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Benha Medical Journal. 2001; 18 (2): 225-244
en Inglés | IMEMR | ID: emr-56408

RESUMEN

The impact of cigarette smoke on fertility of females has been amply documented, but there has been no attention paid to the possible impact of prepubertal exposure to cigarette smoking on female reproductive capacity. Beginning on the day 15 postnatal life, twenty female albino rats were exposed passively to cigarette smoke [0.5 mg/kg body wt. daily for 30 min] in a special container allowing good areation [cigarette smoke-exposed group]. Under similar conditions, twenty female rats were exposed to room air only [Sham-exposed group]. All rats were weighed every two days till the day of puberty; detected by the vaginal membrane rupture. Also, blood samples were collected on the day 35 postnatal life and on the day of puberty for assay of gonadotropins, prolactin and ovarian hormones which are related to sexual maturation as well as ovarian and uterine functions. On the day of puberty, the uteri and ovaries were weighed. Also, the number of ova were counted. In addition, tissue bath experiments were done to assess the effect of pre-pubertal exposure to cigarette smoke on the contractile response of uterine horns of nonpregnant mature female rats to oxytocin or 5 HT [10.90 ng/ml, 10-90 nM respectively]. In rats exposed to cigarette smoke, as compared to shame-exposed rats, it was found: [1] a significant delayed puberty associated with a significant growth retardation, [2] a significant hyperprolactinemia associated with a significant decline in gonadotropins and ovarian hormones at prepubertal and at the day of ovulation, and [3] a significant increase in the strength of spontaneous uterine contractions, prolonged the duration of their cycles and declined their frequency. The stimulatory effects of both spasmogens [oxytocin or SHT] were potentiated and prolonged. It is suggested that: [1] the neurotransmitter systems may be involved in the mechanisms of the sexual maturation, and [2] The mechanism attributed to cigarette smoked - changes in uterine contractility could be due to phosphatidyl inositol signaling


Asunto(s)
Femenino , Animales de Laboratorio , Maduración Sexual , Ratas , Reproducción , Exposición a Riesgos Ambientales , Hormonas Esteroides Gonadales , Hormona Folículo Estimulante/sangre , Hormona Luteinizante/sangre , Prolactina/sangre , Estrógenos/sangre , Progesterona/sangre
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