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.     

Oral administration of Moringa oleifera oil but not coconut oil prevents mercury‐induced testicular toxicity in rats

This study was conducted to compare the effects of administration of coconut oil (CO) and Moringa oleifera oil (MO) on testicular oxidative stress, sperm quality and steroidogenesis parameters in rats treated with mercury chloride (HgCl₂). After 15 days of oral administration of CO (2 ml kg^?1 body weight) and MO (2 ml kg^?1 body weight) along with intraperitoneal (i.p.) administration of HgCl₂ (5 mg kg^?1 body weight) alone or in combination, we found that CO treatment did not protect against HgCl₂‐induced poor sperm quality (motility, count) as well as decreased testosterone level and 17β‐hydroxysteroid dehydrogenase (17β‐HSD) activity. Treatment with CO alone decreased glutathione (GSH), and glutathione peroxidase (GSH‐Px) activities and increased malondialdehyde (MDA) level in rat's testis, whereas MO did not change these parameters. Cotreatment with MO prevented HgCl₂‐induced testicular catalase (CAT) and superoxide dismutase (SOD) activities, poor sperm quality and low testosterone level and also blocks the adverse effect of CO+HgCl₂ (2 ml kg^?1 body weight + 5 mg kg^?1 body weight) on the investigated endpoints. In conclusion, MO and not CO decreased the deleterious effects of HgCl₂ on sperm quality and steroidogenesis in rats and also strengthen the antioxidant defence of the testes. Therefore, MO is beneficial as an antioxidant in HgCl₂‐induced oxidative damage.     

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.     

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.     

Effects of montelukast and zileuton on testicular torsion/detorsion injury in rats

The aim of this study was to evaluate and compare the effects of 5‐lipoxygenase enzyme (5‐LO) inhibitor zileuton and cysteinyl leukotriene receptor (CysLT1R) antagonist montelukast in testicular torsion/detorsion (T/D) injury model in rats. Rats were anaesthetised with 75 mg kg^?1 ketamine hydrochloride and 8 mg kg^?1 xylazine intraperitoneal before the operation. Torsion was created by rotating the right testis 720° clockwise and maintained by fixing the testis. The rats were treated with CysLT1R antagonist montelukast (10 mg kg^?1; i.p.), 5‐LO inhibitor zileuton (3 mg kg^?1; i.p.), and vehicle, at 30 min prior detorsion. After 1 h of torsion, the testis was counter‐rotated to the natural position and replaced into the scrotum. Malondialdehyde (MDA) level was measured in testicular tissue after 3 h of reperfusion. Histological examination was performed after 24 h of reperfusion. T/D caused a significant increase in MDA level and histopathological injury in testes. Montelukast and zileuton treatments prevented the T/D‐induced augmentation in MDA levels. Only zileuton treatment significantly reduced the T/D‐induced histopathological injury. In this study, we demonstrated for the first time that zileuton had protective effects on testicular T/D injury. We have also found that zileuton is more effective than montelukast on histopathological injury.     

Thymoquinone ameliorates testicular tissue inflammation induced by chronic administration of oral sodium nitrite

Although sodium nitrite has been widely used as food preservative, building bases of scientific evidence about nitrite continues to oppose the general safety in human health. Moreover, thymoquinone (TQ) has therapeutic potential as antioxidant, anti‐inflammatory, antibacterial and anticancer. Therefore, we investigated the effects of both sodium nitrite and TQ on testicular tissues of rats. Forty adult male Sprague Dawley rats were used. They received either 80 mg kg^?1 sodium nitrite or 50 mg kg^?1 TQ daily for twelve weeks. Serum testosterone was measured. Testis were weighed and the testicular tissue homogenates were used for measurements of tumour necrosis factor (TNF)‐α, interleukin (IL)‐1β, IL‐4, IL‐6, IL10, caspase‐3, caspase‐8 and caspase‐9. Sodium nitrite resulted in significant reduction in serum testosterone concentration and elevation in testis weight and Gonado‐Somatic Index. We found significant reduction in testicular tissues levels of IL‐4 and IL‐10 associated with elevated levels of TNF‐α, IL‐1β, IL‐6, caspase‐3, caspase‐8 and caspase‐9. In conclusion, chronic oral sodium nitrite induced changes in the weight of rat testis accompanied by elevation in the testicular tissue level of oxidative stress markers and inflammatory cytokines. TQ attenuated sodium nitrite‐induced testicular tissue damage through blocking oxidative stress, restoration of normal inflammatory cytokines balance and blocking of apoptosis.     

Sperm abnormalities induced by pre‐pubertal exposure to cyclophosphamide are effectively mitigated by Moringa oleifera leaf extract

Moringa oleifera L. is a medicinal plant with potential antioxidant property. This study was aimed at investigating the chemoprotective effect of Moringa oleifera leaf extract (MOE) on cyclophosphamide (CP)‐induced testicular toxicity. Two‐week‐old male Swiss albino mice were intraperitoneally injected with phosphate‐buffered saline, 50 mg kg^?1 of CP and 25 mg kg^?1 of MOE. In combination treatment, mice were injected with 25 mg kg^?1 of MOE 24 h prior to CP injection, 24 h prior and post‐CP injection and 24 h post‐CP injection for 5 consecutive days (10 mg kg^?1). Six weeks later, mice were sacrificed to assess epididymal sperm parameters. MOE alone did not have any significant effect on sperm parameters. However, acute injection of CP resulted in significant decline in motility (P < 0.001), increase in head abnormality (P < 0.01) and DNA damage (P < 0.05). Combining MOE with CP increased the sperm density, motility and reduced head defect and DNA damage, irrespective of the schedule and dosage of MOE. Administration of MOE prior to CP significantly elevated the level of superoxide dismutase and catalase with concomitant decrease in lipid peroxidation in the testicular tissue. In conclusion, MOE may have potential benefit in reducing the loss of male gonadal function following chemotherapy.     

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.     

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.     

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.     

Quercetin ameliorates polychlorinated biphenyls‐induced testicular DNA damage in rats

Polychlorinated biphenyls (PCBs) are a group of environmental contaminants widely reported to cause gonadal toxicity in both humans and animals. This study investigated the amelioratory role of quercetin in PCBs‐induced DNA damage in male Wistar rats. Polychlorinated biphenyls were administered intraperitoneally at a dose of 2 mg kg^?1 alone or in combination with quercetin (orally) at 50 mg kg^?1 for 25 days. Quercetin modulation of PCBs‐induced gonadal toxicity was evaluated using selected oxidative stress indices, comet assay, measurement of DNA concentration and histology of the testes. Administration of PCBs alone caused a significant (P < 0.05) depletion in the total thiol level in testes of treated rats. Conversely, the levels of reactive oxygen species (ROS) and thiobarbituric acid reactive substances (TBARS) production were markedly elevated in testes of PCBs‐treated rats compared with control. Further, PCBs exposure produced statistically significant increases in DNA tail migration, degraded double‐stranded DNA (dsDNA) concentration and histological alterations of testes of the treated rats compared to control. Quercetin cotreatment significantly improved the testicular antioxidant status, decreased DNA fragmentation and restored the testicular histology, thus demonstrating the protective effect of quercetin in PCBs‐treated rats.     

Reproductive and toxic effects of methanol extract of Alchornea cordifolia leaf in male rats

Alchornea cordifolia leaf is traditionally used for the treatment of venereal diseases and for the enhancement of fertility throughout its area of distribution in Africa. The effect of oral administration of the methanol extract of the leaf was evaluated on some reproductive and haematological parameters of male rats at 0 (control group), 100, 200, 400, 800 and 1600 mg kg^?1. The toxicity study revealed nonsignificant alterations (P > 0.05) in the values of total and differential white blood cell count, but the erythrocyte count, packed cell volume, haemoglobin concentration and haematometric indices were significantly decreased (P < 0.05) at 1600 mg kg^?1 dose. Markers of hepatic damage (aspartate aminotransferase and alanine aminotransferase) and renal damage (urea and creatinine) were significantly elevated (P < 0.05) at 800 and 1600 mg kg^?1. The bioactivity (reproductive) study revealed significant increases (P < 0.05) in testicular weight, sperm count and motility, and serum testosterone levels, at the 200 and 400 mg kg^?1. The study concludes that the extract of Alchornea cordifolia leaves has toxic potential at 800 mg kg^?1 and 1600 mg kg^?1 doses, but is safe and has beneficial effects on male reproduction when used at doses equal to or lower than 400 mg kg^?1.     

Effects of amlodipine on ischaemia/reperfusion injury in the rat testis

The aim of this study was to examine the effects of amlodipine (AML) in rat testicular torsion/detorsion damage. In this study, rats were divided into eight groups: (i) sham; (ii) testicular ischaemia, 2 h of ischaemia; (iii) testicular ischaemia/reperfusion (I/R), 2 h of ischaemia followed by 2 h of reperfusion; (iv) ischaemia + AML (5 mg kg^?1) administered 30 min before ischaemia; (v) ischaemia + AML (10 mg kg^?1) administered 30 min before ischaemia; (vi) and (vii) I/R + AML (5 mg kg^?1) and I/R + AML (10 mg kg^?1) administered 1.5 h after the induction of ischaemia, respectively, and at the end of a 2‐h ischaemia period and a 2‐h reperfusion period applied; and (viii) sham + AML (10 mg kg^?1). Significant decreases in levels of superoxide dismutase and glutathione were observed in ischaemia and reperfusion groups when compared with healthy controls. These antioxidant levels increased in AML groups while malondialdehyde levels significantly decreased. While increases in tumour necrosis factor‐alpha and transforming growth factor‐beta levels were found in the torsion and detorsion groups, significant decreases in the levels of these inflammatory cytokines were observed in the treatment groups. These results demonstrate that AML significantly produced protective effects on testis tissue damage that occurs in the torsion/detorsion model via biochemical, histopathological and molecular pathways.     

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.     

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.     

Effect of etodolac hydrazone,a new compound synthesised from etodolac,on spermatozoon quality,testicular lipid peroxidation,apoptosis and spermatozoon DNA integrity

The aim of this study was to investigate the effect of etodolac hydrazone (EH), a new compound synthesised from etodolac, on spermatozoon quality, testicular lipid peroxidation, apoptosis and spermatozoon DNA integrity in rats. Group 1 (n = 8) received 1 ml dimethyl sulfoxide (DMSO) daily (Control); group 2 (n = 8) was treated with 5 mg kg^?1 day^?1 EH, dissolved in 1 ml DMSO (EH‐5); and group 3 (n = 8) was treated with 10 mg kg^?1 day^?1 EH, dissolved in 1 ml DMSO (EH‐10). All administrations were performed by gavage and maintained for 8 weeks. Both doses of EH administration caused significant decreases in absolute and relative weights of testis, whole epididymis, right cauda epididymis, and spermatozoon motility, spermatozoon count in comparison with the control group. Only 10 mg kg^?1 day^?1 EH administration caused significant decreases in absolute and relative weights of seminal vesicles and serum testosterone level, and significant increases in testicular lipid peroxidation level, and numbers of TUNEL+ apoptotic germ cells and spermatozoa with damaged DNA along with some histopathological damages when compared to the control group. However, body and ventral prostate weight, and testicular antioxidant markers (glutathione, glutathione‐peroxidase and catalase), were unaffected significantly by both doses of EH administration. In conclusion, two different doses of EH, in particular its high dose, damage to testicular spermatogenic cells and spermatozoon DNA and, it decreases spermatozoon motility, count and testosterone level in healthy rats.     

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.     

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.     

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.     

Effects of Cuminum cyminum L. essential oil on some epididymal sperm parameters and histopathology of testes following experimentally induced copper poisoning in mice

Copper overload can cause sperm cell damage by inducing oxidative stress. On the other hand, cumin has a good antioxidant potential. Therefore, the aim of this study was to evaluate the effects of cumin on sperm quality and testicular tissue following experimentally induced copper poisoning in mice. Forty‐eight mature male mice were divided into four equal groups as follows: group Cu which received 0.1 ml copper sulphate at dose of 100 mg kg^?1, group Cc which received Cuminum cyminum at dose of 1 mg kg^?1, treatment group which received copper sulphate (100 mg kg^?1) and treated with Cuminum cyminum (1 mg kg^?1), and control group which received the same volume of normal saline. Six mice in each group were sacrificed at week 4 and week 6. The results showed that sperm concentration, motility and viability in group Cu were significantly decreased at weeks 4 and 6, and severe degenerative changes were observed in testicular tissues in comparison with the control group. In treatment group, significant improvement in the sperm count, motility and viability, and normal architecture in most seminiferous tubules with organised epithelium was observed compared to the group Cu. The sperm quality parameters in the treatment group approached those of the control group.