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.     

Quercetin prevents 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced testicular damage in rats

The protective effect of quercetin on 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced testicular damage in rats was investigated. Twenty-two rats were equally divided into four groups; first group was kept as control and given corn oil as carrier. In second group, TCDD was orally administered at the dose of 2 μ (kg week)(-1) for 60 days. In third group, quercetin was orally administered at the dose of 20 mg (kg day)(-1) by gavages, and in fourth group TCDD and quercetin were given together at the same doses. Although TCDD increased the formation of thiobarbituric acid reactive substances (TBARS) significantly, it caused a significant decline in the levels of glutathione (GSH), catalase (CAT), GSH-Px and CuZn-Superoxide Dismutase (CuZn-SOD) in rats. In contrast, quercetin significantly increased the GSH, CAT, GSH-Px and CuZn-SOD levels but decreased the formation of TBARS. In addition, sperm motility, sperm concentration and serum testosterone levels were significantly decreased but abnormal sperm rate and testicular damage were increased with TCDD treatment. However, these effects of TCDD on sperm parameters, histological changes and hormone levels were eliminated by quercetin treatment. Our results show that administration of TCDD induces testicular damage (oxidative stress, testes tissue damage, serum hormone level and sperm parameters), and quercetin prevents TCDD-induced testicular damage in rats. Thus, quercetin may be useful for the prevention and treatment of TCDD-induced testicular damage.     

Protocatechuic acid prevents reproductive damage caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in male rats

In this study, it was aimed to determinate beneficial effects of protocatechuic acid (PCA) against reproductive toxicity caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an environmental contaminant. For this purpose, 28 rats were equally divided into four groups (control, TCDD 2 μg kg(-1) per week, PCA 100 mg kg(-1) per day and TCDD + PCA group), and compounds were orally administered for 45 days. The results indicated that TCDD induced oxidative stress via an increase in thiobarbituric acid-reactive substances levels and a decrease in reduced glutathione, catalase, glutathione peroxidise and SOD levels in male rats. In contrast, PCA treatment prevented toxic effects of TCDD in terms of oxidative stress. Additionally, sperm motility, sperm concentration and serum testosterone levels significantly decreased, and pathologic testicular damage increased with TCDD exposure. However, these effects of TCDD on sperm characteristics, histopathological changes and hormone levels were reversed by PCA treatment. In conclusion, it was found that TCDD exposure induced reproductive toxicity (oxidative, hormonal, histopathological and spermatological alternations) in male rats and PCA treatment could prevent toxic effects of TCDD. Thus, PCA may be useful for the prevention and treatment of reproductive toxicity caused by TCDD.     

Acute diethyl nitrosamine and cadmium co‐exposure exacerbates deficits in endocrine balance,sperm characteristics and antioxidant defence mechanisms in testes of pubertal rats

Diethylnitrosamine (DEN) and cadmium are environmental contaminants of known poisonous consequences in animals and humans. We examined the influence of acute oral co‐exposure to DEN (10 mg/kg) and cadmium (5 mg/kg) on endocrine balance, semen and antioxidant status in rat testes. The results indicated decreases (p < 0.05) in the weight of the testis and organo‐somatic index of the testes in rats administered with either DEN or cadmium were aggravated in the co‐exposed rats. Serum concentrations of follicle‐stimulating hormone (FSH), luteinising hormone (LH) and testosterone decreased, and were more pronounced in rats co‐treated with DEN and cadmium. Enzymatic and non enzymatic antioxidant activities decreased following separate exposure to DEN and cadmium, and were increased in rats co‐treated with DEN and cadmium. The significant (p < 0.05) increases in malondialdehyde (MDA) was complemented by marked increase in sperm abnormalities, reduction in the sperm count, motility and viability compared with control. Histologically, co‐exposure to DEN and cadmium aggravates their discrete effects on the testes. Co‐exposure to DEN and cadmium elicited more severe endocrine disruption and testicular oxidative damage in rats, revealing additive adverse effects on testicular functions in rats and as such, may put exposed individual at greater risk.     

Effect of bisphenol A and co-administration of bisphenol A and vitamin C on epididymis of adult rats： A histological and biochemical study

Aim: To study the effect of bisphenol A on the epididymis and epididymal sperm of rats and the possible amelioration action of co-administration with vitamin C. Methods: Male Wistar rats were orally administered bisphenol A (0.2 μg·kg-1·day-1, 2 μg·kg-1·day-1 and 20 μg·kg-1·day-1) and 0.2 μg, 2μg and 20 μg bisphenol A + 40 mg vitamin C·kg-1·day-1 for 60 days. On day 61, rats were killed with anesthetic ether and sperm collected from epididymis were used for assessment of sperm count, motility and viability and biochemical studies. A 1 % homogenate of epididymis was prepared and used for biochemical estimations. Caput, corpus and cauda epididymis were fixed in Bouin's fixative for histological studies. Results: Administration of bisphenol A caused a reduction in the epididymal sperm motility and count and the sperm viability remained unchanged. The activities of superoxide dismutase and glu-tathione peroxidase decreased, while the levels of lipid peroxidation increased in epididymal sperm an     

Effect of kolaviron,a biflavonoid complex from Garcinia kola seeds,on the antioxidant,hormonal and spermatogenic indices of diabetic male rats

The antihyperglycaemic effect of kolaviron (KV), a biflavonoid from Garcinia kola has been established in previous studies. In this study, we investigated the effect of KV (200 mg kg^?1) on the antioxidant, hormonal and spermatogenic indices of alloxan‐diabetic male rats, and metformin hydrochloride (MET) (30 mg kg^?1) served as standard drug. The results showed that KV and MET significantly (P < 0.05) decreased the fasting blood glucose of the diabetic rats. Also, untreated and MET‐treated diabetic groups had significantly (P < 0.05) lower body‐weight gain and relative weights of testes. In addition, epididymal sperm abnormalities were increased, whereas sperm count, motility, testicular protein and sialic acid were decreased in untreated diabetic group. Also, antioxidant parameters, reduced glutathione, catalase, superoxide dismutase, glutathione‐S‐transferase and glutathione peroxidase were significantly (P < 0.05) reduced in the testes with a concomitant increase in lipid peroxidation in untreated diabetic group. Furthermore, untreated diabetic group had significantly (P < 0.05) lower levels of testosterone, luteinising and follicle‐stimulating hormones relative to controls. Treatment with KV restored the relative weights of testes, activities of antioxidant enzymes, sperm and hormonal indices of the diabetic animals. This study demonstrated the role of KV to promote fertility in diabetic male rats by enhancing the hormonal and antioxidant status of the rats.     

6‐Gingerol‐rich fraction from Zingiber officinale ameliorates carbendazim‐induced endocrine disruption and toxicity in testes and epididymis of rats

This study evaluated the protective effects of 6‐gingerol‐rich fraction (6‐GRF) from Zingiber officinale on carbendazim (CBZ)‐induced reproductive toxicity in rats. Adult male rats were treated with either CBZ (50 mg/kg) alone or in combination with 6‐GRF (50, 100 and 200 mg/kg) for 14 consecutive days. Gas chromatography–mass spectrometry (GCMS) analysis revealed that 6‐GRF consists of ten bioactive chemical components with 6‐gingerol being the most abundant (30.76%). Administration of 6‐GRF significantly (p < .05) prevented CBZ‐mediated increase in absolute and relative testes weights as well as restored the sperm quantity and quality in the treated rats to near control. In testes and epididymis, 6‐GRF significantly abolished CBZ‐mediated increase in oxidative damage as well as augmented antioxidant enzymes activities and glutathione level in the treated rats. Moreover, CBZ administration alone significantly decreased plasma levels of testosterone, thyrotropin, triiodothyronine and tetraiodothyronine, whereas follicle‐stimulating hormone was significantly elevated without affecting luteinising hormone and prolactin levels when compared with the control. Conversely, 6‐GRF ameliorated the disruption in the hormonal levels and restored their levels to near normalcy in CBZ‐treated rats. Collectively, 6‐GRF inhibited the adverse effects of CBZ on the antioxidant defence systems, hormonal balance and histology of the testes and epididymis in 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.     

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.     

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.     

Testicular gametogenic and steroidogenic activities in chlorpyrifos insecticide-treated rats: a correlation study with testicular oxidative stress and role of antioxidant enzyme defence systems in Sprague-Dawley rats

The present works examined an adverse effect of chlorpyrifos insecticide on testes and lipid peroxidation at low doses (5 mg-10 mg kg(-1) body weight) and the role of antioxidant enzymes systems at higher doses (20-30 mg kg(-1) body weight) in albino rats. At low doses, reduction in plasma levels of testosterone and FSH and LH hormones along with the significant shrinkage of seminiferous tubules and gametogenic changes in germ cells were noticed. But these changes were restored with the revival of serum testosterone, FSH and LH along with regression of testis at higher doses. Similarly, level of testicular lipid peroxidation was elevated, whereas levels of antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) and steroidogenic enzymes activities (Δ(5) , 3β-hydroxysteroid dehydrogenase and 17β-hydroxysteroid dehydrogenase) were reduced significantly at low doses. But, rat testes showed a significant decrease in lipid peroxidation and concomitant increase in antioxidant enzymes and steroidogenic enzymes activities at higher doses. Results showed that at higher doses of chlorpyrifos treatments, rat testes were shown to trigger their natural defence mechanism which became operative possibly through corrective measure of synthesis of antioxidant defence enzymes and steroidogenic enzymes and pituitary gonadotrophins hormone feedback mechanisms.     

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.     

黄芪注射液对镉诱导大鼠精子畸形的拮抗作用

目的 :观察黄芪注射液拮抗氯化镉诱导的大鼠精子畸形作用。　方法 :将 30只SD雄性大鼠随机分成 5组 :低浓度黄芪组 (A1)、高浓度黄芪组 (A2 )、环磷酰胺组 (CP)、氯化镉组 (Cd)和对照组 (C)。预先连续 7d分别给A1组和A2 组大鼠腹腔黄芪注射液 5g/ (kg·d)和 10g/ (kg·d) ,Cd组和CP组大鼠分别腹腔注射等量蒸馏水作对照 ,之后连续 2 1dA1组、A2 组和Cd组大鼠分别同时腹腔注射氯化镉溶液 [0 .2mg/ (kg·d) ]。CP组大鼠给予 5 0mg/ (kg·d)腹腔注射染镉后第 2 2d处死大鼠 ,观察睾丸脏器系数、精子头计数、每日精子生成量、附睾尾精子计数和畸形率以及睾丸和附睾病理学。　结果 :A2 组睾丸脏器系数、睾丸精子头计数、每日精子生成量和附睾精子计数 [(5 .6 8±1.19)、(4 9.0 1± 8.78)× 10 6/g、(10 .2 5± 2 .30 )× 10 6/ (g·d)、(4 7.5 1± 2 2 .5 1)× 10 6/ml]明显高于Cd组 [(3.11± 0 .16 )、(37.5 9± 10 .6 3)× 10 6/g、(5 .31± 0 .32 )× 10 6/ (g·d)、(10 .89± 2 .4 5 )× 10 6/ml](P <0 .0 5或P <0 .0 1) ;A2 组大鼠精子畸形率 [(7.0 4± 0 .12 ) % ]明显下降 ,与Cd组 [(17.81± 1.5 5 ) % ]相比 ,差异有极显著性 (P <0 .0 1)。　结论 :黄芪注射液可拮抗氯化镉对生殖系统的损害作用 ,对防护     

Biochemical and reproductive effects of gestational/lactational exposure to lead and cadmium with respect to testicular steroidogenesis, antioxidant system, endogenous sex steroid and cauda-epididymal functions

This study investigated the effects of gestational and lactational exposure to lead and cadmium on testicular steroidogenesis, antioxidant system and male accessory gland functions in F1 generation rats to understand the biochemical mechanisms involved in endocrine disruptions. Pregnant rats were subcutaneously administered with 0.05 mg kg(-1) body wt\ day(-1) of sodium acetate (control), lead acetate, cadmium acetate and (lead acetate + cadmium acetate) throughout the gestational-lactational period, and all animals from each of the experimental groups were sacrificed by decapitation on post-natal day 56 for performing various biochemical assays. We observed significant reduction in the activities of testicular key steroidogenic enzymes and serum testosterone concentration along with significant depletion in cholesterol, ascorbic acid and reduced glutathione contents in all the metal-treated groups. Reductions in the activities of catalase and superoxide dismutase with concomitant increase in the levels of thiobarbituric acid reactive substance were observed in experimental groups. Both sperm contents and sperm motility patterns were significantly altered in all the metal-treated groups, suggesting the direct/indirect spermotoxic effects of lead and cadmium. The inhibitory effects of lead, cadmium and combined exposure on testicular steroidogenesis machinery, along with the male accessory gland functions, are indicative of multiple targets of lead and cadmium to disrupt male reproductive functions.     

Effect of piperine on the epididymis of adult male rats

Aim： To study the effect of piperine on the epididymal antioxidant system of adult male rats. Methods： Adult male rats were orally administered piperine at doses of 1 mg/kg, 10 mg/kg and 100 mg/kg body weight each day for 30 consecutive days. Twenty-four hours after the last treatment, the rats were weighed and killed with ether and the epididymis was dissected from the bodies. Sperm collected from the cauda region of the epididymis was used for the assessment of its count, motility and viability. Caput, corpus and cauda regions of the epididymis were separated and homogenized separately to obtain 10 % homogenates. The supernatants were used for the assays of sialic acid, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, lipid peroxidation and hydrogen peroxide generation. Results： Body weight of the piperine-treated rats remained unchanged. The weights of the caput, corpus and cauda regions of the epididymis significantly decreased at dose of 100 mg/kg. Epididymal sperm count and motility decreased at 10 mg/kg and 100 mg/kg, and sperm viability decreased significantly at 100 mg/kg. Sialic acid levels in the epididymis decreased significantly at 100 mg/kg while significant decrease in the cauda region alone was observed at 10 mg/kg. A significant decline in the activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, along with an increase in hydrogen peroxide generation and lipid peroxidation were observed at 10 mg/kg and 100 mg/kg. Conclusion： Piperine caused a decrease in the activity of antioxidant enzymes and sialic acid levels in the epididymis and thereby increased reactive oxygen species levels that could damage the epididymal environment and sperm function.     

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.     

Reproductive aging in the Brown Norway rat is characterized by accelerated germ cell apoptosis and is not altered by luteinizing hormone replacement.

Reproductive aging in the male Brown Norway (BN) rat is characterized by decreased Leydig cell steroidogenesis associated with seminiferous tubule dysfunction. This could be a result of a combination of a primary testicular defect and a secondary hypothalamic pituitary dysfunction. In the present study, we determined in the BN rat whether germ cell loss occurred via apoptosis. We then defined the age of onset of Leydig cell dysfunction and germ cell loss and examined whether chronic luteinizing hormone (LH) replacement would delay or prevent reproductive aging. Plasma hormone levels, testicular sperm concentrations, and germ cell apoptosis were studied in 6, 9, 12, 15, 18, and 21-month-old BN rats. Beginning at 15 months, testicular weight, sperm concentration, total sperm counts, plasma testosterone, LH, and inhibin decreased, whereas the proportion of regressed testes and plasma follicle-stimulating hormone (FSH) levels increased with aging. Accelerated germ cell apoptosis involving spermatogonia, preleptotene and pachytene spermatocytes, and spermatids was evident in some tubules of the relatively normal testes from 21-month-old rats. In the regressed testes, complete cessation of spermatogenesis occurred. The apoptotic index was higher in the testes of old (21-month-old) rats in particular at stages XII-XIV when compared with younger animals. Chronic LH replacement (0.5 microg i.p. twice per day) administered to 15-month-old BN rats for 6 months did not alter plasma hormone levels, testes weight, sperm concentration or content, or the germ cell apoptotic index. In the control group, 3 out of 10 testes were regressed, whereas in the LH-replaced group, only 1 out of 12 testes was regressed. We show in this study that early reproductive aging in the BN rat began at around 15 months. Germ cell loss associated with aging occurs via apoptosis. Replacement therapy with LH for 6 months does not decrease or delay the testicular dysfunction associated with aging. It is unlikely that hypothalamic-pituitary dysregulation is the major cause of testicular aging.     

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.     

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.