Protective effects of the hydroalcoholic extract of Fumaria parviflora on testicular injury induced by torsion/detorsion in adult rats

This study was designed to determine the effects of daily oral administration (250 mg/kg) of the hydroalcoholic extract of Fumaria parviflora (FP) for 14 days on the sperm parameters, oxidative stress parameters, serum testosterone levels, expression of Bax and Bcl‐2 genes, and apoptosis index of germ cells after testicular torsion–detorsion (ischaemia–reperfusion, IR) injury model in rats. Twenty‐eight adult male Wistar rats were divided randomly into four groups of seven each: sham operation, torsion–detorsion (TD), TD plus the hydroalcoholic extract FP (TDFP) and only FP without TD application (FP). Testicular torsion was created by rotating the left testis 720° in a counterclockwise direction; then, after 4 hr, detorsion was performed. The Johnson's score, mean seminiferous tubule diameter (MSTD) and height (thickness) of seminiferous tubule epithelium (HST) were significantly increased in TDFP and FP groups as compared to TD group. The gene expression of Bcl‐2, level of serum testosterone hormone and antioxidant parameters—GPx and SOD—were significantly higher in TDFP and FP groups than TD group. The index of apoptosis, the gene expression of Bax and the level of MDA were significantly higher in TD group than TDFP and FP groups. Therefore, F. parviflora could decrease oxidative stress induced by testicular torsion–detorsion.     

Ferulic acid prevents lead‐induced testicular oxidative stress and suppressed spermatogenesis in rats

Lead affects multiple organ systems including testis. We investigated the effects of ferulic acid (FA) on lead‐induced oxidative stress and spermatogenesis suppression in rats. Animals received lead acetate (500 mg/L in drinking water) and/or FA (50 mg/kg, i.g.) for eight weeks. Lead increased testicular malondialdehyde (MDA) and nitrite levels and decreased glutathione (GSH) content and catalase (CAT) activity. Lead decreased testis weight and testosterone level. Sperm parameters decreased in lead group. FA ameliorated the decreased testis weight, serum testosterone as well as sperm count, viability, motility and normal morphology in lead group. FA improved antioxidant capacity as well as sperm count, viability, motility and normal morphology. FA decreased Johnsen's mean testicular biopsy score (MTBS) criteria by restoring degeneration, atrophy and tubular disarrangement. FA also normalised spermatogonia, spermatocytes and spermatids numbers in lead group and led to increases in number of Leydig and Sertoli cells. FA showed beneficial effects in lead‐induced testicular oxidative stress and spermatological disorders, through inhibiting lipid peroxidation and enhancing antioxidant defence systems. The positive effects of FA on Leydig cells may be involved in restoring testosterone levels in lead group. FA can be considered a potential candidate to protect testis against the deleterious effect of lead intoxication.     

Protective effect of betaine against lead-induced testicular toxicity in male mice

Lead (Pb) is an environmental toxicant reported to impair male reproductive system. Betaine is a natural product which has promising beneficial effects against oxidative stress. In this experimental study, we evaluated the ameliorative effect of betaine on sperm quality and oxidative stress induced by lead (Pb) in the testis of adult male mice. Sixty male Kunming mice were divided equally into four groups: control group, betaine group (1% in drinking water), lead group (100 mg kg⁻¹ bw⁻¹ day⁻¹) and betaine + lead group. In the last group, mice were supplemented with betaine for two weeks prior to the initiation of lead treatment and concurrently during lead treatment for 3 weeks until sacrificed. Our results indicated that in the lead-administrated group, body weights together with sperm count were significantly decreased (p < .05). The numbers of abnormal sperms were found to be higher in lead-treated mice. The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (Cat) were significantly reduced, while the level of malondialdehyde (MDA) content was increased in the testis tissue following lead treatment. The mRNA levels of antioxidant-related genes (SOD1, GPX1 and CAT) were significantly decreased in the lead group. Betaine enhanced these parameters in betaine + lead group. In testis histology span, Johnson score was decreased (p < .05) in lead group and co-treatment with betaine increased Johnson score significantly in betaine + lead group. These results indicate that betaine improves sperm quality and ameliorate oxidative damage in testis of mice exposed to lead.     

Ameliorating effect of kisspeptin‐10 on methotrexate‐induced sperm damages and testicular oxidative stress in rats

The purpose of this study was to determine the kisspeptin‐10 (Kiss) administration on the damages in testicular oxidant–antioxidant system, reproductive organ weights and some spermatological characteristics resulted from methotrexate (MTX) exposure. Group 1 (n:6) received saline only; group 2 (n:6) received 50 nmol/kg kisspeptin‐10 for 10 days; group 3 (n:10) received single‐dose methotrexate 20 mg/kg; and group 4 (n:10) received MTX 20 mg/kg single dose and, after 3 days, received kisspeptin‐10, 50 nmol/kg, lasted for 10 days by intraperitoneal injection. At the end of the study, malondialdehyde levels were found to have increased following the application of MTX while showing a significant reduction in group 4 with Kiss administration. With respect to the spermatological parameters, administering MTX decreased motility and increased the rates of abnormal spermatozoa in group 2, while improvements were observed in group 4 in the form of increased motility in the spermatozoa and fewer abnormal spermatozoa. In addition, Kiss treatment provided statistically significant increases in the absolute weight of the seminal vesicles and the relative weights of the right cauda epididymis and seminal vesicles resulting from MTX administration. MTX administration damaged some spermatological parameters and increased oxidative stress when compared to the control group. However, Kiss treatment was observed to mitigate these adverse effects as demonstrated by the improvements in coadministration of Kiss and MTX when compared to the MTX group. It is concluded that Kiss treatment may reduce MTX‐induced reproductive toxicity as a potential antioxidant compound.     

A potential mechanism associated with lead‐induced testicular toxicity in rats

This study was conducted to investigate the mechanism of lead (Pb)‐induced testicular toxicity. We examined the impact of Pb toxicity on 17β‐oestradiol (E2), oestrogen receptors (ERs) and aromatase P450 which are key factors in spermatogenesis. Treatment of rats with Pb acetate (PbAc, 50 mg/L in drinking water) significantly reduced sperm count, motility, viability and increased sperm abnormalities along with degenerative changes in seminiferous tubules and Leydig cells. Additionally, administration of PbAc resulted in a significant reduction in serum testosterone, serum and testicular E2 as well as increased level of testicular testosterone. Pb also induced testicular oxidative stress as evidenced by a significant decrease in the activities of superoxide dismutase, glutathione peroxidase and catalase antioxidant enzymes, and increased malondialdehyde level in the testis. At the molecular level, Pb treatment downregulated the mRNA expression of P450 arom (Cyp19) and ERα. In conclusion, Pb induces testicular oxidative damage and disrupts spermatogenesis, at least in part, via downregulation of Cyp19 and ERα expression, which further decrease E2 level. These data, therefore, provide insight into the mechanism of lead‐induced testicular toxicity.     

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.     

Protective effect of alpha glucosyl hesperidin (G‐hesperidin) on chronic vanadium induced testicular toxicity and sperm nuclear DNA damage in male Sprague Dawley rats

The study was conducted to evaluate the vanadium‐induced testicular toxicity and its effect on sperm parameters, sperm nuclear DNA damage and histological alterations in Sprague Dawley rats and to assess the protective effect of G‐hesperidin against this damage. Treatment of rats with vanadium at a dose of 1 mg kg bw^?1 for 90 days resulted in significant reduction in serum testosterone levels, sperm count and motility. Further, a parallel increase in abnormal sperm morphology and adverse histopathological changes in testis was also associated with vanadium administration when compared to normal control. Moreover, sperm chromatin dispersion assay revealed that vanadium induces sperm nuclear DNA fragmentation. A marked increase in testicular malondialdehyde levels and decreased activity of antioxidant enzymes such as superoxide dismutase and catalase indicates vanadium‐induced oxidative stress. Co‐administration of G‐hesperidin at a dose of 25 and 50 mg kg bw^?1 significantly attenuated the sperm parameters and histological changes by restoring the antioxidant levels in rat testis. These results suggested that vanadium exposure caused reduced bioavailability of androgens to the tissue and increased free radical formation, thereby causing structural and functional changes in spermatozoa. G‐hesperidin exhibited antioxidant effect by protecting the rat testis against vanadium‐induced oxidative damage, further ensures antioxidant potential of bioflavonoids.     

Therapeutic effect of thymoquinone against lead‐induced testicular histological damage in male Wistar rats

Lead (Pb) is a nonthreshold multi‐targeted toxicant that causes alterations in different organs of the body, especially the gonads. This study was aimed to investigate the possible protective effect of thymoquinone (TQ), the major active ingredient of volatile oil of Nigella sativa seeds, against Pb‐induced testicular histological damage. Adult male rats were randomised into four groups as follows: control group received no treatment, Pb group was exposed to 2000 ppm of Pb acetate in drinking water, Pb‐TQ group was cotreated with Pb plus TQ (5 mg/kg/day, per os) and TQ group receiving only TQ. All treatments were applied for five weeks. Results showed that Pb exposure produced morphological changes in the testis, especially degeneration of germinal epithelium, sloughing of germ cells into the lumen of seminiferous tubules and reduction in the number of luminal spermatozoa. Interestingly, coadministration of TQ to the metal‐treated animals prevented the testicular adverse effects. In conclusion, our data indicate for the first time a remarkable protective effect of TQ against Pb‐induced testicular histopathological lesions in rat. On this basis, TQ deserves more consideration and further examination as a potential therapeutic option.     

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.     

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.     

Protective effects of Urtica dioica L. on experimental testicular ischaemia reperfusion injury in rats

In this study, it was aimed to examine the effects of Urtica dioica L. (UD) that has antioxidant feature in the experimental testicular I/R model in rats in terms of anti‐apoptotic and antioxidative effects. In our study, 24 male rats were divided into three groups: control group, I/R group and I/R + UD (2 mg kg^?1) group. Seminiferous tubule calibre measurement, Johnson score, haematoxylin–eosin staining, proliferative cell nucleus antigen (PCNA) immunohistochemical staining and TUNEL as histopathological have been conducted. The structural deterioration in the testicular on I/R group has reduced after the treatment of UD. Our data indicate a significant reduction in the activity of in situ identification of apoptosis using terminal dUTP nick end labelling (TUNEL), and there was a rise in the expression of proliferating cell nuclear antigen (PCNA) in testis tissues of UD‐treated rats in the I/R group. The I/R + UD group showed a decrease in malondialdehyde levels and an increase in the activities of superoxide dismutase, catalase and glutathione peroxidase in comparison with the I/R group. It could be concluded that protective effects of UD on the I/R testicles are via reduction of histological damage, apoptosis, oxidative stress and lipid peroxidation.     

Protective effects of Lepidium draba L. leaves extract on testis histopathology,oxidative stress indicators,serum reproductive hormones and inflammatory signalling in oxymetholone-treated rat

This study was aimed to investigate the protective effects of Lepidium draba L. (L. draba) extract on oxymetholone (OM)-induced testicular injury in rat. Six groups of n = 5 adult male rats were used as; 1: control, 2: OM (5 mg/kg OM orally), 3, 4 and 5: L. draba extract (100, 200 and 400 mg kg⁻¹ day⁻¹) +OM (5 mg kg⁻¹ day⁻¹ OM) and 6:400 mg/kg/d L. draba extract for 30 days. Serum testosterone (T), follicle-stimulating hormone (FSH) and luteinising hormone (LH), inflammatory cytokines (IL-6, IL-10, TNF-α, IL-1β), oxidative stress (OS) indicators [superoxide dismutase, catalase, glutathione peroxidase and nitric oxide (NO)], apoptotic related genes (Bcl-2, p53, caspase-3 (c3) and Bax) were investigated. OM significantly increased the serum levels of T, proinflammatory cytokines and pro-apoptotic genes expression. Also, it decreased LH and FSH, sperm viability, count and motility. L. draba extract especially could markedly normalise the serum levels of LH and FSH, and T, restore serum antioxidant enzymes and suppressed the pro-inflammatory cytokines. Also, germ cells apoptosis was inhibited against via downregulating the p53, c3, Bax and upregulating Bcl-2. It concluded that L. draba extract could protect the function and structure of testis against OM-induced testicular toxicity via its antioxidant and anti-inflammatory properties.     

Acrocomia aculeata oil: Beneficial effects on cyclophosphamide‐induced reproductive toxicity in male rats

This study aimed to evaluate the effects of the extracted oil of Acrocomia aculeata pulp in preventing or mitigating the reproductive toxicity induced by cyclophosphamide (CP) in male rats. Adult male rats were segregated into seven groups that received vehicle, 100 mg/kg/day of CP, or 10 mg/kg/day of β‐carotene or 3 or 30 mg/kg/day of A. aculeata oil co‐administered with CP. A. aculeata oil exhibited a high content of β‐carotene. CP treatment induced reproductive toxicity in the animals, as it changed the reproductive organs weight, hormone levels, sperm counts and testicular histology. In contrast, co‐administration of A. aculeata improved CP‐induced alterations in these parameters. A. aculeata oil also increased the gene Ckit expression and normalised the antioxidant enzymes levels which were changed by CP. The A. aculeata oil is capable of protecting the male reproductive system from the adverse effects of CP, possibly by acting as an antioxidant and increasing the Ckit gene expression.     

Protective effect of Gallic acid on doxorubicin‐induced testicular and epididymal toxicity

The effect of Gallic acid (GA) on doxorubicin (DOX)‐induced testicular and epididymal toxicity was investigated in experimental rat model. The rats were randomly divided into six groups of 10 animals per group. Rats in group A received clean tap water ad libitum. Rats in group B were administered DOX intraperitoneally at 15 mg/kg on the eighth day of the experiment. Animals in groups C and D received 60 and 120 mg/kg GA orally for 7 days with 15 mg/kg DOX on the eighth day. Rats in groups E and F received 60 and 120 mg/kg GA alone orally for 7 days. The animals were sacrificed 24 hr after the last administration. DOX administration led to a significant (p < 0.05) increase in hydrogen peroxide and malondialdehyde levels with significant reduction in antioxidant enzymes and reduced glutathione levels. DOX administration also led to a significant increase in total sperm abnormalities and prolactin together with a significant decrease in testosterone levels. Immunohistochemistry revealed higher expressions of caspase 3 in the testicular tissues of rats that received DOX alone. Together, pre‐treatment with GA attenuated markers of oxidative stress, reversed sperm abnormality and ameliorated the observed aberration in plasma testosterone and prolactin levels.     

Recovery of lead‐induced suppressed reproduction in male rats by testosterone

The objective of the present study was to investigate the effects of testosterone in recuperation of lead‐induced suppressed reproduction in adult male rats. Lead acetate was administered orally to adult male rats (95 ± 5 days) at dosage level of 0.05 and 0.15% for 55 days through drinking water and injected intraperitoneally with either testoviron depot at a dose of 4.16 mg kg^?1 body weight or vehicle alone on days 1, 7 and 14 respectively. At the end of treatment, control and treated males were cohabited with untreated normal‐cycling females. After cohabitation for 5 days, all the male rats were killed and weights of reproductive organs were determined. Significant increase in the indices of testis, epididymis, seminal vesicles, vas deferens and prostate glands was observed in testosterone (T)‐treated rats when compared to those of lead‐exposed rats. Testosterone treatment significantly increased epididymal sperm count, motile spermatozoa, viable spermatozoa and HOS tail‐coiled spermatozoa and also the activity levels of testicular 3β‐ and 17β‐hydroxysteroid dehydrogenases when compared to those of lead‐exposed males. From the results, it can be hypothesised that supplementation of testosterone mitigated lead‐induced suppressed reproduction in male rats.     

Melatonin abrogates nonylphenol‐induced testicular dysfunction in Wistar rats

Endocrine‐disrupting chemicals present in the environment can bring about hormonal imbalance and be potentially harmful to the human health. Alkylphenols are omnipresent in the environment as they are constituents of several products. The aim of this study was to evaluate the effect of exogenous melatonin treatment on nonylphenol (NP)‐induced oxidative stress and testicular toxicity in Wistar rats using biochemical and histopathological parameters. The oxidative stress biomarkers, activities of enzymatic and non‐enzymatic antioxidants and histopathological evaluation were performed in testicular tissues. NP caused elevated TBARS levels and marked alteration of both nonenzymatic and enzymatic biomarkers. Furthermore, severe histopathological alterations were observed in the testis of NP‐exposed animals as compared with that of the control rats. Melatonin supplementation ameliorated the alterations in these biochemical and histopathological variables in rats. In conclusion, our results demonstrated that melatonin through its antioxidant activity effectively protected against the NP‐induced testicular toxicity.     

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.     

Ameliorative effects of curcumin against acute cadmium toxicity on male reproductive system in rats

The aim of the present study was to investigate the ameliorative effect of curcumin (CMN) against acute cadmium chloride (CdCl(2)) toxicity on male reproductive system in rats. CdCl(2) is known to be a heavy metal and potential environmental pollutant. For this purpose, 28 rats were equally divided into four groups; the first group was kept as control and given distilled water and corn oil as carrier. In second and third groups, CdCl(2) and CMN were administered at the dose with 1 mg kg(-1) day(-1) and 100 mg kg(-1) for 3 days respectively. CdCl(2) and CMN were given together at the same doses in the fourth group. It was determined that acute CdCl(2) exposure caused a significant reproductive damage via increased oxidative stress (increased TBARS levels and decreased SOD, CAT, GPx and GSH levels), histological alterations (necrosis, oedema etc.) and spermatological damage (decreased sperm motility and sperm concentration and increased abnormal sperm rate) in male rats. However, CMN treatment partially reversed these toxic effects of CdCl(2) on the reproductive system. In conclusion, our results show that acute exposure of CdCl(2) may lead to infertility, and CMN could prevent and reverse hazardous effects of CdCl(2) to some degree. Thus, CMN may be useful for the prevention of CdCl(2)-induced reproductive damage.     

Attenuation of the cyproterone acetate‐induced testicular hypofunction by a novel nutraceutical lycopene: a genomic approach

This study was designed to explore the cyproterone acetate (CPA)‐induced andrological hypofunction and its correction by oral administration of lycopene. In this concern, spermatogenic, biochemical, histological and genomic profiles were studied. Cyproterone acetate administration for 1 month helped to develop infertile model rats. A significant recovery was noted in sperm motility, sperm count, sperm viability, hypo‐osmotic swelling tail‐coiled spermatozoa; activities of testicular ?⁵, 3β‐hydroxysteroid dehydrogenase (HSD), 17β‐HSD, catalase (CAT) and superoxide dismutase (SOD); and levels of conjugated diene (CD), malondialdehyde (MDA), testicular cholesterol and serum testosterone after the administration of lycopene at 1.5 mg/0.5 ml Tween‐80/100 g body weight/day for last 1 month to infertile model rats. Simultaneously, qRT‐PCR study of Bax, Bcl‐2, caspase‐3, ?⁵, 3β‐HSD and 17β‐HSD genes in testicular tissue showed a significant rectification towards the control in CPA‐pre‐treated cum CPA–lycopene‐cotreated rats. Side‐by‐side histological and histometric studies showed a significant correction in qualitative analysis of spermatogenesis and seminiferous tubular diameter (STD) in CPA‐pre‐treated cum CPA–lycopene‐cotreated rats. Lycopene showed outstanding efficacy in the management of CPA‐induced testicular hypofunction with special reference to correction in oxidative stress‐induced testicular apoptosis at genomic level.     

Profertility effects of Shilajit on cadmium‐induced infertility in male mice

Shilajit is claimed as a Vajikarak (aphrodisiac) and used for the treatment of male infertility by traditional healers of the Indian subcontinent. Therefore, the present investigation was designed to assess the effectiveness of Shilajit for treatment of male infertility resulting from exposure to perilous chemicals. Effect of daily oral administration (p.o.) of Shilajit (50 mg, 100 mg and 200 mg/Kg BW) was investigated for a single spermatogenic cycle (35 days) in cadmium‐induced (2 mg/Kg BW, p.o. for 35 days) infertile adult (12–14 week) swiss male mice. Shilajit treatment increased weights of reproductive organs, testicular daily sperm production, activities of testicular Δ⁵ 3β‐HSD and 17 β‐HSD enzymes and serum level of testosterone. Histopathological evaluation of testis revealed that Shilajit restored spermatogenesis as reflected by a gradual augmentation in germ cell layers with increased doses of Shilajit compared to cadmium‐treated mice. Further, Shilajit treatment reverted back the adverse effects of cadmium on motility and concentration of spermatozoa. Secretory activities of the epididymis and seminal vesicle and libido, fertility and the number of litters per female were also improved by Shilajit in cadmium‐treated mice. Results thus suggest the potent androgenic nature of Shilajit and its role in fertility improvement against cadmium‐induced infertility.