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A list of all pages that have property "Has abstract" with value "The present study evaluated the ''in vivo'' antitumor effects and toxicity of a new Ru(II) compound, cis-(Ru[phen]2[ImH]2)<sup>2+</sup> (also called RuphenImH [RuC]), against Walker-256 carcinosarcoma in rats. After subcutaneous inoculation of Walker-256 cells in the right pelvic limb, male Wistar rats received 5 or 10mgkg<sup>-1</sup> RuC orally or intraperitoneally (i.p.) every 3 days for 13 days. A positive control group (2mgkg<sup>-1</sup> cisplatin) and negative control group (vehicle) were also used. Tumor progression was checked daily. After treatment, tumor weight, plasma biochemistry, hematology, oxidative stress, histology, and tumor cell respiration were evaluated. RuC was effective against tumors when administered i.p. but not orally. The highest i.p. dose of RuC (10mgkg<sup>-1</sup>) significantly reduced tumor volume and weight, induced oxidative stress in tumor tissue, reduced the respiration of tumor cells, and induced necrosis but did not induce apoptosis in the tumor. No clinical signs of toxicity or death were observed in tumor-bearing or healthy rats that were treated with RuC. These results suggest that RuC has antitumor activity through the modulation of oxidative stress and impairment of oxidative phosphorylation, thus promoting Walker-256 cell death without causing systemic toxicity. These effects make RuC a promising anticancer drug for clinical evaluation. Copyright © 2017 Elsevier Inc. All rights reserved.". Since there have been only a few results, also nearby values are displayed.

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    • Alves 2017 Free Radic Biol Med  + (The present study evaluated the ''in vivo'The present study evaluated the ''in vivo'' antitumor effects and toxicity of a new Ru(II) compound, cis-(Ru[phen]2[ImH]2)<sup>2+</sup> (also called RuphenImH [RuC]), against Walker-256 carcinosarcoma in rats. After subcutaneous inoculation of Walker-256 cells in the right pelvic limb, male Wistar rats received 5 or 10mgkg<sup>-1</sup> RuC orally or intraperitoneally (i.p.) every 3 days for 13 days. A positive control group (2mgkg<sup>-1</sup> cisplatin) and negative control group (vehicle) were also used. Tumor progression was checked daily. After treatment, tumor weight, plasma biochemistry, hematology, oxidative stress, histology, and tumor cell respiration were evaluated. RuC was effective against tumors when administered i.p. but not orally. The highest i.p. dose of RuC (10mgkg<sup>-1</sup>) significantly reduced tumor volume and weight, induced oxidative stress in tumor tissue, reduced the respiration of tumor cells, and induced necrosis but did not induce apoptosis in the tumor. No clinical signs of toxicity or death were observed in tumor-bearing or healthy rats that were treated with RuC. These results suggest that RuC has antitumor activity through the modulation of oxidative stress and impairment of oxidative phosphorylation, thus promoting Walker-256 cell death without causing systemic toxicity. These effects make RuC a promising anticancer drug for clinical evaluation.</br></br>Copyright © 2017 Elsevier Inc. All rights reserved.icancer drug for clinical evaluation. Copyright © 2017 Elsevier Inc. All rights reserved.)