Abstract
Procarbazine (PCZ) (indicated in Hodgkin’s disease), is an alkylating agent known to generate free radicals in vivo, while Quercetin (QCT) is a flavonoid antioxidant with proven free radical scavenging capacity. This study investigated the protective effects of QCT on PCZ-induced oxidative damage in the rat. Male Wistar rats (160–180 g) were randomized into five groups (n = 5/group): I (control), II PCZ-treated (2 mg/kg body weight (bw) for seven days); III pre-treated with QCT (20 mg/kg bw) for seven days, followed by PCZ for seven days; IV co-treated with PCZ and QCT for seven days and V administered QCT alone for seven days. PCZ caused a significant increase in plasma total bilirubin, urea, and creatinine when compared with control (P < 0.05). Similarly, plasma activities of alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and γ-glutamyl transferase (γ-GT) were significantly increased in the PCZ-treated group relative to control. Furthermore, PCZ caused a significant decrease in the activities of hepatic superoxide dismutase (SOD), catalase (CAT) and glutathione-S-transferase (GST) as well as levels of ascorbic acid (AA) and glutathione (GSH). This was followed by a significant increase in hepatic malondialdehyde (MDA) content. However, QCT pre-treatment and co-treatment ameliorated the PCZ-induced changes in plasma levels of urea, creatinine, and bilirubin as well as the activities of ALP, AST, ALT, and GGT. QCT also ameliorated hepatic AA and GSH levels and the activities of SOD, CAT, and GST. This all suggests that QCT protected against PCZ-induced oxidative damage in rats.
Highlights
Procarbazine (N-isopropyl-a-(2-methyl-hydrazine)-p-toluamide hydrochloride) (PCZ) is an orally administered alkylating anticancer agent used for the treatment of Hodgkin’s lymphoma, malignant melanoma, and brain tumors in children (Figure 1a)
Pre-administration and co-administration of QCT with PCZ attenuated the observed elevated plasma urea and creatinine levels when compared with the PCZ-treated group
That is why the present study focused on the ameliorative potential of quercetin (QCT), against procarbazine (PCZ)-induced oxidative damage in rats
Summary
Procarbazine (N-isopropyl-a-(2-methyl-hydrazine)-p-toluamide hydrochloride) (PCZ) is an orally administered alkylating anticancer agent used for the treatment of Hodgkin’s lymphoma, malignant melanoma, and brain tumors in children (Figure 1a). It is administered as a component of a chemotherapeutic cocktail used in the treatment of Hodgkin’s disease, melanoma, and bronchogenic carcinoma [1]. It is first oxidized to azoprocarbazine and further oxidized to a mixture of methylazoxyprocarbazine and benzylazoxyprocarbazine isomers [3]. The methylazoxyprocarbazine produced has been proposed as the active metabolite responsible for anticancer activity in leukaemia [4]. The oxidation of PCZ by microsomal P450 systems and peroxidases produce free radical species
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