Cisplatin is one of the most widely used cytotoxic therapeutic agents for the treatment of cancer. This drug, at effective higher doses or multiple low doses, causes many physiological adverse effects. N,N Diphenyl-р-phenylenediamine (DPPD) and Vit C against cisplatin-induced oxidative stress in rats. Cisplatin was injected once a week (2 mg/kg bwt) for 4 weeks. DPPD (125 mg/kg bwt) and vit C (100 mg/kg bwt) were injected once a week an 24 hour prior to cisplatin injection. In cisplatin treated group, the number of RBCs and WBCs were decreased (P 0.05) compared to that of control rats. However, in rats injected with Vit C or DPPD prior to cisplatin treatment, blood cells counts elevated again to their normal values. Cisplatin toxicity was manifested biochemically by a significant increase (P0.05) of LPO in spleen as well as a decrease in GSH content which associated with a reduction in the activities of antioxidant enzymes, SOD, CAT, GST and γ GGT in spleen and plasma. In addition to the marked decrease in Vit C and Vit E levels. In rats treated with Vit C or DPPD in combination with cisplatin LPO and the activities of SOD, GST, CAT and GGT restored to about normal control levels. In conclusion DPPD and vitamin C are efficient promising compounds for reducing cisplatin-toxic side effects.

Cisplatin is one of the most widely used cytotoxic therapeutic agents for the treatment of cancer. This drug, at effective higher doses or multiple low doses, causes many physiological adverse effects. N,N Diphenyl-р-phenylenediamine (DPPD) and Vit C against cisplatin-induced oxidative stress in rats. Cisplatin was injected once a week (2 mg/kg bwt) for 4 weeks. DPPD (125 mg/kg bwt) and vit C (100 mg/kg bwt) were injected once a week an 24 hour prior to cisplatin injection. In cisplatin treated group, the number of RBCs and WBCs were decreased (P 0.05) compared to that of control rats. However, in rats injected with Vit C or DPPD prior to cisplatin treatment, blood cells counts elevated again to their normal values. Cisplatin toxicity was manifested biochemically by a significant increase (P0.05) of LPO in spleen as well as a decrease in GSH content which associated with a reduction in the activities of antioxidant enzymes, SOD, CAT, GST and γ GGT in spleen and plasma. In addition to the marked decrease in Vit C and Vit E levels. In rats treated with Vit C or DPPD in combination with cisplatin LPO and the activities of SOD, GST, CAT and GGT restored to about normal control levels. In conclusion DPPD and vitamin C are efficient promising compounds for reducing cisplatin-toxic side effects.

Cisplatin is one of the most widely used cytotoxic therapeutic agents for the treatment of cancer. This drug, at effective higher doses or multiple low doses, causes many physiological adverse effects. N,N Diphenyl-р-phenylenediamine (DPPD) and Vit C against cisplatin-induced oxidative stress in rats. Cisplatin was injected once a week (2 mg/kg bwt) for 4 weeks. DPPD (125 mg/kg bwt) and vit C (100 mg/kg bwt) were injected once a week an 24 hour prior to cisplatin injection. In cisplatin treated group, the number of RBCs and WBCs were decreased (P 0.05) compared to that of control rats. However, in rats injected with Vit C or DPPD prior to cisplatin treatment, blood cells counts elevated again to their normal values. Cisplatin toxicity was manifested biochemically by a significant increase (P0.05) of LPO in spleen as well as a decrease in GSH content which associated with a reduction in the activities of antioxidant enzymes, SOD, CAT, GST and γ GGT in spleen and plasma. In addition to the marked decrease in Vit C and Vit E levels. In rats treated with Vit C or DPPD in combination with cisplatin LPO and the activities of SOD, GST, CAT and GGT restored to about normal control levels. In conclusion DPPD and vitamin C are efficient promising compounds for reducing cisplatin-toxic side effects.

Cisplatin is one of the most widely used cytotoxic therapeutic agents for the treatment of cancer. This drug, at effective higher doses or multiple low doses, causes many physiological adverse effects. N,N Diphenyl-р-phenylenediamine (DPPD) and Vit C against cisplatin-induced oxidative stress in rats. Cisplatin was injected once a week (2 mg/kg bwt) for 4 weeks. DPPD (125 mg/kg bwt) and vit C (100 mg/kg bwt) were injected once a week an 24 hour prior to cisplatin injection. In cisplatin treated group, the number of RBCs and WBCs were decreased (P 0.05) compared to that of control rats. However, in rats injected with Vit C or DPPD prior to cisplatin treatment, blood cells counts elevated again to their normal values. Cisplatin toxicity was manifested biochemically by a significant increase (P0.05) of LPO in spleen as well as a decrease in GSH content which associated with a reduction in the activities of antioxidant enzymes, SOD, CAT, GST and γ GGT in spleen and plasma. In addition to the marked decrease in Vit C and Vit E levels. In rats treated with Vit C or DPPD in combination with cisplatin LPO and the activities of SOD, GST, CAT and GGT restored to about normal control levels. In conclusion DPPD and vitamin C are efficient promising compounds for reducing cisplatin-toxic side effects.

Thermal degradation of poly(o-toluidine) (POT) reduced [base form (POT-EB)] and oxidized form [i.e. doped with salicylidine-aniline (SA) and/or salicylidine-o-aminophenol (SAP)] was investigated experimentally and computationally. The results of thermal (TGA) and differential thermal (DTG) gravimetric analysis suggest a higher thermal stability for the oxidized (SA or SAP-doped POT) than that for the respective reduced (POT-EB) chain. Nonisothermal degradation of the reduced POT matrix reveals hydrophilic nature about two times stronger than that for the oxidized form (SA and/or SAP-doped POT) under the same conditions. Molecular mechanics (MM
/) calculations substantiate these observations. FTIR spectroscopic study of the calcined POT-EB showed that the quinoid (Q) ring (iminostructure) is thermally at least twice more stable than for that the benzenoid (B) rings (aminostructure) in the repeating unit of the polymer chain. Isothermal degradation curves [fraction decomposed (a) vs. degradation time (t in min)] of the polymers under investigation revealed that they are characteristically declaratory in shape.

Thermal degradation of poly(o-toluidine) (POT) reduced [base form (POT-EB)] and oxidized form [i.e. doped with salicylidine-aniline (SA) and/or salicylidine-o-aminophenol (SAP)] was investigated experimentally and computationally. The results of thermal (TGA) and differential thermal (DTG) gravimetric analysis suggest a higher thermal stability for the oxidized (SA or SAP-doped POT) than that for the respective reduced (POT-EB) chain. Nonisothermal degradation of the reduced POT matrix reveals hydrophilic nature about two times stronger than that for the oxidized form (SA and/or SAP-doped POT) under the same conditions. Molecular mechanics (MM
/) calculations substantiate these observations. FTIR spectroscopic study of the calcined POT-EB showed that the quinoid (Q) ring (iminostructure) is thermally at least twice more stable than for that the benzenoid (B) rings (aminostructure) in the repeating unit of the polymer chain. Isothermal degradation curves [fraction decomposed (a) vs. degradation time (t in min)] of the polymers under investigation revealed that they are characteristically declaratory in shape.