Methanolic extract of Chlorella vulgaris protects against sodium nitrite-induced reproductive toxicity in male rats

The current study aimed to investigate the protective potential of Chlorella Vulgaris (CV) extract against the reproductive dysfunction induced by sodium nitrite toxicity. Forty-five male Wistar albino rats were assigned into five groups (n = 9). Control group received normal saline orally for 3 months, CV-treated: administered CV extract (70 mg/kg.BW) orally for 3 months, sodium nitrite-treated: received sodium nitrite (80 mg/kg.BW) orally for 3 months, co-treated: simultaneously received CV along with sodium nitrite treatment, orally, daily for 3 months, and CV-pre-treated: pre-treated with CV extract for 4 weeks followed by simultaneous treatment with sodium nitrite and CV extract for additional 8 weeks. Treatment with sodium nitrite significantly decreased serum testosterone and follicle-stimulating hormone concentrations, sperm count, motility, and viability. Besides, it decreased testicular superoxide dismutase and glutathione peroxidase activities while increased malondialdehyde concentration. This effect of sodium nitrite was associated with degenerative, necrotic, vascular, and inflammatory changes in testicular tissues. Treatment of sodium nitrite-intoxicated rats with CV in co-treated and pre-treated groups significantly prevented sodium nitrite-induced alterations of sperm parameters, hormonal concentrations, testicular oxidative–antioxidant status, and histological architecture. This study indicates that CV extract ameliorates the reproductive dysfunction induced by sodium nitrite toxicity via improving reproductive hormonal levels and testicular antioxidant activities.     

Gallic acid and omega-3 fatty acids mitigate epididymal and testicular toxicity in manganese-treated rats

Environmental contamination by manganese is correlated with diverse health outcomes plus reproductive dysfunction. Dietary gallic acid (GA) and omega-3 fatty acids (ω-3-FA) are well reported to elicit beneficial health effects. Though, information on GA and ω-3-FA effects on manganese-induced reproductive toxicity is absent in literature. We examined the effect of GA or ω-3-FA on manganese-induced epididymal and testicular toxicity in rats, exposed to manganese (15 mg/kg b.w.) alone, in combination with GA (30 mg/kg b.w.) or ω-3-FA (20 mg/kg b.w.) by gavage for 14 consecutive days. GA or ω-3-FA significantly (p < .05) prevented manganese-mediated increase in lipid peroxidation, myeloperoxidase activity, reactive oxygen and nitrogen species production but increased antioxidant enzymes activities and glutathione level in epididymis and testes treated rats. GA or ω-3-FA enhanced the activities of testicular function marker enzymes, namely acid phosphatase (ACP), lactate dehydrogenase (LDH), alkaline phosphatase (ALP) and glucose-6-phosphate dehydrogenase (G6PD) in the treated rats. GA or ω-3-FA amelioration of manganese-induced decreases in follicle-stimulating hormone, luteinising hormone, and testosterone levels were complemented by increase (p < .05) sperm functional characteristics in treated rats. Conclusively, GA or ω-3-FA may serve as dietary supplements to improve male reproductive dysfunction associated with manganese toxicity.     

Quercetin and rutin ameliorates sulphasalazine‐induced spermiotoxicity,alterations in reproductive hormones and steroidogenic enzyme imbalance in rats

Certain dietary flavonoids exhibit protective potentials against drug‐induced male reproductive toxicities. We investigated the protective effects of quercetin and rutin on sulphasalazine‐induced alterations in steroidogenic enzyme activity, hormone profile and spermiotoxicity in rats. Sulphasalazine (SASP, 600 mg/kg bw) was administered alone or in combination with quercetin (20 mg/kg bw) or rutin (10 mg/kg bw) for 14 days. SASP treatment significantly increased relative weights of the epididymis and seminal vesicles. Also, testicular and epididymal sperm numbers (TSN, ESN), motility, daily sperm production (DSP) and acrosome reaction (AR) significantly decreased. SASP altered plasma testosterone, luteinising hormone (LH) and follicle‐stimulating hormone (FSH) levels while testicular cholesterol levels, 3β‐hydroxysteroid dehydrogenase (3β‐HSD) and 17β‐hydroxysteroid dehydrogenase (17β‐HSD) activities were decreased. Elevated malondialdehyde levels and concomitant decrease in reduced glutathione, glutathione‐S‐transferase, peroxidase and superoxide dismutase activities were evident in testis and epididymis of SASP‐treated rats. Quercetin or rutin co‐treatment with SASP significantly reversed organ weights, preserved sperm integrity, restored plasma hormone levels and increased cholesterol levels, 3β‐HSD and 17β‐HSD activities in testis. Both flavonoids also prevented oxidative stress in testis and epididymis of SASP‐treated rats. Quercetin and rutin protect against the negative effects of SASP treatment on reproductive capacity in male rats.     

Protective effects of vitamin E on sodium arsenite‐induced toxicity,testicular measurements and histopathological studies of testes in Teddy goat bucks

The objective of this study was to investigate the toxic effects of arsenic on testicular measurements and histology of adult Teddy goats bucks and to examine whether these toxic effects are scavenged by vitamin E. Twelve adult Teddy goat bucks were divided randomly into three groups, A, B and C. Group A was kept as control, the B was given sodium arsenite 5 mg/kg BW per day, and group C was fed with vitamin E 200 mg/kg BW per day + arsenic 5 mg/kg BW per day. This treatment was continued for 84 days. Analysis of data revealed that the testicular measurements (scrotal circumference, width, length and weight) were significantly reduced in arsenic‐treated animals, whereas there were ameliorating effects of vitamin E on these parameters. The major histopathological changes were present in the form of loss of germinal epithelium, atrophy of Leydig cells and vacuolations. Vitamin E in combination with sodium arsenite increased the active spermatogenesis as well as restoration of germinal epithelium. It can be concluded from the present findings that sodium arsenite causes toxicity in the male reproductive system of Teddy goat bucks with major changes in parenchyma of testes. Supplementation of vitamin E has protective effects on the toxicity of sodium arsenite on the reproductive system of male Teddy goat bucks.     

Selenium attenuates diclofenac-induced testicular and epididymal toxicity in rats

The adverse effect of diclofenac administration on the male reproductive organ in both humans and rats has been reported. Selenium, a trace element vital in nutrition, plays a significant part in cellular redox homeostasis, including male reproduction. However, the impact of selenium on male reproductive toxicity associated with diclofenac administration is lacking in the literature. The current investigation assessed the modulatory effects of selenium on diclofenac-mediated reproductive toxicity in rats. Rats were treated for fourteen consecutive days, either with diclofenac (10 mg/kg) or co-treated with selenium (0.125 and 0.25 mg/kg) body weight. Sperm parameters, enzymes of testicular function, luteinizing, follicle-stimulating hormone and testosterone were assessed in addition to oxidative stress indices and histopathological changes. Selenium significantly alleviated diclofenac-induced decreases in sperm count and motility, testicular function enzymes and levels of luteinizing hormone and testosterone in serum. Moreover, selenium co-administration at 0.125 and 0.25 mg/kg inhibited the diclofenac-induced decrease of antioxidant enzyme activities and increased oxidative stress parameters—lipid peroxidation, reactive nitrogen and oxygen species—in epididymis and testes of rats. Selenium (0.25 mg/kg) alone ameliorated diclofenac-mediated histological injuries in exposed rats. Collectively, selenium enhanced testicular and epididymal function in diclofenac-treated rats by suppressing nitrosative and oxidative stress in rats.     

Comparative effect of administration and discontinuation of sildenafil and/or clomipramine on the hepatic,cardiac and testicular tissues of male rats

In this study, we examined the adverse consequences of prolonged treatment with sildenafil and/or clomipramine (CLO) on the hepatic, cardiac and testicular tissues of rats. Additionally, we investigated the potential effects of treatment discontinuation. To this end, 60 adult male rats were randomly assigned into six groups and were orally treated with 4.5 mg sildenafil /kg BW (SLD) and 9 mg/ kg BW (SHD), 2.25 mg CLO/kg BW (CLO), 4.5 mg sildenafil/kg BW + 2.25 mg CLO/kg BW (SLD-CLO) and 9 mg sildenafil/kg BW + 2.25 mg CLO/kg BW (SHD-CLO) while the control rats received 0.5 ml distilled water for 8 weeks. Then, five rats from each group were sacrificed and the other five rats were left untreated for another four weeks to recover from the drug treatment. Long-term administration of sildenafil and/or CLO led to oxidative stress, inflammation and structural changes in the liver, heart and testis, reduction in sperm count and motility, an increase in abnormalities, and a reduction in serum testosterone, FSH and LH levels. All tested parameters returned to the normal state following the four-week discontinuation of sildenafil. Additionally, all the alterations caused by long-term administration of CLO, SLD-CLO and SHD-CLO were significantly improved during the recovery period.     

Dolichandrone serrulata flower extract ameliorates male reproductive damages in type 2 diabetic rats

Dolichandrone serrulata flower (DSF) has been believed to reduce blood glucose in hyperglycaemic persons with sub-fertility but its effect on improvement of male reproductive impairment has never been elucidated scientifically. This study attempted to investigate the hypoglycaemic effects of DSF on male reproductive damages in type 2 diabetes mellitus (T2DM) rats. Adult Sprague Dawley rats were divided into four groups (control, T2DM, DSF200 + T2DM and DSF600 + T2DM; n = 10/each). Control rats received low-fat diet for 14 days before saline injection while streptozocin (50 mg/kg BW) induced T2DM groups received high-fat diet and were orally administered with DSF (200 and 600 mg/kg BW) for 28 days. At the end, fasted blood glucose (FBG), malondialdehyde (MDA), testosterone, sperm quality, histology and protein expressions were examined. The result showed that DSF decreased high FBG and testicular MDA and increased testosterone levels of T2DM-treated rats. Low-sperm quality and histological malfunction were ameliorated in DSF-treated group. There was significant decrease in the expression of androgen receptor, heat-shock 70 and steroidogenic acute regulatory proteins of T2DM-treated rats. Our study demonstrated changes of six bands (116, 51, 45, 39, 35 and 29 kDas) of tyrosine-phosphorylated proteins. In conclusion, DSF could reduce the FBGand ameliorate the reproductive damages in male T2DM rats.     

Fertility enhancing activity and toxicity profile of aqueous extract of Chasmanthera dependens roots in male rats

This study evaluated the fertility‐enhancing activity and safety of aqueous extract of Chasmanthera dependens root (AECDR) in male rats. In the fertility study, twenty, sodium arsenite (10 mg/kg) body weight (BW)‐treated male rats (171.02 ± 3.36 g), assigned into four groups (I–IV), received 1 ml of distilled water (DW), 25, 50 and 100 mg/kg BW of AECDR for 60 days, whereas the control received DW. After 7 days of pairing with female rats (153.67 ± 2.24 g), spermatogenic, fertility, testicular function indices and enzymatic antioxidant activities were evaluated. The animal groupings in the toxicity study were similar to the fertility study except no administration of sodium arsenite. Sodium arsenite treatment‐related decreases (p < .05) in the semen and sperm parameters, testicular function indices, antioxidant activities and female rat fertility indices were reversed/ameliorated by AECDR. AECDR significantly altered the function indices of the liver and kidney and the lipid profile and selectively altered the haematological parameters. There was no treatment‐related histoarchitectural changes in the organs. Overall, the aqueous extract of C. dependens roots exhibited pro‐spermatogenic, fertility enhancing, antioxidant and androgenic activities in male rats. It also exhibited functional toxicity. Therefore, the chronic use of AECDR may not be completely safe as oral remedy.     

Protective effects of royal jelly on testicular torsion induced ischaemia reperfusion injury in rats

This study was performed to investigate the protective effects of royal jelly (RJ) on a testicular torsion-induced ischaemia/reperfusion (I/R) injury in adult rats. A total of 40 male Wistar rats were divided into four groups, including 10 rats in each group: Group 1 (sham), Group 2 (Control), group 3 (I/R rats treated with 100 mg/kg RJ for 50 days after torsion) and group 4( I/R rats treated with 20 mg/kg vitamin C for 50 days after torsion). Testicular torsion was created by rotating the right testes 720° a clockwise direction for 90 min. The levels of testosterone were measured by ELISA. Pathological evaluation, mean maturity and quality of the seminiferous tubules were used. Results showed that the testicular histopathology standards and testosterone levels changes were statistically significant in groups 3 and 4. The results obtained in this study may suggest that RJ like vitamin C had protective effects on a testicular ischaemia/reperfusion-induced injury in rats.     

Effects of curcumin on sperm quality,lipid profile,antioxidant activity and histopathological changes in streptozotocin-induced diabetes in rats

In this study, the effect of low-dose curcumin on sperm parameters, reproductive hormones, lipid profile, biochemical antioxidant parameters and the histopathological structure of the testis in diabetic male rats were evaluated. In the study, 28 male Wistar albino rats weighing 300–370 g and aged 8–10 weeks were used. Four groups of equal numbers have been created. Diabetes mellitus was induced with 45 mg/kg streptozotocin (STZ) in seven rats. Curcumin was administered to the rats in curcumin and the diabetes + curcumin group by gavage for 15 days at a dose of 10 mg/kg. Then, the rats were sacrificed. Blood samples and testis tissues were obtained, while the rats were under anaesthesia. Glucose, lipid profile, reproductive hormones, sperm parameters, biochemical antioxidant parameters and histopathological examination of the testis were performed. Abnormal sperm ratio, malondialdehyde, glucose, cholesterol, low-density lipoprotein, and triglyceride levels and caspase-3 expression were increased in diabetic rats, while the sperm motility and intensity and reduced glutathione, catalase and testosterone levels were decreased. When low-dose curcumin (10 mg/kg) was administered to diabetic rats, we found that curcumin significantly increased sperm motility and density, and decreased abnormal sperm rate according to the diabetic group. Moreover, curcumin significantly suppressed the lipid profile and increased follicle-stimulating hormone (FSH) and testosterone levels compared to the diabetic group. On testicular damage and decreased reproductive hormones caused by diabetes, curcumin may have a protective effect with indirect effect of glycaemic control by curcumin.     

Testicular toxicity following separate and combined administration of PDE5 inhibitors and opioid: assessment of recovery following their withdrawal

We previously observed that PDE5 inhibitors and opioids were widely abused in Nigeria. Here, we examined the effect of high doses of sildenafil, tadalafil, tramadol and sildenafil + tramadol on reproductive toxicity in male rats. Rats were either administered normal saline (0.2 ml), sildenafil (10 mg/kg), tadalafil (10 mg/kg), tramadol (20 mg/kg) or sildenafil + tramadol (10 and 20 mg/kg respectively) p. o. for 8 weeks. The recovery groups were allowed 8‐week recovery period before sacrifice. Results showed that body weight change, testicular and epididymal weights, epididymal sperm count and sperm viability were significantly reduced in all treated groups compared with the control. Spermatozoa with abnormal morphology were significantly increased in all treated groups compared with the control. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione (GSH) were significantly reduced, while malondialdehyde (MDA) was significantly increased in all treated groups compared with the control. The severity of toxicity was highest in sildenafil + tramadol group. There was no complete recovery from reproductive toxicity following withdrawal of the various treatments. High doses of sildenafil, tadalafil, tramadol or sildenafil + tramadol result in testicular oxidative stress‐induced reproductive toxicity with poor reversal following withdrawal.     

Comparison of the protective effects of curcumin and caffeic acid phenethyl ester against doxorubicin-induced testicular toxicity

Whether testicular toxicity is mediated by matrix metalloproteinases (MMPs) is an important question that has not been examined. This study investigated the suppressive effect of curcumin and caffeic acid phenethyl ester (CAPE) on oxidative stress, apoptosis, and whether MMPs mediate doxorubicin (DOX)-induced testicular injury. Male rats were randomly divided into eight groups (n = 8 per group). The groups were as follows: sham, dimethyl sulphoxide (100 µL), DOX (3 mg/kg), CAPE (2.68 mg/kg), curcumin (30 mg/kg), DOX+CAPE (3 mg/kg DOX and 2.68 mg/kg CAPE), DOX+curcumin (3 mg/kg DOX and 30 mg/kg curcumin) and DOX+CAPE+curcumin (3 mg/kg DOX, 2.68 mg/kg CAPE and 30 mg/kg curcumin). Injections were administered daily for 21 days. The oxidative stress, MMPs, proinflammatory cytokines and apoptotic markers in the DOX group were higher than the sham group (p < .05); these measures were lower in the groups treated with CAPE and curcumin together with DOX compared with the DOX group (p < .05). The results showed that MMPs mediated DOX-induced testicular injury, but CAPE and especially curcumin suppressed testis injury and cell apoptosis by suppressing DOX-induced increases in MMPs, oxidative stress and proinflammatory cytokines. However, curcumin exhibited more pronounced effects than CAPE in terms of all studied parameters.     

Protocatechuic acid inhibits testicular and epididymal toxicity associated with methotrexate in rats

We examined the effect of protocatechuic acid (PCA) on methotrexate (MTX)‐induced testicular and epididymal toxicity in Wistar rats, treated with MTX (20 mg/kg) alone or in combination with PCA (25 and 50 mg/kg) body weight for a week. PCA significantly abated MTX‐mediated increase in reactive oxygen and nitrogen species generation and lipid peroxidation as well as enhances glutathione balance and antioxidant enzymes in the testes and epididymis of treated animals. PCA suppressed MTX‐mediated increases in interleukin‐1β, tumour necrosis factor alpha and caspase‐3 activity in treated animals. Additionally, PCA treatment mediated increases in luteinising and follicle‐stimulating hormones, prolactin and testosterone levels with marker enzymes of testicular function, accompanied with increase in sperm functionality in treated animals. Conclusively, PCA may serve as potential supplementation, enhancing reproductive health in males undergoing MTX therapy.     

High dose of standardised extract of Costus afer leaves potentiates cadmium reproductive toxicity in Wistar rats

Protective effects of standardised extract of Costus afer leaves (CAME), an extract with good antioxidants on cadmium‐induced reproductive toxicity in male rats, were investigated in this study. Forty‐two adult male Wistar rats were randomly divided into six groups and were treated every day regularly for 4 weeks. G1 (control) rats received 1 ml of vehicle treatment. G2 rats were intoxicated with 2.5 mg kg^?1 day^?1 s.c cadmium chloride for 1 week. G3 and G4 rats were intoxicated with cadmium as in G2 rats and were treated orally with 100 and 200 mg/kg bwt/day of CAME, respectively, for 4 weeks. Group G5 and G6 rats were orally treated with 100 and 200 mg kg^?1 day^?1 bwt of CAME, respectively, for 4 weeks. Significant changes (p < 0.05) in andrological parameters (sperm count, sperm morphology, serum testosterone and nitric oxide concentration) and testicular antioxidant parameters (reduced glutathione, lipid peroxidation and activities of catalase, glutathione S‐transferase and glutathione peroxidase) caused by Cd toxicity were improved in cadmium‐intoxicated rats treated with 100 mg/kg body weight of CAME. Administration of 200 mg/kg body weight of CAME to cadmium‐intoxicated rats potentiated reproductive toxic effects of cadmium. In conclusion, lower dose of CAME is preferred over high dose in treatment of cadmium‐induced reproductive toxicity in rats.     

Ethanol‐induced male infertility: Effects of aqueous leaf extract of Tetracarpidium conophorum

This study investigated the effects of Tetracarpidium conophorum leaf extract on infertility induced by ethanol in male rats. Thirty rats were randomly divided into six groups of five animals each: Group 1 (positive control) received 0.9% saline only; Group 2 (ethanol alone) were given only 30% ethanol orally at 7 ml/kg body weight per day, thrice in a week; groups 3, 4 and 5 were given ethanol and co‐treated with 50, 500 and 1,000 mg/kg body weight of leaf extract, respectively, while Group 6 was given ethanol and co‐treated with a fertility drug, clomiphene citrate. Ethanol treatment resulted in significant (p < .05) decrease in LDH activity, G‐6PDH activity, glycogen content, 3β and 17β HSD activities and testicular and epididymal Zn and Se contents and furthermore decrease in testicular sperm count, viability and marked increment in total sperm abnormalities, rate of sperm analysis parameters and consequently decreased reproductive hormone levels. Interestingly, co‐administration of ethanol with either T. conophorum extract or drug almost ameliorated the toxic assault imposed by ethanol on reproductive organs and improved seminal qualities of the rats.     

Evaluation of protective effects of gallic acid on cisplatin-induced testicular and epididymal damage

Cisplatin is an effective chemotherapeutic drug used to treat many types of tumours. However, it may cause male reproductive toxicity. Gallic acid exhibits beneficial effects such as antioxidant, anti-inflammatory and antitumor. The current study investigated the beneficial effects of gallic acid against testis and epididymis toxicity induced by cisplatin. Male rats were divided into 4 groups as follows (n = 7): Control, cisplatin (a single dose of 8 mg/kg), Gallic acid (50 mg/kg) and cisplatin +Gallic acid groups. Testis was examined morphometrically by stereological methods. In addition, apoptosis, DNA damage, oxidative stress parameters in testis and testosterone in serum were measured. Epididymis was histopathologically evaluated. As a result, a significant decrease was observed in the number of spermatogonia, Leydig and Sertoli cells, testicular volume, height of germinal epithelial, Bcl-2 immunopositive cell number, activity of CAT, GSH and SOD enzymes and serum testosterone levels compared with the cisplatin group control group, while a significant increase was observed in the number of Caspase-3, Bax and 8-OHdG immunopositive cells and the MDA levels. However, Gallic acid significantly restored these parameters. Our study reveals that Gallic acid may improve Cisplatin-induced male reproductive toxicity by reducing oxidative stress, suppressing apoptosis and DNA damage and restoring structural and functional deterioration.     

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.     

Reversal of the toxic effects of cyclosporine on male reproduction and kidney function of rats by simultaneous administration of hCG + FSH

We have shown earlier that the administration of cyclosporine impairs testicular function and causes a decrease in sperm counts, sperm motility and fertility. In order to determine whether or not the deleterious effects of CsA could be reversed by hormonal therapy, we injected sexually mature male Sprague Dawley rats with cremaphor + saline or CsA (40 mg./kg./d) alone or in combination with human chorionic gonadotropin (hCG; five micrograms./d/rat) and follicle stimulating hormone (FSH; five micrograms./d/rat). The injections were given subcutaneously for 14 days. As expected, CsA administration decreased the body and reproductive organ weights, testicular and epididymal sperm counts, sperm motility and fertilizing ability. Serum levels of LH were elevated and testosterone was decreased. The administration of FSH + hCG to the CsA treated rats restored the body and reproductive organ weights, sperm counts and motility. Seventy five percent of gonadotropin treated males were fertile as compared to 25% in the CsA treated group. In the hormone treated group, the blood levels of CsA were 50% of that of CsA treated group. In order to verify whether or not the decline in the blood levels of CsA was the cause for the amelioration of CsA-induced changes in the reproductive function, we compared the CsA + hormone treated group with another group treated with five mg./kg./d CsA which had blood levels of CsA comparable to the former group. In the five mg./kg./d group the reproductive functions were significantly lower than the CsA + hormone treated group suggesting, therefore, that the restoration of reproductive functions in the CsA + hormone treated group is a result of hormonal treatment. Administration of CsA (40 mg./kg./d) reduced the kidney weight and increased the levels of serum creatinine: these changes were also ameliorated by the administration of hCG + FSH.     

Tocotrienol‐rich fraction supplementation prevents foetal loss in females mated with corticosterone‐treated male Sprague–Dawley rats

This study examined whether tocotrienol supplementation to corticosterone‐treated male rats could prevent foetal loss in females upon their mating. Epididymides of adult male Sprague–Dawley (SD) rats with proven fertility were surgically separated at the testis‐caput junction. Twenty‐four hours post‐surgery, these animals received for 7 days either: tocopherol‐stripped corn oil (Control), corticosterone 25 mg/kg s.c. (CORT), CORT 25 mg/kg s.c. and tocotrienol‐rich fraction (TRF) 100 mg/kg orally (CORT + TRF) or TRF 100 mg/kg orally (TRF). On day 8, males were cohabited with proestrus females. A spermatozoa‐positive vaginal smear indicated pregnancy. Males were euthanised for analysis of testosterone and antioxidant activities. Reproductive organs were weighed. On day 8 of pregnancy, females were laparotomised to count the number of implantation sites. Pregnancy was continued until term. Number of pups delivered and their weights were determined. Data were analysed using ANOVA. Malondialdehyde levels were significantly lower in CORT + TRF group compared with CORT group. Enzymatic antioxidant activities, testosterone level and reproductive organ weights were significantly higher in CORT + TRF group compared with CORT group. Number of implantation sites and live pups delivered, and their birth weights from females mated with CORT + TRF males were significantly higher compared to CORT group. Therefore, TRF prevents foetal loss in females mated with CORT + TRF‐treated males.     

The effects of hesperidin on colistin-induced reproductive damage,autophagy, and apoptosis by reducing oxidative stress

This study has been conducted to investigate the effect of hesperidin on colistin-induced reproductive damage in male rats. Twenty-four adult male Sprague Dawley rats were used as animal material. They were divided into four groups: control group, received physiological saline for 7 days by oral gavage; hesperidin group, received 300 mg/kg day hesperidin for 7 days; colistin group, received 73 mg/kg (total dose) colistin during 7 days; and colistin + hesperidin group, received 300 mg/kg day hesperidin following the colistin treatment. At the end of the study, routine spermatological parameters and biochemical evaluations were assayed. Also, apoptosis and autophagy biomarkers in testes were evaluated. Colistin increased oxidative stress, apoptosis and autophagy expression levels in testis. Hesperidin supplementation significantly decreased the oxidative stress levels in the testes of the colistin + hesperidin group when compared to the colistin group. The highest apoptosis and autophagy expression levels were detected in the colistin group. These values were statistically lower in the colistin + hesperidin group when compared to the colistin group. Colistin treatment decreased the percentage of sperm motility and increased sperm abnormality. Hesperidin supplementation mitigated significantly mentioned side effects compared to the colistin group. In conclusion, hesperidin supplementation can be a good strategy to mitigate colistin-induced testicular toxicity.