Oxidative Effects of Na+- Specific Ionophore Monensin on the Rat Epididymis

The carboxylic antibiotic ionophore monensin is well-known for the Na⁺/H⁺ exchanger activity across the biological membranes. The current study has been designed to investigate the effect of monensin on spermatozoal concentration, motility, and oxidative stress–related parameters in the rat epididymis. Monensin was administered orally at a dose of 3.5 mg/kg body weight daily for 70 days, a duration that coincides with the completion of the spermatogenic cycle. At the end of the respective treatment, the epididymis was isolated into three separate regions—the capitum, corpus, and the cauda—successively away from the head of the testis. Marked changes were noted in the body weight, organ (epididymis) weight, sperm concentration and motility, as well as the morphologic observations of the sperm and the histologic architecture of the epididymal epithelium. Significant alterations were also recorded in the oxidative stress parameters such as the lipid peroxidation product, malonyldialdehyde, and the activity of superoxide dismutase, glutathione sulfotransferase, glutathione reductase, and catalase. The nonenzymatic thiol content such as the total, oxidized, and reduced glutathione showed significant changes and the tissue phosphatases such as alkaline and acid phosphatase were increased, indicative of the interference of the drug in lysosomal and Golgi membrane complex. The findings of the current study indicate interactions during the spermatozoal maturational process in the epididymis, and a significant potential use of monensin in male contraception may be suggested.     

Oxidative effects of Na+--specific ionophore monensin on the rat epididymis

The carboxylic antibiotic ionophore monensin is well-known for the Na+/H+ exchanger activity across the biological membranes. The current study has been designed to investigate the effect of monensin on spermatozoal concentration, motility, and oxidative stress-related parameters in the rat epididymis. Monensin was administered orally at a dose of 3.5 mg/kg body weight daily for 70 days, a duration that coincides with the completion of the spermatogenic cycle. At the end of the respective treatment, the epididymis was isolated into three separate regions--the capitum, corpus, and the cauda--successively away from the head of the testis. Marked changes were noted in the body weight, organ (epididymis) weight, sperm concentration and motility, as well as the morphologic observations of the sperm and the histologic architecture of the epididymal epithelium. Significant alterations were also recorded in the oxidative stress parameters such as the lipid peroxidation product, malonyldialdehyde, and the activity of superoxide dismutase, glutathione sulfotransferase, glutathione reductase, and catalase. The nonenzymatic thiol content such as the total, oxidized, and reduced glutathione showed significant changes and the tissue phosphatases such as alkaline and acid phosphatase were increased, indicative of the interference of the drug in lysosomal and Golgi membrane complex. The findings of the current study indicate interactions during the spermatozoal maturational process in the epididymis, and a significant potential use of monensin in male contraception may be suggested.     

Therapeutic and fertility restoration effects of Ionidium suffruticosum on sub-fertile male albino Wistar rats: effects on testis and caudal spermatozoa

Context: Ionidium suffruticosum (L.) Ging (Violaceae) is an important medicinal plant widely used as a herbal traditional medicine in Ayurveda for the treatment of infertility. Currently, little pharmacological information is available on its male fertility properties following prolonged use.

Objective: To investigate I. suffruticosum leaf extracts for male fertility parameters.

Materials and methods: The ethanol lyophilized fraction was administered orally on carbendazim-induced sub-fertility rats (250?mg/kg body weight for 28 days). The effects of fractions on rat’s fertility parameters i.e., body and testes weight, sperm motility, sperm vitality, epididymal sperm counts, its morphology, enzyme and antioxidant stress and histopathology were studied and compared with clomiphene citrate.

Results: The sub-fertile male rats treated with I. suffruticosum leaf extract increased the body weight of 7?g, testis weight of 97?mg, increased cauda epididymal sperm counts of 34.2?×?10⁶ sperm/mL, motility of sperm 46% and vitality 28% also increased and normal sperm morphology also improved up to 32%. The carbendazim-treated group showed loss in body weight of 33?g, testis weight of 851?mg, decreased epididymal sperm counts of 15?×?10⁶ sperm/mL, with sluggish motility and a highly significant fall in the live sperms of about 57%.

Discussion and conclusion: The leaf fraction of I. suffructicosum increased the testicular weight, spermatogenesis, sperm counts, lessened sperm agglutination, and increased testicular oxidative biomarkers, SOD, and CAT. This study therefore supports the usage of I. suffructicosum in traditional medicine for infertility.     

Involvement of Sertoli cells in spermatogenic failure induced by carbendazim

The aim of this study is to determine whether Sertoli cells are involved in spermatogenic failure induced by carbendazim, a benzimidazole fungicide that is widely used in agriculture. Total 40 rats were treated with carbendazim by oral gavage at dosages of 0, 20, 100 and 200mg/kg for 60 days. The testis weight, sperm counts, sperm motility and Sertoli cell morphology and secretions including vimentin, ABP, inhibin B, SCFs and SCFm in testis were examined. In 100 and 200mg/kg groups, the testis weight, the sperm counts and motility and SCFm levels were significantly decreased, the sloughing of germ cells and ABP levels were increased, and the vimentin filaments and Sertoli cell morphology were altered. Inhibin B and SCFs levels were unchanged. The results suggested that alterations of Sertoli cell morphology and function were involved in spermatogenic failure induced by carbendazim.     

Effect of continuous inhalation of allethrin-based mosquito coil smoke in the male reproductive tract of rats

Objectives: Continuous inhalation of allethrin-based mosquito coil smoke may affect fertility, an aspect that has not received much attention. In this study, we attempt to understand the harmful effects on the male reproductive system caused by continuous exposure to allethrin-based mosquito coil smoke.

Methods: Adult Wistar rats were allowed to inhale mosquito coil smoke for 15–180 days, and male reproductive tract tissues (caput, cauda, and testes) were collected. Using standard biochemical techniques, changes in oxidative stress (lipid peroxidation) and antioxidant status was measured. Histopathological analyses were carried out to assess pathomorphological damage in the caput, cauda, and testis. Real-time polymerase chain reaction was carried out to determine the expression pattern of the stress-response gene, p53, and the spermatogenic factors c-Kit, Scf, and Tgf-β1.

Results: In rats exposed to allethrin-based mosquito coil smoke for 15–180 days, compared to the unexposed controls, lipid peroxidation was increased in the cauda and testes. The activity of antioxidant enzymes remained largely unchanged in the all the tissues analyzed. Histopathological analyses revealed loss of tubule architecture, epithelial cell disruption, increase in lumen size, interstitial edema, and presence of dead spermatozoa. p53 gene expression was differentially altered in the epididymis and testes. The expression of spermatogenic factors, namely, stem cell factor and its ligand c-Kit was unaltered though decreased levels of Tgf-β1 were observed.

Conclusion: Results of this study demonstrate that prolonged exposure to allethrin-based mosquito coil smoke could lead to oxidative stress and compromise germ cell production.     

The inductive effects of <Emphasis Type="Italic">Centella asiatica</Emphasis> on rat spermatogenic cell apoptosis in vivo

Centella asiatica (L.) Urban has been traditionally used for the treatment of various disease and as a food for thousands of years in various parts of the world including eastern Asia, China and India. The goal of this study was to investigate the effects of Centella asiatica aqueous leaf extract on the induction of spermatogenic cell apoptosis in male rats. After lethal dose (LD₅₀) assessment of plant extract, rats were divided in five groups. The experimental groups received orally 10, 50, 80 and 100 mg/kg aqueous leaf extract daily for 60 days and the control group received just water. After 60 days, body and testis weight were measured and blood samples were taken from the heart. To evaluate apoptosis and histological changes, tissue samples obtained from rat testes were stained by TUNEL assay and hematoxylin and eosin stain. Results showed that the sperm count, motility, and viability and the number of spermatogenic cells in the seminiferous tubules were significantly decreased compared with the control group. The number of apoptotic germ cells per seminiferous tubule cross-section was significantly increased in the experimental group (18.11 ± 3.5) compared with the control group (8.7 ± 0.81) (P < 0.05). Serum testosterone, follicle-stimulating hormone, and luteinizing hormone levels also showed significant decreases in the experimental groups (P < 0.05). There was also a significant decrease in testis weight in experimental groups compared with the control group (P < 0.05). It is concluded that Centella asiatica has toxicological effects on the reproductive system in male rats and, therefore, it is suggested that leaf extracts of Centella asiatica possess antifertility effects in the male rat.     

Evaluation of ameliorative effect of curcumin on imidacloprid‐induced male reproductive toxicity in wistar rats

This study was undertaken to investigate the toxic effects of imidacloprid (IM) on male reproductive system and ameliorative effect of curcumin (CMN) in male Wistar rats. For this purpose, IM (45 and 90 mg/kg, body weight) and CMN (100 mg/kg, body weight) were administered orally to the rats either alone or in combinations for a period of 28 days. At the end of experiment, male reproductive toxicity parameters (total sperm count and sperm abnormalities), testosterone level, steroidal enzymatic activity [3β‐hydroxysteroid dehydrogenase (3β‐HSD) and 17β‐HSD], and oxidative stress indicators were estimated in testis and plasma. IM treatments resulted in significant decrease (p < 0.05) in total epididymal sperm count, sperm motility, live sperm count, and increase (p < 0.05) in sperm abnormalities. Activities of gamma‐glutamyl transpeptidase, lactate dehydrogenase‐x, and sorbitol dehydrogenase were significantly increased (p < 0.05), while, 3β‐HSD and 17β‐HSD enzymatic activity along with testosterone concentration in testis and plasma were decreased significantly (p < 0.05) in IM‐treated rats. IM exposure resulted in significant increase (p < 0.05) in LPO and decrease (p < 0.05) in GSH level along with decreased activities of CAT, SOD, GPx, and GST. IM‐treated rats showed histopathological alterations in testis and epididymis. However, the reproductive toxicity parameters, oxidative stress indicators, and histopathological changes were minimized and functional restorations were noticed by co‐administration of CMN in IM‐treated rats. The results of this study suggest that IM‐induced male reproductive toxic effects could be ameliorated by CMN supplementation. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1250–1263, 2016.     

The Effects of l‐Carnitine Against Cyclophosphamide‐Induced Injuries in Mouse Testis

In order to explore the possibility of l ‐carnitine (LC) as a protector of male fertility in chemotherapy, we observed the damage of cyclophosphamide (CTX) to Sertoli cells and the protective effect of LC on the testis Sertoli cells from such damage in this study. Healthy adult male mice were divided into three groups: chemotherapy group were injected intraperitoneally with the CTX; protective agent group were injected both LC and CTX; control group mice were injected only with isochoric physiological saline; all once a day for 5 days. After 5 days, the mice were, respectively, killed at 24 hr after the last injection. The testis and epididymis were removed. Epididymis was for sperm analysis immediately, and immunohistochemistry, RT‐PCR and Western blot for the assessments of occludin, glial cell‐derived neurotrophic factor (GDNF) and TGF‐β3 mRNA and protein expression. The sperm analysis of epididymis showed that CTX can significantly decrease sperm count and motility; and administration of LC resulted in significant recovery of the sperm count and sperm motility. Compared with control group, the expressions of occludin and GDNF decreased and the expression of TGF‐β3 increased significantly (p < 0.05) in the CTX group. In the LC + CTX group, the expressions of occludin and GDNF were higher than those of the CTX group and similar to those of the control group; the TGF‐β3 expression was lower (p < 0.05) than that of the CTX group and similar to that of the control group. The results of this study showed that CTX could damage the spermatogenesis and reduce the expression of occludin and GDNF, and increase the expression of TGF‐β3 in testis of mouse, which indicates CTX's damage or efficacy to testis Sertoli cells. LC could protect the Sertoli cells of testis from these damages caused by CTX, and promote or protect the spermatogenesis. In conclusion, this study provides meaningful information about the possible damage to male fertility by chemotherapeutics and potential of LC in the protection of male fertility during chemotherapy.     

五子衍宗丸调控睾丸线粒体融合蛋白2减轻内质网应激改善肥胖大鼠生精功能

目的 观察五子衍宗丸对高脂饮食诱导肥胖大鼠生精功能的影响,并从睾丸内质网应激角度探讨可能机制。方法 30 只雄性 SD 大鼠随机分为对照组、模型组和五子衍宗丸低、中、高剂量（0.5、1.0、2.0 g·kg^-1）组。对照组给予普通饮食,其余组给予高脂饲料喂养,16 周后各组 ig 给予相应剂量药物,连续 4 周;取附睾进行精子功能分析;血清 ELISA 分析性激素水平变化;苏木素-伊红染色观察睾丸组织病理改变;透射电镜观察睾丸支持细胞线粒体和内质网结构改变;免疫荧光染色检测睾丸线粒体融合蛋白 2（Mfn2）及内质网应激标识蛋白葡萄糖调节蛋白 78（GRP78）的定位及表达;Western blotting 检测睾丸组织 Mfn2 和蛋白激酶 R 样内质网激酶（PERK）通路 相 关 蛋 白 相 对 表 达 。结果 与对照组比较, 模型组大鼠体质量明显增加（P＜0.01）,血清雌二醇水平明显升高（P＜0.01）,睾酮水平明显降低（P＜0.01）;睾丸生精细胞排列稀疏,细胞变性;精子活力明显降低（P＜0.05）,精子畸形率明显升高（P＜0.01）;睾丸支持细胞内质网和线粒体肿胀,呈空泡状,部分网膜断裂,Mfn2 表达明显降低,GRP78 荧光表达明显增加;PERK、 活 化 转 录 因 子 -4 （ATF4） 和 CHOP 蛋白量明显升高（P＜0.01）。与模型组比较,五子衍宗丸高剂量组体质量减轻明显（P＜0.05）;中、高剂量组血清雌二醇水平明显降低（P＜0.05、0.01）,睾酮水平明显升高（P＜0.05、0.01）;高剂量组精子活力明显升高（P＜0.05）,精子畸形率明显降低（P＜0.05）;睾丸病变减轻,排列较致密,支持细胞内质网和线粒体肿胀改善;Mfn2 荧光表达逐渐增强,蛋白相对表达明显增加 （P＜0.05、0.01）,GRP78 荧光表达逐渐减弱;低剂量组 ATF4 蛋白量明显降低 （P＜0.01）,中剂量组PERK、ATF4 蛋白量明显降低（P＜0.05、0.01）,高剂量组 PERK、ATF4 和 CHOP 蛋白量均明显降低（P＜0.01）。结论 五子衍宗丸可改善高脂饮食诱导肥胖引起的大鼠生精障碍,其机制可能与调控睾丸支持细胞Mfn2表达,减轻内质网应激有关。     

Effect of the anti-androgenic endocrine disruptor vinclozolin on embryonic testis cord formation and postnatal testis development and function

Vinclozolin is a systemic dicarboximide fungicide that is used on fruits, vegetables, ornamental plants, and turf grass. Vinclozolin and its metabolites are known to be endocrine disruptors and act as androgen receptor antagonists. The hypothesis tested in the current study is that transient embryonic exposure to an anti-androgenic endocrine disruptor at the time of testis determination alters testis development and subsequently influences adult spermatogenic capacity and male reproduction. The effects of vinclozolin on embryonic testicular cord formation in vitro were examined, as well as the effects of transient in utero vinclozolin exposure on postnatal testis development and function. Embryonic day 13 (E13, sperm-positive vaginal smear DAY = E0) gonads were cultured in the absence or presence of vinclozolin (50–500 μM). Vinclozolin treated gonads had significantly fewer cords (P < 0.05) and the histology of the cords that formed were abnormal as compared to vehicle-treated organs. Pregnant rats were exposed to vinclozolin (100 mg/kg/day) between embryonic days 8 and 14 (E8–E14) of development. Testis morphology and function were analyzed from postnatal day (P) 0, pubertal P20, and adult P60. No significant effect of vinclozolin on testis histology or germ cell viability was observed in P0 testis. The pubertal P20 testis from vinclozolin exposed animals had significantly higher numbers of apoptotic germ cells (P < 0.01), but testis weight was not affected. The adult P60 sperm motility was significantly lower in vinclozolin exposed males (P < 0.01). In addition, apoptotic germ cell number in testis of vinclozolin exposed animals was higher in adult P60 animals. Observations demonstrate that vinclozolin can effect embryonic testicular cord formation in vitro and that transient in utero exposure to vinclozolin increases apoptotic germ cell numbers in the testis of pubertal and adult animals. This correlated to reduced sperm motility in the adult. In conclusion, transient exposure to vinclozolin during the time of testis differentiation (i.e. cord formation) alters testis development and function. Observations indicate that transient exposure to an anti-androgenic endocrine disruptor during embryonic development causes delayed effects later in adult life on spermatogenic capacity.     

The effect of thiamine pyrophosphate on ethambutol-induced ocular toxicity

Context: Ethambutol-induced retinal oxidative damage in patients with tuberculosis is still not being adequately treated. The protective effect of thiamine pyrophosphate against oxidative damage in some tissues has been reported, but no information on the protective effects of thiamine pyrophosphate against ethambutol-induced oxidative retinal damage has been found in the medical literature.

Objective: The objective is to investigate whether thiamine pyrophosphate has a protective effect against oxidative retinal damage in rats induced by ethambutol.

Materials and methods: Experimental animals divided into four groups (n?=?10): the healthy group (HG), the ethambutol control group (EMB), thiamine?+?ethambutol group (Thi–EMB) and thiamine pyrophosphate?+?ethambutol group (TPP–EMB). The rats in the TPP–EMB and Thi–EMB groups were administered thiamine pyrophosphate and thiamine, respectively, at doses of 20?mg/kg intraperitoneally. Distilled water was administered intraperitoneally to the HG and the EMB groups as a solvent in the same volumes. One hour after drug injection, 30?mg/kg ethambutol was administered via an oral gavage to the TPP–EMB, Thi–EMB and EMB groups. This procedure was repeated once a day for 90 days. At the end of this period, all rats were euthanized under high-dose thiopental sodium anesthesia, and biochemical and histopathological investigations of the retinal tissue were performed.

Results: Malondialdehyde (MDA) and DNA damage product 8-hydroxyguanine levels were significantly lower in the retinal tissue of TPP–EMB and HG groups compared to those of the Thi–EMB and EMB groups, and total glutathione (tGSH) was also found to be higher. In addition, severe retinal tissue vascularization, edema and loss of ganglion cells were observed in the Thi–EMB and EMB groups, whereas histopathological findings for the TPP–EMB group were observed to be close to normal.

Discussion and conclusion: These findings suggest that thiamine pyrophosphate protects retinal tissues from ethambutol-induced oxidative damage, and thiamine does not. This positive effect of thiamine pyrophosphate may be useful in the prevention of ocular toxicity that occurs during ethambutol use.     

Cadmium exposure increases susceptibility to testicular autoimmunity in mice

Cadmium, one of various environmental toxicants, is known to suppress systemic immunity and to injure the testicular capillary endothelia with resultant necrosis of testicular tissues in mice and rats treated with high doses. Recently, it also became evident that cadmium can affect the integrity of the blood–testis barrier (BTB), the endocrine function of Leydig cells, apoptosis of germ cells and systemic immunity, even on treatment with a low dose that does not induce spermatogenic disturbance. Experimental autoimmune orchitis (EAO), i.e., an organ‐specific autoimmunity of the testis, can be induced by repeated immunization with testicular antigens, and its pathology is characterized by lymphocytic inflammation and spermatogenic disturbance. In the present study, we investigated the morphological and functional changes of testes in mice treated with a low dose of cadmium chloride (CdCl₂) and also examined its toxicity as to susceptibility to EAO. The results showed that exposure to 3 mg CdCl₂ kg^?1 body weight did not affect the spermatogenic state. However, the BTB at the tubuli recti and the rete testis, but not the seminiferous tubules, was slightly weakened, and intra‐testicular mRNA expression of interleukin (IL)‐6, tumor necrosis factor‐α and IL‐1β was significantly increased by the CdCl₂ treatment. Furthermore, immunization with testicular antigens after the CdCl₂ exposure significantly augmented the EAO severity. Therefore, exposure to a low dose of CdCl₂ induces no significant disturbance of spermatogenesis, however, it does change the immunological microcircumstances in the testis, resulting in increased susceptibility to testicular autoimmunity. Copyright © 2012 John Wiley & Sons, Ltd.     

Tribulus terrestris ameliorates metronidazole-induced spermatogenic inhibition and testicular oxidative stress in the laboratory mouse

Objective:The present study was undertaken to evaluate the protective effects of the fruit extract of Tribulus terrestris (TT) on the metronidazole (MTZ)-induced alterations in spermatogenesis, sperm count, testicular functions, and oxidative stress.Results:Metronidazole caused marked alterations in the testicular weight, spermatogenesis, activities of antioxidant enzymes, lactate dehydrogenase, alkaline phosphatase, and the level of LPO. The epididymal sperm count also declined significantly in MTZ-treated group. These changes were partially restored following co-administration of 500 mg/kg BW/day of MTZ and 100 mg/kg BW/day of TT. However, in the mice co-administered with 500 mg/kg BW/day of MTZ and 200 mg/kg BW/day of TT, the changes reverted back completely, similar to that of the controls.Conclusion:The fruit extract of TT ameliorates the MTZ-induced alterations in the testis.KEY WORDS: Antioxidant enzymes, free radicals, metronidazole, testis, Tribulus terrestris     

Sperm quality and fertility in rats after prenatal exposure to low doses of TCDD: A three-generation study

Exposure to Tetrachlorodibenzo-p-dioxin (TCDD) in male rats promotes, decreased sperm concentration, alterations in motility and in sperm transit time. We evaluated the effect transgenerational of in utero exposure to low doses TCDD in the sperm quality. Pregnant rats (F0) were exposed to 0.1; 0.5 and 1.0 μg of TCDD, on gestational day 15, coincides with the end of most organogenesis in the fetus. Adult male offspring (F1, F2 and F3 generation) were investigated for fertility after artificial insemination in utero. After collection of the uterus and ovaries, the numbers of corpora lutea and implants were determined. TCDD provoked alterations in sperm morphology and diminution in serum testosterone levels and sperm transit time in the cauda epididymis. The fertility significantly decreased in all the generations, at least at one dose. In conclusion, TCDD exposure decreases rat sperm quality and fertility in adult male offspring and this effects persist into the next generation.     

Effects of high doses of testosterone propionate and testosterone enanthate on rat seminiferous tubules — a stereological and cytological study

The effects of exogenous testosterone on various testicular variables has become of increasing significance because of its potential use in male contraception. For this reason, high doses of two testosterone esters [testosterone propionate (TP) and testosterone enanthate (TE)] were used in a study of their influence on the morphology, length and curvature of the seminiferous tubules of the rat testis, and on cytological smears of the seminiferous tubules epithelium. TP was given for 14 days (3 mg/100 g body weight, i. m.) to assess the acute effects of testosterone on the seminiferous tubules. TE was administered for 60 days (in the same manner as TP) to study possible chronic effects on the rat testis. After TP and TE treatment the seminiferous tubule epithelium showed disorganization and desquamation of spermatogenic cells. In the TP-treated testes the tubules lined with Sertoli cells only were observed. The values for the length and curvature of seminiferous tubules of the TP- and TE-treated rats were significantly reduced (p<0.001). All these changes were observed earlier in the TP-treated than in the TE-treated animals. In cytological smears of the testis of the TP- and TE-treated rats an increase of vacuoles and residual bodies in Sertoli cell cytoplasm was noted. In addition, a reduction of spermatogenic cells, particularly sperms, was manifest in the smears after treatment. Large groups of Sertoli cells were seen in the smears from these testes.The study was supported by a Grant for Scientific Research No. 3-01-041 from the Ministry of Science, Technology and Informatics of the Republic of Croatia     

Effects of subchronic samarium exposure on the histopathological structure and apoptosis regulation in mouse testis

To evaluate the reproductive toxicity of samarium, a widely used rare earth element, male ICR mice were orally exposed to samarium nitrate for 90 days for lesion evaluation in the testis. Decreased organ coefficients, disorganized seminiferous tubules, and decreased spermatogenic cells and sperm of the testis were observed extensively in the treated groups, indicating that the testis is a target organ of samarium. Electron microscopy confirmed that the lesions inside the spermatogenic cells and sperm mainly included mitochondrial swelling, mitochondrial vacuolization, fuzzy nuclear membranes, and marginated chromatin. Increased spermatogenic cell apoptosis rate in the testis was confirmed with a TUNEL assay. And expression up-regulation of p53 and Bax, and down-regulation of Bcl-2 were observed (p < 0.05), indicating the apoptosis is related to p53 mediated pathway.     

Sexual and fertility adverse effects associated with chemotherapy treatment in women

Introduction: Earlier diagnosis and novel chemotherapy strategies have resulted in a considerable improvement in cancer survival, but the quality of that survival is influenced by late effects of chemotherapy. Premature ovarian failure is a common consequence of chemotherapy in reproductive-aged women, and, as a result, fertility issues and sexual dysfunction occur frequently in women who have undergone chemotherapy.

Areas covered: This article reviews what is known about the effects of chemotherapy on fertility and sexuality. We also discuss risk factors for premature ovarian failure, fertility preservation options in patients willing to have a child after treatment, and sexual changes associated with estrogen withdrawal and psychological factors.

Expert opinion: Chemotherapy-induced ovarian failure in young women is associated with poorer quality of life, decreased sexual functioning, psychosocial distress related to fertility concerns, and infertility. Fertility preservation options should be considered in women at risk of premature ovarian failure caused by chemotherapy. Sexual dysfunction associated with estrogen withdrawal and psychological stress is common in cancer survivors. Women who suffer from sexual dysfunction may benefit from brief counseling and targeted intervention.     

Testicular effects of di-n-butyl phthalate (DBP): Biochemical and histopathological alterations

Di-n-butyl phthalate (DBP) was administered to young male rats by gavage at the doses of 250, 500 and 1000 mg/kg body weight/day for 15 days. A significant decrease in testes weight was observed at 500 and 1000 mg/kg doses of DBP. Histopathological examination revealed marked degeneration of seminiferous tubules. The activities of testicular enzymes associated with postmeiotic spermatogenic cells, such as sorbitol dehydrogenase and acid phosphatase, were decreased significantly, while that of lactate dehydrogenase was significantly increased, coincident with degeneration of spermatogenic cells. The activities of enzymes associated with premeiotic spermatogenic cells, Sertoli cells or interstitial cells, -glucuronidase, -glutamyl transpeptidase and glucose-6-phosphate dehydrogenase were significantly increased. Thus the alterations in activity of these testicular cell specific enzymes suggest that DBP exposure during early life could affect the testicular functions.     

Effects of L-ascorbic acid supplementation on dieldrin toxicity in rats

Chronic dieldrin administration to rats (5 mg/kg/day) produced pathological changes in liver and kidney tissues. Dieldrin treated rats showed high levels of liver ascorbic acid and increased activities of inorganic pyrophosphatase in brain and glucose-6-phosphatase in liver. The activities of Mg²⁺-ATPase in liver and acetylcholinesterase in brain were decreased under toxic doses of dieldrin. L-Ascorbic acid supplements in treated animals could partially prevent the pathological alterations, as observed histologically in liver and kidney tissues. Administration of this vitamin could also prevent alterations in some enzyme activities produced by toxic dieldrin doses.     

Gonad histology and vitellogenin concentrations in brown trout (Salmo trutta) from Danish streams impacted by sewage effluent

Brown trout (Salmo trutta) collected from a number of Danish streams impacted by sewage effluent were examined for alterations to gonadal development and induction of vitellogenin synthesis. Among fish collected in June/July 2000/2001 and November 2002 higher levels of plasma vitellogenin were found in males from six streams impacted by sewage effluent compared to males from their respective reference sites. A direct non-competitive ELISA was developed for brown trout vitellogenin in order to perform the vitellogenin measurements. Intersex in females with no apparent relation to sewage effluent exposure was observed at all sites. In one stream, male brown trout with a very high level of vitellogenin were concomitantly found to have a high degree of vacuolation of the testes and a presence of only the early spermatogenic stage, spermatogonia. The cause of these alterations to the testis structure is unclear. However, as a high level of plasma vitellogenin in these males indicated estrogenic exposure, the vacuolation might also be a result of endocrine disruption causing delayed or disrupted spermatogenesis.