Effects of mecobalamin on testicular dysfunction induced by X-ray irradiation in mice]

Experimental testicular dysfunction were produced by X-ray irradiation to the testes in mice. Mecobalamin (CH3-B12) was orally administered at a daily dose of 0.01, 0.1 or 1 mg/kg six times a week for 8 weeks from the next day after the irradiation. The control mice received physiological saline in the same manner. On 4th- and 6th-week after the irradiation, the weights of testes and epididymides were decreased, although those of the body and accessory sex glands (seminal vesicle, coagulating gland and prostate) were nearly equal to those of non-irradiated mice. At the same time, the diameter of seminiferous tubules decreased and sperm parameters (sperm count, sperm motility and sperm abnormality) deteriorated. When CH3-B12 (1 mg/kg) was administered, the diameter of seminiferous tubules increased and sperm parameters improved as compared to those of the control. The results indicate that CH3-B12 improved the experimental testicular dysfunction in mice induced by the irradiation. These results suggest that CH3-B12 might accelerate testicular function.     

Effect of alpha-tocopherol and simvastatin on male fertility in hypercholesterolemic rats.

The effect of alpha-tocopherol, simvastatin and both on male fertility in hypercholesterolemic rats was studied. Induction of hypercholesterolemia was done by feeding rats on a diet containing 1% cholesterol for 30 days. Hypercholesterolemic rats were orally given alpha-tocopherol (3 mg kg(-1) BW) or simvastatin (1 mg kg(-1) BW) or both for 65 days. Fertility index, serum testosterone level, sex organs weight, semen analysis and histopathological examination of testes, seminal vesicles and prostate glands were the parameters used to evaluate the reproductive efficiency of rats. In hypercholesterolemic rats (control +ve), there was a marked decrease in fertility index, testicular weight, sperm cell count, and percentages of sperm motility and viability associated with a significant increase in sperm cell abnormalities. Oral administration of either alpha-tocopherol or simvastatin to hypercholesterolemic rats for 65 days significantly improved the fertility index, testicular weight and semen quality. Concomitant administration of alpha-tocopherol and simvastatin to hypercholesterolemic rats markedly increased fertility index and sperm motility and viability associated with a significant reduction of sperm cell abnormalities. Histopathological examination revealed that testes of hypercholesterolemic rats (control +ve) had degenerated, non-functioning and atrophied seminiferous tubules associated with arrest of spermatogenesis. Oral administration of alpha-tocopherol and simvastatin concomitantly to hypercholesterolemic rats resulted in active mature and full functioning seminiferous tubules. In conclusion, concomitant administration of alpha-tocopherol and simvastatin to hypercholesterolemic male rats improved their reproductive efficiency and produced additional protection against reduced fertility induced by hypercholesterolemia.     

The effect of vomitoxin (Deoxnivalenol) on testicular morphology, testicular spermatid counts and epididymal sperm counts in IL-6KO [B6129-IL6 [TmlKopf] (IL-6 gene deficient)] and WT [B6129F2 (wild type to B6129-IL6 with an intact IL-6 gene)] mice.

The potential of vomitoxin (VT) to affect testicular morphology and testicular and epididymal sperm counts was assessed in three strains of mice: IL-6KO [B6129-IL6 (tmlKopf) (IL-6 gene deficient)], WT [B6129F2 (wild type to B6129-IL6 with an intact IL-6 gene)] and B6C3F1 mice in a 90-day feeding study. The treated mice received VT at a concentration of 10 ppm in their diet. The body weight of VT-treated animals was significantly reduced compared with control animals. Slight changes, not statistically significant, were observed in relative testis weight and testicular spermatid counts. Histological changes were not apparent in the testes of VT-treated animals. The diameter of the seminiferous tubules, the height of the seminiferous epithelium and the number of Sertoli cell nucleoli per cross-sectioned seminiferous tubule in the VT-treated groups were not significantly different from their respective untreated controls. The IL-6KO and B6C3F1 VT-treated mice had significantly reduced cauda epididymal weights compared with their respective controls. These changes were not attributed to decreased sperm counts and this finding suggests that VT may exert an adverse affect on the epididymis.     

Evaluation of protective effect of vitamin e on acrylamide induced testicular toxicity in wister rats

Male wistar rats (weighting 160-180 g) were divided in six groups of 6 animals per group. Group A and F served as control. Groups B, C, D and E received acrylamide at 20 mg/kg body weight for 28 days and groups C and E received additionally vitamin E (50 IU/kg body weight) for 1 to 28 days and 29 - 42(nd) days of experiment, respectively. The animals from groups A, B, and C were sacrificed on day 28(th) of experiment and from groups D, E, and F on 42(nd) day of experiment, respectively. There was significant decrease in the total sperm count and significant increase in the dead sperm count on day 28(th) of study due to acrylamide toxicity. At recovery period, there was significant increase in the total sperm count of vitamin-E-treated group of animals as compared to untreated toxicated rats. But, values were significantly lower than control animals. Microscopically, the lesions in the testes of acrylamide intoxicated rats at 28(th) day revealed destruction of seminiferous tubules at periphery. No spermatid and spermatocytes were seen in the seminiferous tubules. Detachment of spermatogonial cells started at periphery of seminiferous tubules. Atrophy of seminiferous tubules was a constant finding. Some tubules showed vacuolar degenerative changes in germinal epithelium. During the recovery period, destruction of seminiferous tubules, detachment of spermatogonial cells, and atrophy of seminiferous tubules were observed in group D and E. Few sections revealed only spermatogonial cells. At recovery period vitamin-E-treated rats revealed somewhat better architecture of the seminiferous tubules. Late spermatids were seen in few seminiferous tubules and other revealed starting of spermatogenesis. Thus, it appears that Vitamin E is not able to protect testes from acrylamide toxicity during active feeding, but after cessation of acrylamide feeding treatment with vitamin E revealed faster recovery as compare to not treated group.     

Cyclophosphamide treatment causes impairment of sperm and its fertilizing ability in mice

This study is focused on the toxicological effect of cyclophosphamide on male mice reproductive system. In the present study, cyclophosphamide was injected intraperitoneally (ip) at the level of 50-200mg/kg body weight into 6-weeks old ICR male mice once in a week for a period of 5 weeks. The animals were sacrificed after 1st and 5th week of last injection. Reduction in weight of testis and epididymis were observed both in 1st and 5th week group mice after administration with increasing concentration of cyclophosphamide. The weight of the body significantly decreased in both 1st and 5th week group in mice treated with 200mg/kg cyclophosphamide. The weight of the testis significantly decreased with all doses of cyclophosphamide in 1st week group, whereas, in 5th week group significant reduction was observed only in 200mg/kg dose of cyclophosphamide. The sperm motility was analyzed with Computer-Assisted Sperm Analysis (CASA). The motility of caudal sperm decreased with increasing concentration of cyclophosphamide in the 1st week group, whereas, it revived after 5th week. The total sperm counts in the epididymis of 1st week group mice declined significantly while significant restoration of the same was observed with mice treated with 50,100 and 150 mg/kg doses in the 5th week group. The intact acrosome was lower with 150 and 200mg/kg doses in both 1st and 5th week group. The live sperm was reduced to 29% in mice treated with 200mg/kg in the 5th week group. The decrease in the pregnancy rate of female mice was 17, 50, 58 and 100% when mated with male mice injected with 50, 100, 150 and 200mg/kg dose, respectively. Seminiferous tubules of mouse testis were severely damaged in the 1st week group. However, reinstate of sperm within the seminiferous tubules was observed in the 5th week group mice. Significant decrease in serum luteinizing hormone (LH) was observed in the 1st week group treated with 50, 100, 150 and 200mg/kg dose of cyclophosphamide. However, no significant difference was observed in the serum follicle-stimulating hormone (FSH), whereas, a decrease of about 98% in serum testosterone level was observed in cyclophosphamide treated mice. The decrease in the mean testosterone levels of cyclophosphamide treated mice served as proof for the damage of testis. These results demonstrate that cyclophosphamide caused temporary interference of normal male reproductive system with low dose treatment, but might be permanent dysfunction in high dose treatment.     

Perinatal exposure to low doses of tributyltin chloride reduces sperm count and quality in mice

Exposure to endocrine disruptors (EDs) during early development might lead to adverse health outcomes later in life. Tributyltin (TBT), a proven ED, is widely used in consumer goods and industrial products. Herein we demonstrate the effects of low doses of tributyltin chloride (TBTCl) on reproduction of male KM mice. Pregnant mice were administered by gavage with 0, 1, 10, or 100 μg TBTCl/kg body weight/day from day 6 of pregnancy through the period of lactation. TBTCl dramatically decreased sperm counts and motility on postnatal days (PNDs) 49 and 152. Meanwhile, a significant increase in sperm abnormality was observed in exposed mice on PND 49, but comparable to that in the control on PND 152. The histopathological analysis of testes of treated animals showed a dose‐dependent increase in sloughing of germ cells in seminiferous tubules. Mice treated with 10 μg TBTCl/kg exhibited decreased intratesticular 17β‐estradiol (E2) levels on PND 49, and then followed by an obvious recovery on PND 152. While, no significant differences in serum E2, testosterone (T) levels and intratesticular T levels were detectable between control and TBTCl‐exposed offspring at the sacrifice. These results suggest that perinatal TBTCl exposure is implicated in causing long lasting alterations in male reproductive system and these changes may persist far into adulthood. © 2013 Wiley Periodicals, Inc. Environ Toxicol 30: 44–52, 2015.     

Effects of subchronic ifosfamide-mesna treatment on testes and semen characteristics in the rabbit

Ifosfamide, a chemotherapeutic agent with a broad spectrum of antineoplastic activity, is concurrently administered with the uroprotectant mesna to avoid the urotoxic effect. This study was undertaken to investigate possible effects of ifosfamide-mesna treatment on the testes and semen characteristics in rabbits. Sexually mature New Zealand White male rabbits received intravenously 10 weekly treatments of ifosfamide+mesna (groups A, B and C received 30, 45 or 60 mg/kg of body weight ifosfamide+6, 9 or 12 mg/kg of body weight mesna, respectively, followed by a second equal dose of mesna 4 h later); groups MA, MB and MC received mesna alone at corresponding doses; and group S received normal saline. Reproductive organ weight as well as various qualitative and quantitative parameters of testis histology (minor diameter of seminiferous tubules, the most advanced germ cell type in seminiferous tubule identified in cross sections, and the number of germ cells per stage 1 seminiferous tubule cross section) were determined 1 day and 20 weeks after the treatment period, while semen quality (sperm count, sperm morphology and sperm progressive motility) and libido were evaluated on a weekly basis. Changes were noted only in the ifosfamide+mesna treated animals. One day after treatment, reproductive organ weights were decreased in groups A–C. Major histopathological lesions were not found; however, quantitative histological endpoints were altered in groups A–C. Transient oligospermia and teratozoospermia were noted in groups B and C, while asthenozoospermia was observed in group C only. The time course of these sperm alterations suggested possible bioaccumulation and residual activity of ifosfamide. Libido remained normal. The decrease in reproductive organ weights persisted in groups B and C to 20 weeks after treatment but only one quantitative histological endpoint, the number of the round spermatids per stage 1 seminiferous tubule cross section, remained decreased in group C. These results suggest that subchronic treatment with ifosfamide-mesna suppressed spermatogenesis and epididymal sperm maturation in the rabbit. Germinal epithelium recovery was not complete because although sperm characteristics returned to pretreatment values, not all histological alterations were ameliorated.     

Antispermatogenic and antifertility effects of 20,25-diazacholesterol dihydrochloride in mice

The effect of intraperitoneal administration for 28 days of 10, 20, and 30 mg/kg body weight per day of 20,25-diazacholesterol dihydrochloride (SC 12937), a hypocholesterolemic agent, on the testis of Parkes (P) strain mice was investigated. Histologically, testes in mice treated with 10 or 20 mg/kg body weight of SC 12937 showed non-uniform degenerative changes in the seminiferous tubules as both affected and normal tubules were observed in the same section; the affected tubules showed intraepithelial vacuolation, occurrence of giant cells, exfoliation of germ cells, and marginal condensation of chromatin in round spermatids. In both dosage groups, only 11-12% of the seminiferous tubules were affected, and no significant differences were found in the frequency of affected tubules between the two groups. By contrast, testes in mice treated with 30 mg/kg body weight of the drug exhibited a degenerated appearance of germ cells in all seminiferous tubules. The treatment also had adverse effects on motility, viability, morphology, and number of spermatozoa in the cauda epididymidis, and on fertility. Even 56 days after drug withdrawal, the above parameters remained markedly affected. Our results thus suggest that SC 12937 treatment causes antispermatogenic and antifertility effects in P mice and that the effects are not reversible up to 56 days after drug withdrawal. This compound may prove useful in the control of rodent populations.     

The influence of aluminum exposure on male reproduction and offspring in mice

The dominant lethal assay was utilized to assess the reproductive performance in male mice, possible genetic hazards, and persistent damage of aluminum (Al). Al chloride, AlCl(3), was administered subcutaneously to CD-1 adult male mice at dosages of 0, 7, or 13mg Al/kg body weight/day for 2 weeks of pre-mating periods. Females were not dosed at any time during this study. At the end of the exposure period, each male was caged with three virgin females each day. The mean mating frequencies of the Al-treated groups reduced consistently from week 4 to 6, and a dramatic reduction in male fertility was also observed. However, the mating frequency restored to near normal control levels as the experiment terminated. Results showed significantly higher numbers of post-implantation losses, foetal mortality, and induced petechial haemorrhage; also significant decreases in body weights of viable foetus throughout weeks 3-8 in the Al-treated groups. The weights of the reproductive organs of the Al-dosed animals decreased significantly as Al accumulation increased in the testes. The spermatogenetic impairment within the seminiferous tubules was also apparent. Nevertheless, these disturbances disappeared at the end of the experiments. In summary, the results demonstrated that Al exerted substantial hazards on male reproductive function and produced genetic toxicity. However, these effects were found to be reversible.     

Testicular toxicity in sodium fluoride treated rats: association with oxidative stress

This study examined the effect of sodium fluoride, a water pollutant important through the world, including India, on testicular steroidogenic and gametogenic activities in relation to testicular oxidative stress in rats. Sodium fluoride treatment at 20mg/kg/day for 29 days by oral gavage resulted in significant diminution in the relative wet weight of the testis, prostate, and seminal vesicle without alteration in the body weight gain. Testicular delta(5),3beta-hydroxysteroid dehydrogenase (HSD) and 17beta-HSD activities were decreased significantly along with significant diminution in plasma levels of testosterone in the fluoride-exposed group compared to the control. Epididymal sperm count was decreased significantly in the fluoride-treated group and qualitative examination of testicular sections revealed fewer mature luminal spermatozoa in comparison to the control. The seminiferous tubules were dilated in treated animals. Fluoride treatment was associated with oxidative stress as indicated by an increased level of conjugated dienes in the testis, epididymis, and epididymal sperm pellet with respect to control. Peroxidase and catalase activities in the sperm pellet were decreased significantly in comparison to the control. The results of this experiment indicate that fluoride at a dose encountered in drinking water in contaminated areas exerts an adverse effect on the male reproductive system and this effect is associated with indicators of oxidative stress.     

Induction of antifertility with lupeol acetate in male albino rats

The present study was undertaken to evaluate the antifertility activity of the active principle, i.e. lupeol acetate, isolated from benzene extract of Alstonia scholaris in male albino rats. The treatment with lupeol acetate at the dose level of 10 mg/rat/day did not cause any significant change in the body weights, but significant reduction in the weight of reproductive organs, i.e. testes, epididymides, seminal vesicle and ventral prostate, was observed. Testicular sperm count, epididymal sperm count and motility were found significantly declined when compared with controls, which resulted in reduction of male fertility by 100%. Arrest of spermatogenesis was noted at various stages with production of primary spermatocytes (preleptotene and pachytene), secondary spermatocytes and step-19 spermatids were decreased by 52.36, 54.91, 55.67 and 69.65%, respectively. The seminiferous tubules appeared reduced in size by 24.62%. Cross-sectional surface area of Sertoli cells as well as their counts were found to be significantly depleted. Leydig cell nuclear area and number of mature Leydig cells were decreased by 27.65 and 35.47%. Biochemical parameters of tissues i.e. protein, sialic acid, glycogen and cholesterol content of testes and seminal vesicular fructose also showed significant reduction.     

Reproductive effects of endosulfan on male offspring of rats exposed during pregnancy and lactation.

1. The reproductive effects of endosulfan on the male offspring of rats were examined. Dams were treated orally with 0, 1.5 or 3.0 mg endosulfan/kg from day 15 of pregnancy to postnatal day (PND) 21 of lactation. The male offspring rats were investigated at PND 65 or 140, corresponding to the pubertal and adulthood stage of development. 2. The dose of 3.0 mg endosulfan/kg induced a decrease in maternal body weight during pregnancy, but litter size and mean birth weight were not affected. Similarly, the age at testis descent and preputial separation was not affected on the male offspring. 3. The daily sperm production (x10(6)) was permanently decreased in the highest dose group when investigated at puberty and at adulthood. At the lowest dose, however, the daily sperm production was significantly reduced only at puberty. 4. Histologically, the percentage of seminiferous tubules showing complete spermatogenesis was significantly decreased at puberty. This finding may explain the decrease in daily sperm production observed in the endosulfan-exposed male rats. 5. The results of this study show that low doses of endosulfan have no apparent effect on developmental landmarks or on the weight of reproductive and accessory sex organ. Daily sperm production was the most susceptible endpoint in the male offspring exposed to endosulfan during pregnancy and lactation. To further understand the reproductive effects of endosulfan on male rat offspring, additional reproductive and toxicokinetic studies should be carried out to determine the extent of endosulfan exposure in male rat offspring in utero and during lactation.     

Effects of chlorpyrifos on reproductive toxicology of male rats

The aim of this study is to investigate the effects of subchronic exposure to chlorpyrifos on reproductive toxicology of male rats. Forty healthy male rats were divided into four groups: three exposure groups and a control group. Chlorpyrifos was administered orally to male rats at 0, 2.7, 5.4, and 12.8mg/kg for 90 days to evaluate the toxic alterations in testicular histology, testicular marker enzyme activities and related genes expression levels, sperm dynamics, and testosterone levels. The body weight and the testis weight of animals did not show any significant changes. Chlorpyrifos brought about marked reduction in testicular sperm counts, sperm motility, and significant growth of sperm malformation rate in exposed males. Histopathological examination of testes showed mild to severe degenerative changes in seminiferous tubules at various dose levels. The levels of testosterone (T) showed a decreasing tendency, and there was a statistical difference between the 5.4, 12.8 mg/kg groups, and the control group. The levels of follicle stimulating hormone (FSH) were significantly increased in 5.4 and 12.8 mg/kg groups, but there were no obvious effects on the levels of luteinizing hormone (LH) and estradiol (E₂). A significant increase in the activities of LDH and LDH‐x was observed in chlorpyrifos exposed rats in 5.4 and12.8 mg/kg groups, but the expression levels of related genes had no significant differences between chlorpyrifos exposure groups and the control group. These results suggest that chlorpyrifos has adverse effects on reproductive system of male rats. © 2013 Wiley Periodicals, Inc. Environ Toxicol 29: 1083–1088, 2014.     

Silver nanoparticles effects on epididymal sperm in rats

The motivation of our study was to examine the acute effects of intravenously administered a single bolus dose of silver nanoparticles (AgNPs) on rat spermatogenesis and seminiferous tubules morphology. In the treated rats compared to the vehicle treated control animals, the experiments revealed a size-dependent (20 nm and 200 nm), dose-dependent (5 and 10 mg/kg body mass) and time-dependent (24 h, 7 and 28 days) decrease the epididymal sperm count measured by histological methods. In parallel AgNPs injection increased the level of DNA damage in germ cells, as measured by alkaline comet assay. Histological examination of the testes showed change in the testes seminiferous tubule morphometry in 200 nm Ag NPs treated rats. No change of body weight, adipose tissue distribution and the frequency of abnormal spermatozoa was observed. Twenty nanometers AgNP appeared to be more toxic than 200 nm ones.     

Testicular effects of acrylonitrile in mice

Daily oral administration of acrylonitrile (10 mg/kg body weight) to mice for a period of 60 days caused a significant decrease in the activity of testicular sorbitol dehydrogenase and acid phosphatase, and an increase in that of lactate dehydrogenase and beta-glucuronidase. Histopathological studies revealed degeneration of the seminiferous tubules. A decrease in the sperm counts of the epididymal spermatozoa was also observed in the animals of the acrylonitrile-exposed group. These observations suggest that acrylonitrile may affect the male reproductive function by causing testicular injury.     

Distribution of microcystin-LR to testis of male Sprague–Dawley rats

Microcystins (MCs) are a group of cyclic heptapeptide toxins produced by naturally freshwater cyanobacteria. Among more than 90 identified analogues of microcystins, microcystin-LR (MC-LR) is the most abundant and toxic. Our previous investigations indicated that MC-LR displays male reproductive toxicity, but the target of MC-LR in testes remains unclear. To this end, the present study is designed to elucidate whether microcystin-LR could be distributed to testes and explore the target cells in testes. In the in vivo study, male Sprague–Dawley rats were injected intraperitoneally with MC-LR at a dose of 300 μg/kg per day for 6 days. MC-LR was detected in testes, mainly within seminiferous tubules, which was further validated by Western blot. The concentrations of MC-LR were determined by LC–MS analysis, with a result of 0.0252 ± 0.0037 and 0.0056 ± 0.0012 μg/g dry weight in liver and testis respectively. In the in vitro study, Primary cultured spermatogonia, Sertoli cells and Leydig cells were exposed to MC-LR respectively, and MC-LR was observed to enter spermatogonia and Sertoli cells, but not Leydig cells. These results suggested that the reproductive toxicity of MC-LR were induced by its distribution in testis. Spermatogonia and Sertoli cells are important target cells.     

Propolis protection from reproductive toxicity caused by aluminium chloride in male rats

Different forms of aluminium (Al) are environmental xenobiotics that induce free radical-mediated cytotoxicity and reproductive toxicity. Propolis has been reported to be important antioxidant. Therefore, this study aimed at elucidating the protective effects of propolis against reproductive toxicity of aluminium chloride (AlCl₃) in male rats. The first group served as control. Group 2 received 34 mg AlCl₃/kg bw (1/25 LD₅₀). Group 3 was administered 50 mg propolis/kg bw/day. Group 4 was treated with AlCl₃ plus propolis. Treatment was continued for 70 days. AlCl₃ caused a decrease in testes, seminal vesicle and epididymis weights, sperm concentration, motility, testosterone level and the activities of 17-ketosteroid reductase, CAT and GST, and GSH content. While, dead and abnormal sperm and testes TBARS concentrations were increased. In the AlCl₃-treated group, histopathologic examinations revealed apparent alterations in the testes, where it induced marked lesions in seminiferous tubules. Propolis alone decreased dead and abnormal sperm and TBARS, and increased testosterone, GSH, 17-ketosteroid reductase, CAT and GST. Results showed that propolis antagonized the harmful effects of AlCl₃. This was proved histopathologically by the great improvement in testes. In conclusion propolis could be effective in the protection against the reproductive toxicity of AlCl₃.     

Reproductive toxicity of 1-bromopropane, a newly introduced alternative to ozone layer depleting solvents, in male rats.

1-Bromopropane has been newly introduced as an alternative to ozone-depleting solvents. We aimed to clarify its dose-dependent reproductive toxicity in male rats. Thirty-six Wistar male rats were randomly divided into 4 groups of 9. The groups were exposed to 200, 400, or 800 ppm 1-bromopropane or only fresh air, 8 h per day for 12 weeks. Epididymal sperm indices were evaluated after a 12-week exposure. The testes, epididymides, seminal vesicle, prostate, and other organs were weighed and examined histopathologically. Spermatogenic cells, in stage VII seminiferous tubules, and retained spermatids, at the basal region of stages IX-XI seminiferous epithelium, were counted. Plasma testosterone levels were measured by radioimmunoassay. The testicular weight did not significantly change, but the weight of epididymides, seminal vesicle, and prostate dose-dependently decreased. The weight of seminal vesicle decreased significantly at the lowest concentration of 200-ppm and over. 1-Bromopropane induced a dose-dependent decrease in the epididymal sperm count and in motility, as well as an increase in tailless sperm and sperm with an immature head shape. The spermatogonia, preleptotene spermatocytes, pachytene spermatocytes, and round spermatids did not decrease significantly at stage VII. Retained, elongated spermatids near the basement membrane at the postspermiation stages IX-XI increased dose-dependently. Plasma testosterone levels significantly decreased at the 800-ppm dosage. 1-Bromopropane caused failure of spermiation. Its reproductive toxicity is different from that of 2-bromopropane, which specifically impairs spermatogonia. Thus, this solvent may have serious reproductive toxic effects in men, and should be used very cautiously in the workplace.     

Testicular toxicity of Nigerian bonny light crude oil in male albino rats

The purpose of this work was to investigate the testicular effects of Nigerian bonny light crude oil on male albino rats. Male albino rats were administered 200, 400, and 800 mg/kg body weight of bonny light crude oil dissolved in Tween 80 in their drinking water for 7 days, while the control group received Tween 80 in their drinking water only. After 7 days, the rats were sacrificed and testis excised, weighed, and processed for histological examination. Treatment with bonny light crude oil showed a dose-dependent decrease in the absolute weight of the testes, and a significant (P < 0.05) dose-dependent reduction in the epididymal sperm number (ESN). The final body weights of the animals treated with crude oil were also significantly (P < 0.05) decreased. Histological evaluation of the testes showed slight to severe degeneration or even complete absence of seminiferous tubules and necrosis of cells depending on the dose of the crude oil. This study suggests that the Nigerian bonny light crude oil is a testicular toxicant and its use as a folklore medicine may cause infertility.     

Expression of calmodulin in germ cells is associated with fenvalerate-induced male reproductive toxicity

Exposure to fenvalerate was demonstrated to be toxic to the male reproductive system. Our previous data revealed that intracellular calcium plays an important role in regulating the above toxicity, through actions on both T-type calcium channels and endoplasmic reticulum calcium signals. The present study explored the effects of fenvalerate on the expression of calmodulin in mouse testis and GC-2spd(ts) cells, and its association with fenvalerate-induced male reproductive toxicity. Male mice were subjected to different doses (3.71, 18.56, 37.12, 92.81?mg/kg bw) of fenvalerate or vehicle control for 4?weeks. Expression of calmodulin was determined by real-time polymerase chain reaction (PCR) and Western blot analysis in mouse testis. Similar approaches were utilized in GC-2spd(ts) cells cultured with 5?μM fenvalerate at different time points. In the in vivo study, all mice survived through the entire 4?weeks. Administration of fenvalerate resulted in a dose-dependent reduction in testis weight/body weight, sperm motility, and increased head abnormality rate. By histological staining, mice treated with fenvalerate at higher doses showed dilated seminiferous tubules and disturbed arrangement of spermatogenic cells. Meanwhile, both mRNA and protein expression of calmodulin were significantly increased in the testes of mice exposed to fenvalerate compared to control mice. Moreover, in the in vitro study, 5?μM fenvalerate significantly increased the expression of calmodulin at the mRNA and protein levels in GC-2spd(ts) cells after 8?h of incubation and sustained these levels for at least 24?h. Collectively, these data suggested that enhanced expression of calmodulin correlates with male reproductive damage induced by fenvalerate.