxicity is an entity not as extensively explored as nephrotoxicity as it does not manifest itself as a dose limiting factor [48]. With our ethylenediamine derivative of gold, in the acute toxicity component of the study, varying extent of steatosis was the main finding. In the sub acute toxicity component, varying extent of ballooning degeneration with accompanying congestion and focal portal inflammation comprised the predominant histopathological lesion. One of the samples revealed an occasional focus of lobular inflammation. Capsular inflammation was also a consistent finding. Other drugs like cisplatin produce hepatoxicity in high doses [49,50]. El-Sayyad et al investigated the effects of cisplatin, doxorubicin and 5-FU belonging to different chemical classes on rats liver and showed that groups receiving cisplatin and doxorubicin exhibited increased hepatoxicity in comparison to 5-FU treatment. The most pronounced histopathlogical abnormalities observed were hepatic cord dissolution [51]. Avci et al demonstrated that a dose of 10 mg/kg cisplatin could induce sinusoidal congestion, hydropic 1326631 and vacuolar degeneration, extensive disorganization in hepatocytes, and significant fibrosis around central venules and expanded periportal areas [48]. In another multidrug, multimodal study by Kart et al, moderate to severe hydropic degeneration in centrilobular zones extendingRenal and Hepatic Toxicity of a Gold (III) CompoundFigure 6. Spectrum of hepatic Rubusoside custom synthesis Microscopic findings as seen in the acute toxicity study of a gold (III) compound [Au(en)Cl2]Cl. a: Marked mixed micro and macrovesicular steatosis, H E 640. b c: Marked sinusoidal congestion and dilatation, H E 620 and 640 respectively. d: Marked ballooning degeneration along with two microgranulomas, H E 640. doi:10.1371/journal.pone.0051889.gFigure 7. Microscopic pictures of renal tubules, with no evidence of necrosis as seen in sub-acute toxicity study 
of a gold (III) compound [Au(en)Cl2]Cl, H E at magnifications of : a. 610. b. 620. c. 640. doi:10.1371/journal.pone.0051889.gRenal and H.After a single intraperitoneal dose of 7.5 mg/kg of cisplatin [39].In a study by Ravindra et al, rats injected intraperitoneally with 0.4 mg/kg of cisplatin for a period of 8 weeks showed different alterations comprising marked proximal tubular dilation and desquamation along with acute tubular necrosis [40]. Other drugs like methrotrexate and cyclosporine have been reported to have a nephrotoxic effect culminating to cell death by direct tubular toxicity and intratubular precipitation [41,42] along with proximal tubular apoptosis and necrosis [43] respectively, but studies evaluating their dose dependent renal histopathological manifestations are not available.Nephrotoxicity is an integral and inherent accompaniment of multiple anti-neoplastic drugs [23,24,44?6] which usually have a narrow therapeutic index and the minimum dosage required to significantly decrease tumor burden is usually associated with substantial nephrotoxicity. The significantly diminished renal toxicity 
of N-substituted ethylenediamine complexes of gold could be attributed to their different anti-proliferative mechanism of action and selective sparing of the proximal tubular epithelial cells. Their mechanism although not precisely delineated, comprises a cumulative impact on induction of cell cycle blockage, interruption of the cell mitotic cycle, programmed cell death (apoptosis) or premature cell death (necrosis) [47]. Hepatotoxicity is an entity not as extensively explored as nephrotoxicity as it does not manifest itself as a dose limiting factor [48]. With our ethylenediamine derivative of gold, in the acute toxicity component of the study, varying extent of steatosis was the main finding. In the sub acute toxicity component, varying extent of ballooning degeneration with accompanying congestion and focal portal inflammation comprised the predominant histopathological lesion. One of the samples revealed an occasional focus of lobular inflammation. Capsular inflammation was also a consistent finding. Other drugs like cisplatin produce hepatoxicity in high doses [49,50]. El-Sayyad et al investigated the effects of cisplatin, doxorubicin and 5-FU belonging to different chemical classes on rats liver and showed that groups receiving cisplatin and doxorubicin exhibited increased hepatoxicity in comparison to 5-FU treatment. The most pronounced histopathlogical abnormalities observed were hepatic cord dissolution [51]. Avci et al demonstrated that a dose of 10 mg/kg cisplatin could induce sinusoidal congestion, hydropic 1326631 and vacuolar degeneration, extensive disorganization in hepatocytes, and significant fibrosis around central venules and expanded periportal areas [48]. In another multidrug, multimodal study by Kart et al, moderate to severe hydropic degeneration in centrilobular zones extendingRenal and Hepatic Toxicity of a Gold (III) CompoundFigure 6. Spectrum of hepatic microscopic findings as seen in the acute toxicity study of a gold (III) compound [Au(en)Cl2]Cl. a: Marked mixed micro and macrovesicular steatosis, H E 640. b c: Marked sinusoidal congestion and dilatation, H E 620 and 640 respectively. d: Marked ballooning degeneration along with two microgranulomas, H E 640. doi:10.1371/journal.pone.0051889.gFigure 7. Microscopic pictures of renal tubules, with no evidence of necrosis as seen in sub-acute toxicity study of a gold (III) compound [Au(en)Cl2]Cl, H E at magnifications of : a. 610. b. 620. c. 640. doi:10.1371/journal.pone.0051889.gRenal and H.