Nitric oxide synthase inhibition ameliorates nicotine-induced sperm function decline in male rats
Autor: | Adeyombo F. Bolarinwa, IP Oyeyipo, Yinusa Raji |
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Rok vydání: | 2015 |
Předmět: |
Infertility
Nicotine medicine.medical_specialty Inhibitor medicine.medical_treatment media_common.quotation_subject lcsh:Medicine Fertility Plant Science Nitric oxide chemistry.chemical_compound Internal medicine medicine Saline media_common General Veterinary biology business.industry lcsh:R Obstetrics and Gynecology medicine.disease Sperm Rats Nitric oxide synthase Endocrinology Reproductive Medicine chemistry biology.protein Animal Science and Zoology business Hormone medicine.drug |
Zdroj: | Asian Pacific Journal of Reproduction, Vol 4, Iss 3, Pp 212-216 (2015) |
ISSN: | 2305-0500 |
DOI: | 10.1016/j.apjr.2015.06.004 |
Popis: | Objectives To evaluate the effects of inhibiting nitric oxide synthase as a means of intervention in nicotine-induced infertility in male rats. Methods Forty-eight male and thirty female Wistar rats (180–200 g) were randomly assigned to six groups and treated orally for 30 days with saline (control), nicotine (0.5 mg/kg, 1.0 mg/kg) with or without NG Nitro- l -Arginine Methyl Ester ( l -NAME, 50 mg/kg). Treated male rats were cohabited with untreated females in ratio 1:2 for fertility studies. Sperm analysis was done by microscopy. Results There was a significant decrease in the epididymal sperm motility and count after nicotine treatment. However, the percentage of abnormality significantly increased in nicotine treatment groups. Fertility studies revealed that nicotine reduced libido in male rats and decreased litter weight and number delivered by the untreated female during the experiments. Co-treatment with l -NAME effectively reversed the nicotine-mediated alterations in the sperm functional parameters, fertility indexes and hormone when compared to nicotine only. Conclusion Taken together, the present data indicate the abilities of l -NAME to ameliorate nicotine-induced spermatotoxic effects in male rats via a mechanism dependent on the circulating testosterone level. |
Databáze: | OpenAIRE |
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