Cadmium chloride–induced testicular toxicity in male wistar rats; prophylactic effect of quercetin, and assessment of testicular recovery following cadmium chloride withdrawal

Nna, Victor Udo; Ujah, Godwin Adakole; Mohamed, Mahaneem; Etim, Kingsley Bassey; Igba, Benedict O.; Augustine, Ele R.; Osim, E. E.

doi:10.1016/j.biopha.2017.07.087

Cited by 94 publications

(58 citation statements)

References 46 publications

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“…Its efficacy is due to its antioxidant potential which plays a major protective role against oxidative stress and prevents the production of lipid peroxides which are toxic by‐products of many metabolic processes in biological membranes. Vitamin E is known to inhibit the xanthine oxidase enzyme system which is known to produce large amounts of ROS (Koizumi & Li, ; Nna et al., ). By inhibiting this enzyme system, vitamin E reduces the amount of ROS, hence reducing oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Vitamin E attenuates nicotine- and noise-induced reproductive impairment in male albino Wistar rats

et al. 2018

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Previous studies showed that exposure to stress or nicotine induced reproductive impairment in male rats. Here, we assessed the effect of an antioxidant (vitamin E) on nicotine-, stress- and nicotine + stress-induced reproductive impairment in male rats. Forty-eight male albino Wistar rats were divided into eight groups as follows; control, stress (generator noise 90-120 dB, 8 hr/day), nicotine (1.5 mg kg day ), nicotine + stress, vitamin E (100 mg kg day ), stress + vitamin E, nicotine + vitamin E and stress + nicotine + vitamin E. Sperm count, viability, motility and rapid progressive forward movement decreased significantly (p < 0.05), while percentage of nonmotile spermatozoa increased significantly (p < 0.05) in stress, nicotine and nicotine + stress groups, compared with control. Serum testosterone and follicle-stimulating hormone decreased significantly (p < 0.05) in stress, nicotine and nicotine + stress groups, compared with control. Serum luteinising hormone decreased (p < 0.05) significantly in stress and nicotine + stress groups, compared with the control. Histology of the testes showed loss of germ cells in numerous seminiferous tubules, and epididymal histology showed decreased sperm density in stress, nicotine and nicotine + stress groups compared with the control. These negative changes were more severe in the nicotine + stress group. Vitamin E ameliorated the negative changes in the above parameters. This may be attributable to its antioxidant property.

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Section: Discussionmentioning

confidence: 99%

Vitamin E attenuates nicotine- and noise-induced reproductive impairment in male albino Wistar rats

et al. 2018

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“…Epididymal epithelial thickness was measured using image analyzer. For Leydig cell count, the number of Leydig cells in 20 random intertubular areas (area enclosed by three seminiferous tubules) was counted using 40x objective (Mohamed et al ., 2011b; Nna et al ., 2017b). The mean Johnsen testicular biopsy score (MJTBS) was determined in 10 randomly selected seminiferous tubules using the method shown in Table , as reported earlier (Nna et al ., 2017b).…”

Section: Methodsmentioning

confidence: 99%

Down‐regulation of steroidogenesis‐related genes and its accompanying fertility decline in streptozotocin‐induced diabetic male rats: ameliorative effect of metformin

et al. 2018

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Background: Metformin has long been used for glycemic control in diabetic state. Recently, other benefits of metformin beyond blood glucose regulation have emerged. Objectives: To investigate the effect of metformin on the expression of testicular steroidogenesis-related genes, spermatogenesis, and fertility of male diabetic rats. Materials and methods: Eighteen adult male Sprague Dawley rats were divided into three groups, namely normal control (NC), diabetic control (DC), and metformin-treated (300 mg/kg body weight/day) diabetic rats (D+Met). Diabetes was induced using a single intraperitoneal injection of streptozotocin (60 mg/kg b.w.), followed by oral treatment with metformin for four weeks. Results: Diabetes decreased serum and intratesticular testosterone levels and increased serum but not intratesticular levels of luteinizing hormone. Sperm count, motility, viability, and normal morphology were decreased, while sperm nuclear DNA fragmentation was increased in DC group, relative to NC group. Testicular mRNA levels of androgen receptor, luteinizing hormone receptor, cytochrome P450 enzyme (CYP11A1), steroidogenic acute regulatory (StAR) protein, 3b-hydroxysteroid dehydrogenase (HSD), and 17b-HSD, as well as the level of StAR protein and activities of CYP11A1, 3b-HSD, and 17b-HSD, were decreased in DC group. Similarly, decreased activities of epididymal antioxidant enzymes and increased lipid peroxidation were observed in DC group. Consequently, decreased litter size, fetal weight, mating and fertility indices, and increased pre-and post-implantation losses were recorded in DC group. Following intervention with metformin, we observed increases in serum and intratesticular testosterone levels, Leydig cell count, improved sperm parameters, and decreased sperm nuclear DNA fragmentation. Furthermore, mRNA levels and activities of steroidogenesis-related enzymes were increased, with improved fertility outcome. Discussion and conclusion: Diabetes mellitus is associated with dysregulation of steroidogenesis, abnormal spermatogenesis, and fertility decline. Controlling hyperglycemia is therefore crucial in preserving male reproductive function. Metformin not only regulates blood glucose level, but also preserves male fertility in diabetic state. Research has shown that DM impairs several aspects of the male reproductive function (Nna et al., 2017a). Decreased daily sperm production, sperm count, motility and viability, increased 110

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“…Rats exposed to a single dose of (0.67-1.1 mg/kg) of Cd for 7 days show disorganization of the seminiferous epithelium (Cupertino et al, 2017). After 28 days of oral administration of Cd (5 mg/kg) for 28 days, rat's sperm count, motility, and viability decline (Nna et al, 2017). When rats are exposed to Cd (0.2 mg/kg, sc) for 15 days, the seminiferous tubules of their testes are disarranged, the number of germ cells decreases (Jahan et al, 2014).…”

Section: Effect Of CD On Sperm Developmentmentioning

confidence: 99%

Toxicological Effects of Cadmium on Mammalian Testis

Zhu

2020

Front. Genet.

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Cadmium is a heavy metal, and people are exposed to it through contaminated foods and smoking. In humans and other mammals, cadmium causes damage to male testis. In this review, we summarize the effects of cadmium on the development and function of the testis. Cadmium causes severe structural damage to the seminiferous tubules, Sertoli cells, and blood-testis barrier, thus leading to the loss of sperm. Cadmium hinders Leydig cell development, inhibits Leydig cell function, and induces Leydig cell tumors. Cadmium also disrupts the vascular system of the testis. Cadmium is a reactive oxygen species inducer and possibly induces DNA damage, thus epigenetically regulating somatic cell and germ cell function, leading to male subfertility/infertility.

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Cadmium chloride–induced testicular toxicity in male wistar rats; prophylactic effect of quercetin, and assessment of testicular recovery following cadmium chloride withdrawal

Cited by 94 publications

References 46 publications

Vitamin E attenuates nicotine- and noise-induced reproductive impairment in male albino Wistar rats

Vitamin E attenuates nicotine- and noise-induced reproductive impairment in male albino Wistar rats

Down‐regulation of steroidogenesis‐related genes and its accompanying fertility decline in streptozotocin‐induced diabetic male rats: ameliorative effect of metformin

Toxicological Effects of Cadmium on Mammalian Testis

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