Gallic acid protects against cyclophosphamide‐induced toxicity in testis and epididymis of rats

The protective role of gallic acid (GA) on reproductive toxicity induced by cyclophosphamide (CPA), an antineoplastic drug, was investigated in male Wistar rats. Sixty rats were grouped into 10 rats per group. Group 1 (control) received distilled water. Rats in groups 2 and 3 received GA alone at 60 and 120 mg kg^?1 for 14 consecutive days, respectively. Group 4 received a single intraperitoneal dose of CPA at 200 mg kg^?1 on day 1. Groups 5 and 6 received a single dose of CPA (200 mg kg^?1) intraperitoneally on day 1 followed by treatment with GA at 60 and 120 mg kg^?1 for 14 consecutive days, respectively. In testes and epididymis of the treated rats, CPA administration resulted in significant elevation (P < 0.05) in malondialdehyde (MDA), nitrite and hydrogen peroxide levels. There was a significant decrease in the activities of superoxide dismutase and glutathione‐S‐transferase. Furthermore, there were significant reductions in plasma luteinising hormone (LH), follicle stimulation hormone (FSH) and testosterone levels, which were accompanied by significant decrease in sperm motility and viability in CPA‐treated rats. Histological examination revealed marked testicular and epididymal atrophy in CPA alone treated rats and these aberrations were reversed by GA. In conclusion, GA has capacity to protect against reproductive toxicity induced by cyclophosphamide.     

Rutin ameliorates cisplatin‐induced reproductive damage via suppression of oxidative stress and apoptosis in adult male rats

Cisplatin (CP) treatment causes damage in the male reproductive system. Rutin (RUT) is a naturally occurring flavonoid glycoside that has antioxidant and anti‐inflammatory properties. This study aimed to investigate effects of RUT against cisplatin‐induced reproductive toxicity in male rats. Twenty‐one adult male Sprague Dawley rats were used. The control group received physiological saline with oral gavage during 14 days, and physiological saline was injected intraperitoneally (IP) in 10th days of study. CP Group received physiological saline during 14 days, and 10 mg kg^?1 CP was injected IP in 10th day. RUT + CP group received RUT (150 mg kg^?1) during 14 days, and 10 mg kg^?1 CP was injected IP in 10th day. Spermatological parameters (including motility, cauda epididymal sperm density, dead sperm percentage and morphological sperm abnormalities), biochemical (MDA, GSH, GSH‐px, SOD and CAT), histological (H&E dye) and immunochemistry evaluations of testicles were evaluated. CP treatment caused damage on some spermatological parameters, increased the oxidative stress and induced testicular degeneration and apoptosis when compared to the control group. However, RUT treatment mitigates these side effects when compared to the CP alone group. IT is concluded that RUT treatment may reduce CP‐induced reproductive toxicity as a potential antioxidant compound.     

Cisplatin‐induced testicular dysfunction and its amelioration by Launaea taraxacifolia leaf extract

This study investigates the ameliorative potential of Launea taraxacifolia (LT) aqueous leaf extract on cisplatin‐induced testicular dysfunction in Wistar rats. Thirty rats were randomly divided into six groups (A–F) of 5 rats each: Group A which served as control received water; Group B was intraperitoneally (ip) injected 10 mg kg^?1 body wt cisplatin on day 21; Groups C and D were given 100 and 400 mg of LT via oral administration, respectively, for 21 days while Groups E and F received similar treatment as Groups C and D, respectively, and then exposed to ip administration of 10 mg kg^?1 body weight cisplatin on the 21st day. Exclusively, Cisplatin‐exposed Group B rats showed reduced sperm characteristics and increased sperm morphological abnormalities; distorted histological architecture of seminiferous tubules; significantly increased lipid peroxidation (LPO) and decreased activities of superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH)levels in the testes. These parameters in LT alone treated Groups C and D were not markedly different compared with the control group. The rats with the combined treatment in Groups E and F showed significantly improved sperm parameters, testicular histo‐architecture and antioxidant enzymatic activities. Conclusively, aqueous extract of L. taraxacifolia has protective potential against cisplatin damage.     

Evaluation of the protective effect of quercetin against cisplatin‐induced renal and testis tissue damage and sperm parameters in rats

The protective effect of quercetin on cisplatin‐induced renal and testicular tissue damage was investigated using biochemical, histopathological and histological approaches. A total of 40 male rats were divided into 5 groups as follows: control; cisplatin alone; quercetin alone; cisplatin + quercetin; and quercetin + cisplatin. Cisplatin was administered to rats at a single dose of 7 mg kg^?1 intraperitoneal. Quercetin was administered by gavage daily for 10 days at dosage 50 mg kg^?1. At the end of the study serum, total antioxidant capacity (TAC) levels and total oxidant status (TOS) were determined. Malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and xanthine oxidase (XO) were studied separately in serum, renal tissue and testicular tissue. Renal and testicular morphological alterations were assessed, histopathologically. Epididymal sperm concentration, motility and morphology were investigated. Testicular and renal TAC and TOS values did not alter significantly. Renal CAT levels were increased by cisplatin and cisplatin plus quercetin groups that is reversed by administration of quercetin before cisplatin. MDA, CAT, SOD ve XO levels of testicular tissue did not differ significantly. Cisplatin and cisplatin plus quercetin groups had decreased sperm motility ratio and increased abnormal spermatozoa. Quercetin partially reverses some of the cisplatin‐related pathological effects on kidney and testis.     

Strontium fructose 1, 6‐diphosphate alleviate cyclophosphamide‐induced oligozoospermia by improving antioxidant and inhibiting testicular apoptosis via FAS/FASL pathway

This study investigated the treatment effects of a new compound, strontium fructose 1, 6‐diphosphate (FDP‐Sr), in cyclophosphamide (CP)‐induced oligozoospermia. FDP‐Sr, with extra high‐energy supply, could reverse male hypogonadism in the testis. Male Wistar rats were randomly divided into three groups: control group (vehicle treated), CP group and CP + FDP‐Sr group. Both CP group and CP + FDP‐Sr groups were orally administered CP (20 mg kg^?1) consecutively for the first 7 days to establish CP‐induced testicular toxic models. Subsequently, CP group was given orally distilled water per day, whereas CP + FDP‐Sr group was received FDP‐Sr (200 mg kg^?1) for 49 days. Compared to the CP group, the FDP‐Sr group showed significantly increased levels of serum testosterone, testis relative weights and epididymal sperm counts in rats. In addition, rats treated by FDP‐Sr showed the recuperative activities of testicular marker enzymes and normalised levels of antioxidants in tissue. Testicular protection of FDP‐Sr was further demonstrated by enhancing expression of P450scc, reducing ability of FAS/FASL and generating cytoprotection in the histopathological study. FDP‐Sr appeared to possess an ability to attenuate CP‐induced reproduction toxicity via the activation of antioxidants and steroidogenesis enzymes, and alleviate oligozoospermia via inhibition of testicular apoptosis by FAS/FASL pathway.     

Nortriptyline protects testes against germ cell apoptosis and oxidative stress induced by testicular ischaemia/reperfusion

We designed this experiment to evaluate the effects of nortriptyline on testicular injury after torsion/detorsion (T/D). Ninety‐six adult Wistar rats were divided into six groups 16 each in control group (Group 1), sham operated (Group 2), T/D + saline (Group 3), and in groups 4–6; were administered 2, 10 and 20 mg kg^?1, i.p. of nortriptyline 30 and 90 min after torsion respectively. Testicular torsion was created by twisting the right testis 720° in clockwise direction for 1 h. In six rats of each group, tissue MDA level and caspase‐3 activity increased and the activities of catalase, superoxide dismutase and glutathione peroxidase decreased in compared with control group 4 h after detorsion (P < 0.001). In six rats of each group 24 h after detorsion, histopathological changes and germ cell apoptosis were significantly deteriorated by measuring mean of seminiferous tubules diameters (MSTD) and TUNEL test. Moreover, 30 days after T/D, sperm concentration and motility were examined in rest of rats. Pre‐ and post‐reperfusion nortriptyline could reduce MDA and caspase‐3 levels and normalise antioxidant enzymes activities, dose dependently. Germ cell apoptosis was significantly decreased, and the MSTD, as well as sperm functions, were significantly improved. Inhibition of mitochondrial permeability transition pore is probably involved in protective effects of nortriptyline against testicular T/D cell damages.     

Quercetin prevents docetaxel‐induced testicular damage in rats

The protective effect of quercetin on docetaxel – an anticancer agent – induced testicular damage in rats was investigated. Thirty‐two rats were randomly divided into four groups: group 1 – control, carrier solutions were given; group 2 – quarcetin 20 mg kg^?1 day^?1 was given orally; group 3 – docetaxel 5 mg kg^?1 was given intraperitoneally as single dose; group 4 – docetaxel and quarcetin were given together. The histopathological changes; the specific biochemical markers, including antioxidants; and the sperm characteristics were evaluated. Docetaxel caused a significant increase in TBARS level and a significant decrease in SOD, GPX, CAT and GSH levels in the testicular tissues compared with the control group, whereas quercetin led to a significant decrease in lipid peroxidation, which was caused by docetaxel, via reducing TBARS level and increasing the levels of SOD, CAT, GPX and GSH. In addition, after docetaxel administration, sperm motility, sperm concentration, testicular and epididymis weights were significantly decreased and abnormal sperm rate and histopathological changes were increased. However, these effects of docetaxel on sperm parameters, histological changes and the tissue weights were eliminated by quercetin treatment. Our results show that the administration of docetaxel induced the testicular damage (oxidative stress, testes tissue damage and sperm parameters), and quercetin prevented docetaxel‐induced testicular damage in rats.     

Quercetin mitigates fenitrothion‐induced testicular toxicity in rats

Fenitrothion (FNT) is a widely used organophosphorus pesticide in agriculture. Quercetin (QR), a plant‐derived flavonoid, has a free radical scavenging property. This study investigated the protective effect of QR on FNT‐induced testicular toxicity in rats. Twenty‐four male rats were divided into four groups. Group I (control) received normal saline. Group II was administered QR at the dose of 50 mg kg^?1 b.wt. Group III was orally administered FNT (20 mg kg^?1 b.wt). Group IV was gavaged FNT and QR together at the same doses. All administrations were performed daily by gavage and maintained for 70 days. Sperm parameters and histopathological changes in testes were investigated. Serum testosterone and luteinising hormone were estimated using radioimmunoassay kits. In testes, expressions of steroidogenic genes (3β‐hydroxysteroid dehydrogenase type 6, 17 β‐hydroxysteroid dehydrogenase type 3 and steroidogenic factor‐1) and oxidative stress genes (catalase and superoxide dismutase) were determined using real‐time PCR. FNT administration caused significant decreases in sperm count, motility and hormonal levels, a significant increase in abnormal sperm morphology and a significant down‐regulation of steroidogenic and antioxidant genes in the testis. However, QR administration ameliorated FNT‐induced toxic effects. Our results concluded that QR effectively mitigated testicular damage induced by FNT in rats.     

Protective effects of quercetin against arsenic‐induced testicular damage in rats

This study investigated the effect of quercetin on changes in testes due to arsenic exposure. Twenty‐seven male rats were divided into three groups: control (10 ml kg^?1 day^?1 saline), arsenic (10 mg kg^?1 day^?1 sodium arsenite) and arsenic + quercetin (arsenic + 50 mg kg^?1 day^?1 quercetin). The rats were sacrificed at the end of 15‐day experiment. There was no difference between control group and arsenic group in body weight gain, testicular weight and serum total testosterone level. Quercetin treatment did not cause a significant difference in these parameters. In the arsenic group rats, we determined deterioration in the structure of seminiferous tubules, a decrease in the number of spermatogenic cells, an increase in the number of apoptotic cells, a decrease in the number of PCNA‐positive cells, a decrease in SOD, CAT and GSH‐Px activities, and an increase in the MDA level in testicular tissue. In all these changes, arsenic+quercetin group showed an improved compared to arsenic group. The amount of arsenic increased in the arsenic group was compared to the control group, and there was no difference between arsenic group and arsenic + quercetin group in the amount of arsenic. In conclusion, quercetin prevented arsenic‐induced testicular damage with its anti‐apoptotic and antioxidant effects.     

Ameliorative effect of resveratrol on testicular oxidative stress,spermatological parameters and DNA damage in glyphosate‐based herbicide‐exposed rats

In this study, the reproductive impacts of being exposed to glyphosate (GLF) and the protective impacts of resveratrol (RES) were assessed in 28 Wistar male rats, which were equally separated into four groups. Control group were fed normal diet without GLF or RES, group II received normal feed containing 20 mg kg^?1 daily^?1 RES, group III received normal feed containing 375 mg kg^?1 daily^?1 GLF, and group IV received normal feed containing 375 mg kg^?1 daily^?1 GLF+20 mg kg^?1 daily^?1 RES. GLF administration decreased sperm motility, sperm plasma membrane integrity, glutathione level and superoxide dismutase in the testicular tissue of rats. On the other hand, abnormal sperm rate, malondialdehyde level, and DNA damage were detected to be high in the group treated with GLF. The findings indicate that RES protects spermatological parameters and DNA damage, decreases GLF‐induced lipid peroxidation, improves the antioxidant defence mechanism and regenerates tissue damage in the testis of rats.     

Chemotherapeutic efficacy of an ethanolic Moringa oleifera leaf extract against chromium‐induced testicular toxicity in rats

This study was conducted to determine the mechanism underlying the chemotherapeutic efficacy of an ethanolic Moringa oleifera leaf extract (MOLEE) against chromium‐induced impairments of rat testes using biochemical methods. Twenty male Wistar rats were divided into four groups of five animals each. Group I (control), group II injected potassium dichromate (8 mg kg^?1) i.p., group III gastrogavaged MOLEE (500 mg kg^?1) p.o. and group IV received (potassium dichromate plus MOLEE) by the same doses for 60 days. After the blood samples were collected, the animals were sacrificed to determine the testicular antioxidant status and sperm parameters. The chromium‐treated group exhibited a significant decrease in testicular antioxidant enzymatic activities, local immunity and sperm parameters as well as an increase in inflammatory markers when compared with the control and MOLEE‐treated group. However, concurrent administration of chromium and MOLEE significantly ameliorated the chromium effects on the sperm parameters, local immunity, inflammatory markers and antioxidant enzymatic activities compared with rats exposed to chromium alone. This study concludes that chronic exposure to chromium produces clear testicular toxicity, which can either be prevented or at least decreased by concomitant administration of MOLEE. Interestingly, the metal ion chelation could attribute partly the antioxidant activities of MOLEE.     

Mitigation of paracetamol‐induced reproductive damage by chrysin in male rats via reducing oxidative stress

Paracetamol (PRC) is a nonsteroidal anti‐inflammatory drug used widely as a painkiller for various diseases and as the symptomatic flu cure in several countries worldwide. PRC toxicity may occur under conditions of the overdose usage. Chrysin (CR) is a flavonoid that is naturally present in several plants, honey and propolis. The aim of this study was to investigate the effects of CR (at the doses of 25 mg kg⁻¹ and 50 mg kg⁻¹) pre‐treatment over seven consecutive days against PRC‐induced reproductive toxicity in male rats. Our results showed that PRC toxicity decreased the sperm motility, and increased dead sperm rate, abnormal sperm cell rate, apoptosis and MDA levels in testicular tissues. Pre‐treatment with CR at the dose of 25 and 50 mg kg⁻¹ for 7 days mitigated side effects of acute PRC toxicity in male reproductive system proportionally in a dose‐dependent manner. This possible protection mechanism might be dependent on the antioxidant activity of CR. In conclusion, pre‐treatment with CR at the dose of 25 and 50 mg kg⁻¹ for 7 days can be the beneficial against PRC‐induced reproductive toxicity proportionally in a dose‐dependent manner.     

Fenugreek seed extract attenuates cisplatin‐induced testicular damage in Wistar rats

Cisplatin (CIS) provides oxidative stress and inflammations in testicular tissues. Fenugreek seed extract (FSE) is a widely used herbal medicine with potent antioxidant and anti‐inflammation properties. The purpose of this study was to investigate the protective effects and the possible mechanisms of FSE against CIS‐induced testicular damage in rats. Adult male Wistar rats were given vehicle, single dose of CIS alone (10 mg kg^?1), single dose of FSE alone or single dose of CIS followed by FSE (50, 100 or 200 mg kg^?1) every day for 5 days. On day 6, oxidative stress and apoptotic testicular toxicity were evaluated. FSE attenuated both germ cell degenerations and apoptosis in seminiferous tubules in CIS‐treated rats. Furthermore, FSE counteracted CIS‐induced oxidative stress in rats as assessed by the restoration of superoxide dismutase and catalase activities and reduction in the myeloperoxidase activity and malondialdehyde levels in testes. CIS increased expressions of inducible nitric oxide synthase and nuclear factor‐kappa B in testicular tissues. Importantly, treatment with FSE at all doses effectively alleviated all of these inflammatory parameters in testes. Based on these results, we concluded that FSE reduces CIS‐induced reproductive toxicity in rats by the suppression of testicular oxidative stress, apoptosis and inflammations.     

Aminoguanidine prevents testicular damage–induced‐2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) in male rats

In this study, it was aimed to determinate protective effects of aminoguanidine (AG) against reproductive toxicity caused by 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD), an environmental contaminant. Thirty‐two rats were equally divided into four groups; the first group was kept as control and given corn oil as carrier. In second and third groups, TCDD and AG were orally administered at the dose of 2 μg kg^?1 per week and 100 mg kg^?1 per day for 45 days, respectively. In fourth group, TCDD and AG were given together at the same doses. Although TCDD significantly increased the formation of TBARS, it caused a significant decline in the levels of GSH, CAT, GPx and SOD in rats. On the other hand, AG, given together TCDD, reversed TCDD effects on TBARS SOD, GSH, GPx and CAT. In addition, sperm characteristics negatively affected and histopathological deformation occurred with TCDD exposure. However, AG treatment partly prevented these toxic effects of TCDD on spermatological parameters and histopathological changes. In conclusion, TCDD exposure induces testicular damage (oxidative stress, histopathological damage and sperm parameters), and AG treatment reversed TCDD‐induced testicular damage in rats. Thus, AG may be useful for the prevention and treatment of TCDD‐induced male infertility problems.     

Protective effects of udenafil citrate,piracetam and dexmedetomidine treatment on testicular torsion/detorsion‐induced ischaemia/reperfusion injury in rats

The aim of this study was to investigate the antioxidant properties of udenafil citrate (1.4 mg kg^?1–2.8 mg kg^?1), dexmedetomidine 25 μg kg^?1 and piracetam 200 mg kg^?1 administered on ipsilateral/contralateral testes after ischaemia in a rat model of testicular torsion/detorsion (T/D) and define its protective effect histologically. Fifty‐six Wistar albino rats were included and randomly assigned into 6 groups. No intervention was performed in control group (Group 1, n = 8) and in torsion/detorsion group, (Group 2, n = 8). Udenafil 1.4 mg kg^?1 was given to torsion/detorsion group (Group 3, n = 10), udenafil 2.8 mg kg^?1 was given to torsion/detorsion group (Group 4, n = 10), piracetam 200 mg kg^?1 was given to torsion/detorsion group (Group 5, n = 10) and dexmedetomidine 25 μg kg^?1 was given to torsion/detorsion group (Group 6, n = 10) intraperitoneally after 60 mins of testicular torsion. Biochemical and histopathological testicular injury were evaluated. When the tissue was examined by TOS values, Group 3, Group 4 and Group 5 were significantly lower than Group 2. In contrary Group 6 values were significantly higher than Group 2. The increasing doses of udenafil demonstrated antioxidant properties on the testis tissue and histopathological that protects the testicles.     

Ameliorative effect of polydatin on oxidative stress‐mediated testicular damage by chronic arsenic exposure in rats

Arsenic causes lipid peroxidation leading to alterations in antioxidant status in organisms. In this study, the reproductive effects of chronic exposure to arsenic and the protective effects of polydatin (PD) were evaluated in 35 Wistar male rats, which were divided equally into five groups. The control group received a normal diet and tap water, arsenic (100 mg l^?1, approximately 1/50 of oral LD₅₀) was given via drinking water to experimental groups except control group, and PD was orally given to the other groups at dose of 50, 100 and 200 mg kg^?1 for 60 days. Arsenic administration decreased sperm motility, glutathione level, superoxide dismutase and catalase activities in testicular tissue of rats. In contrast, malondialdehyde level and DNA damage were found to be high levels in arsenic‐treated group. Histopathologically, it was observed that decreased sperm concentration and degeneration of Sertoli cells in testicular tissue. PD administration, partially 200 mg kg^?1, reversed arsenic‐induced lipid peroxidation, DNA damage, antioxidant enzyme activity and cell integrity in testis of rats. These results demonstrate that PD decreases arsenic‐induced lipid peroxidation, enhances the antioxidant defence mechanism and regenerates tissue damage in testis of rats.     

Protective effects of fish omega‐3 fatty acids on doxorubicin‐induced testicular apoptosis and oxidative damage in rats

The aim of this study was to examine the protective effects of fish omega‐3 (n‐3) fatty acids on acute doxorubicin (DOX)‐induced testicular apoptosis and oxidative damage. 24 male rats were divided into three groups: control, DOX‐treated and DOX+fish n‐3 fatty acids. Fish n‐3 fatty acids (400 mg kg^?1) were given for 30 days by intragastric gavage. The rats received a single intraperitoneal injection of DOX (30 mg kg^?1) and were sacrificed after 48 h. The DOX+fish n‐3 fatty acids group showed a decrease in malondialdehyde levels and increased activities of superoxide dismutase and glutathione peroxidase in comparison with the DOX‐treated group. Acute DOX treatment caused severe damage such as disorganisation and separation of germ cells. The fish n‐3 fatty acids‐pretreated rats showed an improved histological appearance in the DOX‐treated group. Our data indicate a reduction in the activity of terminal deoxynucleotidyl transferase mediated dUTP nick end labelling; there was a rise in the expression of proliferating cell nuclear antigen in testis tissues of the DOX+fish n‐3 fatty acids group compared with DOX‐treated group. These data suggested that fish n‐3 fatty acids pre‐treatment may be beneficial for spermatogenesis following acute DOX‐induced testicular damage by decreasing germ cell apoptosis and oxidative stress.     

Protective role of Diospyros lotus on cisplatin‐induced changes in sperm characteristics,testicular damage and oxidative stress in rats

The aim of this study was to investigate the protective effect of Diospyros lotus (DL) on cisplatin (CP)‐induced testicular damage in male rats. Twenty‐eight male rats were randomly divided into four groups: group 1 – control, given isotonic saline solution; group 2 – CP 7 mg kg⁻¹ given intraperitoneally as single dose; group 3 – DL 1000 mg kg⁻¹ per day given orally for 10 days; group 4 – CP and DL given together at the same doses. CP caused a significant increase in thiobarbituric acid‐reactive substances (TBARS) level and a significant decrease in superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and glutathione (GSH) levels in rats testis tissues compared to the control group. CP caused a significant increase in lipid peroxidation in testis tissues compared to the control group, whereas DL led to a significant increase in SOD and GSH levels. However, there were no statistically significant changes in GPx and CAT levels. In addition, serum testosterone levels, sperm concentration and sperm motility were significantly decreased, but abnormal sperm rate and histological changes were increased with CP. However, these effects of CP on sperm parameters, histological changes and the tissue weights were eliminated by DL treatment. In conclusion, our study showed that the reproductive toxicity caused by CP may be prevented by DL treatment.     

Dose‐dependent effects of ethanol extract of Salvia haematodes Wall roots on reproductive function and copulatory behaviour in male rats

This study was aimed to investigate the dose‐dependent effects of Salvia haematodes Wall roots (SHW) extract on male reproductive function and copulatory behaviour in rats. Sexually mature males were assigned to four groups: control and treated (5, 50 and 300 mg kg^?1 day^?1 for 30 days). At the end of treatment regimes, the reproductive activity viz. body/organ weights, testicular spermatogenesis, daily sperm production rate (DSP) and epididymal sperm counts, and sexual behaviour including mounting latency (ML), mounting frequency (MF), intromission latency (IL), intromission frequency (IF), ejaculation latency (EL), post‐ejaculatory interval (PEI) and penile reflexes (PE) were assessed. Results showed significant increase in body weight (at 300 mg kg^?1), testis/epididymis weights (at 50 and 300 mg kg^?1), testicular spermatids, DSP, tubular diameter and epididymal sperm counts (at 50 and 300 mg kg^?1doses) in treated compared with control rats. It also produced dose‐dependant changes in sexual behaviour. The 5 mg kg^?1 dose of extract increased MF and PE, whereas 50 and 300 kg^?1 doses caused significant increase in MF, IF, PE, EL (but less than sildenafil citrate treatment), hit rate and seminal plug weight. It is concluded that SHW extract enhances anabolic activity, testicular function and sexual behavioural performance in a dose‐dependant manner.