This study evaluated the role of quercetin against cyclophosphamide‐induced distortion of rat testicular function. Adult rats were administered cyclophosphamide (100 mg/kg), quercetin (50 mg/kg) and in combination for seven days. Cyclophosphamide caused a significant increase in the activities of indoleamine 2, 3‐dioxygenases (IDO), tryptophan 2, 3‐dioxygenase (TDO), myeloperoxidase (MPO), and elevated the concentrations of interleukin 6 (IL‐6) and interferon‐γ (IFN‐γ). Cyclophosphamide increased testis malondialdehyde (MDA) concentrations but depleted superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH‐Px) and glutathione (GSH). However, quercetin co‐administration significantly (p < 0.05) prevented the increased values of IDO, TDO, MPO, IL‐6, IFN‐γ, MDA, SOD, CAT, GSH‐Px and GSH compared with control rats. Also, quercetin co‐treatment significantly increased serum testosterone, follicle‐stimulating hormone (FSH), prolactin, luteinizing hormone (LH), activities of testicular 3β‐hydroxysteroid dehydrogenase (3 β‐HSD), 17β‐hydroxysteroid dehydrogenase (17 β‐HSD) as well as sperm count, motility and viability but reduced abnormal sperm morphology. Quercetin exposure alone did not alter any of the parameters evaluated relative to control. Thus, quercetin protected the testes against cyclophosphamide‐induced alterations in immunosuppressive IDO/TDO activities elicited by oxidative‐inflammatory mediators.

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This study investigated the influence of rutin against EtOH‐induced testicular impairment in rats and the involvement of the indole‐aminergic pathway. Four groups of eight rats each were orally exposed to drinking water (Group 1), EtOH (5 g/kg bwt, Group 2), R (5 g/kg bwt, Group 3), and EtOH + R (5 g/kg bwt + 50 mg/kg bwt, Group 4) via gavage for 15 days. Results showed that exposure to EtOH significantly (p < 0.0001) reduced the testicular antioxidant system and increased lipid peroxidation (LPO) relative to control. We observed a significant (p < 0.0001) increase in the inflammatory biomarkers, with attendant disruption in the testicular histological structure and concomitant elevation in the activities of indoleamine 2,3‐dioxygenase (IDO), in comparison with control and no noticeable effects in tryptophan 2,3‐dioxygenase (TDO) activity across the groups. Rutin‐only exposed group did not show any alteration in the measured parameters when compared with the control. Rutin co‐exposure augmented the antioxidant system, prevented histological damage, reduced LPO and inflammation, and thus, lowered EtOH‐mediated increase in IDO activity, compared with control. Overall, these findings reveal the involvement of the indole‐aminergic pathway in rutin's protective influence against EtOH‐induced testicular impairment in rats.