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.

Bicalutamide (BCT) is a potent anti-androgen chemotherapeutic drug indicated for prostate cancer. However, BCT is known to cause oxidative stress and impairment of male reproductive function. Whereas Morin (MOR), a flavonoid has been found to be a potent antioxidant, with free radical scavenging capacity. This study investigated the protective effect of MOR on BCT-induced testicular toxicity in Wistar rats. Twenty-four male albino rats were randomized into four groups (n=6/group). Group I which served as control received distilled water. Group II, received 3 mg/kg body weight (bwt) BCT orally (per os); group III received 3 mg/kg/day BCT p.o. plus 100 mg/kg/d MOR p.o. and group IV received 100 mg/kg/d MOR p.o. All treatments lasted for 14 days, thereafter, animals were sacrificed and epididymis and testis were collected for sperm and biochemical analyses. The result revealed that BCT treatment caused a significant increase in abnormal sperm morphology. Sperm production, sperm count, motility and viability were significantly reduced when compared with control (p<0.05). Similarly, testicular superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx),glutathione S-transferase (GST) and acid phosphatase (ACP) activities, as well as ascorbic acid and GSH levels were significantly reduced in the BCT- treated animals when compared to control (p<0.05). Conversely, testicular alkaline phosphatase (ALP), gamma glutamyl transferase (GGT) and lactate dehydrogenese (LDH) activities as well as malondialdehyde (MDA) levels of BCT-treated animals  increased significantly relative to control (p<0.05). However, co-treatment with Morin ameliorated BCT-induced alterations in sperm parameters, ascorbic acid, GSH and MDA levels, as well as LDH, SOD, CAT, GST, GPX, ACP, ALP and GGT activities. Data obtained from this study suggest that Morin protected against altered sperm parameters and testicular oxidative stress caused by BCT. Keywords: Bicalutamide, Anti-androgen, Testis, Oxidative stress, Morin, Antioxidant, Rat