Melatonin prevents dexamethasone‐induced testicular oxidative stress and germ cell apoptosis in golden hamster,Mesocricetus auratus

This study investigated the protective effect of melatonin on dexamethasone (Dex), an extensively used anti‐inflammatory and immunosuppressive synthetic glucocorticoid, induced testicular oxidative stress and germ cell apoptosis in golden hamster. Hamsters were randomly divided into four groups (n = 7): group I – control; group II – melatonin treated (10 mg kg^?1 day^?1); group III – Dex treated (7 mg kg^?1 day^?1) and group IV – combination of Dex and melatonin. All the injections were administered intraperitoneally for seven consecutive days. The histopathological changes, specific biochemical markers, including antioxidative enzymes, plasma melatonin level and the markers for germ cell apoptosis were evaluated. Dex administration decreased antioxidant enzyme activities (SOD, CAT, GSH‐P_X), plasma melatonin level and melatonin receptor (MT1) expression with a concomitant increase in lipid peroxidation (TBARS) and altered testicular histopathology which might culminate into increased germ cell apoptosis as evident from increased Bax/Bcl‐2 ratio and caspase‐3 expression. However, melatonin pre‐treatment enhanced enzyme activities for SOD, CAT, GSH‐P_X with a simultaneous decrease in Bax/Bcl‐2 ratio and caspase‐3 expression. Our findings clearly suggest that melatonin improved defence against Dex‐induced testicular oxidative stress and prevented germ cell apoptosis, suggesting a novel combination therapeutic approach for management of male reproductive health.     

LY294002, a PI3K pathway inhibitor,prevents leptin‐induced adverse effects on spermatozoa in Sprague‐Dawley rats

This study examined the effects of PI3K and AMPK signalling pathway inhibitors on leptin‐induced adverse effects on rat spermatozoa. Sprague‐Dawley rats, aged 14–16 weeks, were randomised into control, leptin‐, leptin + dorsomorphin (AMPK inhibitor)‐, and leptin+LY294002 (PI3K inhibitor)‐treated groups with six rats per group. Leptin was given once daily for 14 days via the intraperitoneal (i.p.) route at a dose of 60 ug kg^?1 body weight. Rats in the leptin and inhibitor‐treated groups received concurrently either dorsomorphin (5 mg kg^?1 day^?1) or LY294002 (1.2 mg kg^?1 day^?1) i.p. for 14 days. Controls received 0.1 ml of normal saline. Upon completion, sperm count, sperm morphology, seminiferous tubular epithelial height (STEH), seminiferous tubular diameter (STD), 8‐hydroxy‐2‐deoxyguanosine (8‐OHdG) and phospho‐Akt/total Akt ratio were estimated. Data were analysed using ANOVA. Sperm count, STEH and STD were significantly lower, while the percentage of spermatozoa with abnormal morphology and the level of 8‐OHdG were significantly higher in rats treated with leptin and leptin + dorsomorphin when compared to those in controls and LY294002‐treated rats. Testicular phospho‐Akt/total Akt ratio was significantly higher in leptin and leptin + LY294002‐treated rats. In conclusion, LY294002 prevents leptin‐induced changes in rat sperm parameters, suggesting the potential role of the PI3K signalling pathway in the adverse effects of leptin on sperm parameters.     

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.     

Improvement in erectile function in a rat model of high cholesterol diet‐induced atherosclerosis by atorvastatin in a manner that is independent of its lipid‐lowering property

The purpose of the present study is to explore the effects of a lipid‐lowering drug atorvastatin, a three‐hydroxy‐3‐methylglutaryl coenzyme A (HMG‐CoA) reductase inhibitor, in the treatment of erectile dysfunction (ED) in a rat model of atherosclerosis (AS) and the possible mechanisms underneath. A high‐cholesterol diet was administrated to Sprague‐Dawley rats in an attempt to induce an ASED model, which was later confirmed by abdominal aorta histopathology and erectile function evaluation. ASED rats were further assigned to non‐treatment group, atorvastatin low‐dose treatment group (5 mg kg^?1 day^?1), high‐dose group (10 mg kg^?1 day^?1) and sildenafil (1.5 mg kg^?1 day^?1) treatment group. Lipid profile, erectile function, oxidative stress biochemical markers, endothelial nitric oxide synthase (eNOS) and extracellular superoxide dismutase (SOD_EX) mRNA expression were evaluated after 8‐week treatment duration. Erectile function was impaired in AS rat model, which was preserved in atorvastatin and sildenafil intervention groups. The oxidative stress biochemical markers were attenuated, while eNOS and SOD_EX mRNA expression were restored in atorvastatin and sildenafil groups, which were found to be involved in ED pathogenesis. However, the lipid profile remained unaltered in the treatment group, and it was elevated in ASED rats. This kind of lipid‐lowering agent, or atorvastatin, has the utilisation potential in ASED treatment, even before lipid profiles altered. This effect on erectile function preservation of atorvastatin was attributed to its preservation of endothelial function, possibly through amelioration of oxidative stress and improvement in eNOS expression.     

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.     

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.     

Vitamin E attenuates nicotine‐ and noise‐induced reproductive impairment in male albino Wistar rats

Previous studies showed that exposure to stress or nicotine induced reproductive impairment in male rats. Here, we assessed the effect of an antioxidant (vitamin E) on nicotine‐, stress‐ and nicotine + stress‐induced reproductive impairment in male rats. Forty‐eight male albino Wistar rats were divided into eight groups as follows; control, stress (generator noise 90–120 dB, 8 hr/day), nicotine (1.5 mg kg^?1 day^?1), nicotine + stress, vitamin E (100 mg kg^?1 day^?1), stress + vitamin E, nicotine + vitamin E and stress + nicotine + vitamin E. Sperm count, viability, motility and rapid progressive forward movement decreased significantly (p < 0.05), while percentage of nonmotile spermatozoa increased significantly (p < 0.05) in stress, nicotine and nicotine + stress groups, compared with control. Serum testosterone and follicle‐stimulating hormone decreased significantly (p < 0.05) in stress, nicotine and nicotine + stress groups, compared with control. Serum luteinising hormone decreased (p < 0.05) significantly in stress and nicotine + stress groups, compared with the control. Histology of the testes showed loss of germ cells in numerous seminiferous tubules, and epididymal histology showed decreased sperm density in stress, nicotine and nicotine + stress groups compared with the control. These negative changes were more severe in the nicotine + stress group. Vitamin E ameliorated the negative changes in the above parameters. This may be attributable to its antioxidant property.     

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.     

Effects of leptin on sperm count and morphology in Sprague‐Dawley rats and their reversibility following a 6‐week recovery period

Altered epididymal sperm count and morphology following leptin treatment has been reported recently. This study examined the effects of 42 days of leptin treatment on sperm count and morphology and their reversibility during a subsequent 56‐day recovery period. Twelve‐week‐old male Sprague‐Dawley rats were randomised into four leptin and four saline‐treated control groups (n = 6). Intraperitoneal injections of leptin were given daily (60 μg Kg^?1 body weight) for 42 days. Controls received 0.1 ml of 0.9% saline. Leptin‐treated animals and their respective age‐matched controls were euthanised on either day 1, 21, 42 or 56 of recovery for collection of epididymal spermatozoa. Sperm concentration was determined using a Makler counting chamber. Spermatozoa were analysed for 8‐hydroxy‐2‐deoxyguanosine and DNA fragmentation (Comet assay). Data were analysed using anova . Sperm concentration was significantly lower but fraction of abnormal spermatozoa, and levels of 8‐hydroxy‐2‐deoxyguanosine were significantly higher in leptin‐treated rats on day 1 of recovery. Comet assays revealed significant DNA fragmentation in leptin‐treated rats. These differences were reduced by day 56 of recovery. It appears that 42 days of leptin treatment to Sprague‐Dawley rats has significant adverse effects on sperm count and morphology that reverse following discontinuation of leptin treatment.     

Sperm nuclear histone to protamine ratio in fertile and infertile men: evidence of heterogeneous subpopulations of spermatozoa in the ejaculate

Sperm protamine deficiency is observed in a subset of infertile men, suggesting that the relative histone to protamine ratio may be altered in the spermatozoa of these men. We measured the ratio of nuclear histones to protamines in the spermatozoa of fertile (n = 10) and infertile men (n = 20). Sperm nuclear proteins were extracted and subsequently separated by acid-urea (AU) polyacrylamide gel electrophoresis. The relative histone (H2B) to protamine (PRM1 + PRM2) and PRM1 to PRM2 ratios were estimated by densitometric analysis of the AU gels. Immunoblotting experiments (using H2B, PRM1, and PRM2 antibodies) were conducted to confirm the specificity of the bands. The pattern and intensity of H2B staining in human spermatozoa was assessed by immunocytochemistry. Sperm samples from the infertile men in this study had a significantly higher proportion of histone H2B to protamine (PRM1 + PRM2) than did samples from the fertile men in this study (0.38 vs 0.08, P < .001). Immunocytochemistry experiments demonstrated a punctuated staining pattern (with strong, intermediate, or weak H2B staining intensity) throughout the sperm head. Infertile men had a higher proportion of spermatozoa exhibiting strong and intermediate staining than did samples from fertile men. These findings suggest that infertile men possess a higher proportion of spermatozoa with an increased histone to protamine ratio than fertile controls.     

Toxic effects of arsenic on semen and hormonal profile and their amelioration with vitamin E in Teddy goat bucks

The present environmental study has been planned to investigate the toxic effects of arsenic on reproductive functions of Teddy bucks as well as to examine whether these toxic effects are ameliorated by vitamin E. Sixteen adult Teddy bucks were divided randomly into four equal groups A, B, C and D with following treatment: A (control), B (sodium arsenite 5 mg kg^?1 BW day^?1), C (vit E 200 mg kg^?1 BW day^?1 + Arsenic 5 mg kg^?1 BW day^?1) and D (vit E 200 mg kg^?1 BW day^?1). This treatment was continued for 84 days. Semen quality parameters were evaluated weekly. Male testosterone, luteinising hormone (LH), follicle‐stimulating hormone (FSH) and cortisol levels were measured through enzyme‐linked immunosorbent assay (ELISA) after every 2 weeks. The data were subjected to two‐way analysis of variance followed by Duncan test for multiple comparisons. Semen evaluation parameters were reduced significantly (P < 0.05) in arsenic‐treated animals. The serum hormonal profile of testosterone, LH and FSH was reduced significantly (P < 0.05) in arsenic group, while the serum level of cortisol was increased. Vitamin E alleviated the toxic effects of arsenic on semen and hormonal parameters. It may be concluded from this study that sodium arsenite causes major toxicity changes in semen and hormonal profile in Teddy goat bucks and vitamin E has ameliorative effects on these toxic changes.     

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.     

Chemoprotective effects of kolaviron on ethylene glycol monoethyl ether‐induced pituitary‐thyroid axis toxicity in male rats

Endocrine disrupting chemicals cause reproductive dysfunction by interacting with intricate regulation and cellular processes involve in spermatogenesis. This study investigated the probable mechanism of action of ethylene glycol monoethyl ether (EGEE) as an antiandrogenic compound as well as the effects of kolaviron upon co‐administration with EGEE in rats. Adult male rats were exposed to EGEE (200 mg kg^?1 bw) separately or in combination with either kolaviron [100 (KV1) and 200 (KV2) mg kg^?1 bw] or vitamin E (50 mg kg^?1 bw) for 14 days. Western blot analysis revealed that the administration of EGEE adversely affected steroidogenesis in experimental rats by decreasing the expression of steroid acute regulatory (StAR) protein and androgen‐binding protein (ABP). EGEE significantly decreased the activities of 3β‐hydroxysteroid dehydrogenase (3β‐HSD) and 17β‐hydroxysteroid dehydrogenase (17β‐HSD) but markedly increased sialic acid concentration in rat testes. EGEE‐treated rats showed significant decreases in plasma levels of luteinising hormone (31%), testosterone (57.1%), prolactin (80.9%), triiodothyronine (65.3%) and thyroxine (41.4%), whereas follicle‐stimulating hormone was significantly elevated by 76.9% compared to the control. However, co‐administration of kolaviron or vitamin E significantly reversed the EGEE‐induced steroidogenic dysfunction in rats. This study suggests that kolaviron may prove promising as a chemoprotective agent against endocrine pathology resulting from EGEE exposure.     

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 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.     

Effect of rutin on diabetic‐induced erectile dysfunction: Possible involvement of testicular biomarkers in male rats

The present study aimed to investigate effects of rutin on diabetic‐induced impairments of sexual behaviour, spermatogenesis and oxidative testicular damage. Diabetes was induced by a single injection of STZ (65 mg/kg) in male adult Wistar rats. Two weeks later, rutin (50 and 100 mg kg^?1 day^?1) was treated to normal and diabetic rats for 5 weeks. Sexual behaviour of the animals was observed by taking stimulus females. At the end of the study, sperm count, motility and viability were recorded. Serum levels of glucose, inflammatory markers and testosterone were also estimated. In penile tissue, cGMP levels were measured, while lipid peroxidation and antioxidant molecules and enzyme activities were determined. Finally, histopathological changes were evaluated in a cross‐section of testis. Diabetic‐induced alterations in male sexual behaviour and sperm count, motility and viability were markedly corrected following 5 weeks of rutin treatment to the diabetic animals. Rutin also attenuated the inhibited serum testosterone and penile cGMP content, while improved diabetic‐associated inflammation and testicular lipid peroxidation and oxidative stress. Histopathological evaluation revealed damaged testicular tissues in diabetic rats, which was protected following rutin treatment. In conclusion, treatment with rutin improved sexual functionality and also protects against diabetic‐induced testicular damage.     

Melatonin prevents gentamicin‐induced testicular toxicity and oxidative stress in rats

This study investigated the protective effects of melatonin (MT) against gentamicin (GM)‐induced testicular toxicity and oxidative damage in rats. GM (100 mg kg^?1) was injected intraperitoneally (i.p.) to rats for 6 days. MT (15 mg kg^?1) was administered i.p. to rats for 6 days at 1 hr after the GM treatment. GM caused a decrease in prostate and seminal vesicle weights, sperm count and sperm motility. Histopathological examination showed various morphological alterations in the testis, characterised by degeneration of spermatogonia/spermatocytes, decrease in the number of early spermatogenic cells and vacuolisation. In addition, an increased malondialdehyde concentration and decreased glutathione content and glutathione reductase, catalase and glutathione‐S‐transferase activities were found in the testis. In contrast, MT treatment significantly attenuated the testicular toxicity of GM, including decreased reproductive organ weights, sperm count, and sperm motility and increased histopathological alterations. MT also had an antioxidant benefit by decreasing the lipid peroxidative product malondialdehyde and increasing the level of the antioxidant glutathione and the activities of antioxidant enzymes in the testis. These results indicate that MT prevents testicular toxicity induced by GM in rats, presumably due to its potent antioxidant activity, and its ability to inhibit lipid peroxidation, and restore antioxidant enzyme activity.     

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.     

Prostate‐specific targeting of the aqueous root extract of Croton membranaceus in experimental animals

Croton membranaceus Müll.Arg. (Euphorbiaceae) is used for benign prostate hyperplasia (BPH) treatment. The study aimed at investigating organs that the aqueous root extracts of C. membranaceus (CMARE) target, which is absent in literature. Twenty‐four male Sprague‐Dawley rats (100–140 g) were randomly divided into 4 groups. Group 1, the control group received distilled water. Groups 2, 3 and 4 received 30, 150 and 300 mg kg^?1 b.wt CMARE respectively (oral gavage). Rats fed 90 days the standard chow diet ad libitum. Upon sacrifice, major organs were histologically examined and serum prostate‐specific antigen (PSA) biochemically determined. Only the prostate was abnormal. Histologically, H&E staining revealed thickness and infoldings of the epithelial cells shrinking with increasing dose. The 30 mg kg^?1 group showed low columnar or flattened epithelium cells, whereas the columnar epithelium infoldings of the 150 mg kg^?1 b.wt and 300 mg kg^?1 b.wt groups were virtually nonexistent. The acini of the control, 30 mg kg^?1 b.wt group and the 150 mg kg^?1 b.wt groups showed clear pinkish secretion. However, secretion of the high‐dose group appeared light pink in colour and the stroma cells appeared much darker than all the treated and control group. C. membranaceus targets the prostate with significant PSA reduction (P < 0.01).