Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

These studies examined the cellular mechanisms for lower adiposity seen with nicotine ingestion. Rats were infused with nicotine or saline for 1 wk and adipocytes isolated from epididymal fat pads. Nicotine-infused rats gained 37% less weight and had 21% smaller fat pads. Basal lipolysis was 78% higher, whereas the maximal lipolytic response to isoproterenol was blunted in adipocytes from nicotine-infused rats. The antilipolytic actions of adenosine and the levels of serum catecholamines were unaffected by nicotine. The nicotine-induced alteration in lipolysis was not associated with any changes in hormone-sensitive lipase. Nicotine caused a 30% decrease in lipoprotein lipase (LPL) activity, without any changes in LPL mass or mRNA levels, in epididymal fat in the fed state. In contrast, LPL activity, mass, and mRNA levels in heart were increased by nicotine whether animals were fed or fasted. These studies provide evidence for multiple mechanistic events underlying nicotine-induced alterations in weight and suggest that nicotine diverts fat storage away from adipose tissue and toward utilization by muscle.
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PMID:Alterations of lipolysis and lipoprotein lipase in chronically nicotine-treated rats. 877 41

We evaluated the effects of smoking on testicular function and fertilizing potential in rats. Twenty rats (group A) were exposed to the smoke of 20 cigarettes for 1 h per day. Ten rats (group B) were exposed to the smoke of 40 incense sticks for 1 h per day, and an additional 10 rats served as a control group (group C). After 10 weeks of daily exposure, serum levels of nicotine and cotinine were assessed, and a mating test was conducted. Five days later, serum concentrations of testosterone before and after human chorionic gonadotropin (hCG) stimulation, gonadotropins, and epididymal sperm content and motility were evaluated. In addition, in vitro fertilization was carried out. Nicotine and cotinine were detected in group A, but not in groups B and C. Basal serum testosterone and gonadotropin concentrations did not differ significantly among the three groups, but the testosterone response to hCG stimulation was significantly lower in group A than in groups B and C. Group A showed significant reductions in epididymal sperm content and motility, and in fertility in vivo and in vitro. These findings suggest that smoking leads to a secretory dysfunction of the Leydig cells, and also a deficiency in sperm maturation and spermatogenesis. In addition, smoking has a detrimental effect on sperm fertilizing potentials in vivo and in vitro.
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PMID:Effects of smoking on testicular function and fertilizing potential in rats. 953 96

Adult male albino rats were treated with 0.4 mg nicotine/100 g body weight either orally or intraperitoneally for 30 days. All animals were autopsied on the 31st day. Epididymis and vas deferens were dissected out, weighed and processed for biochemical estimations. Nicotine caused a reduction in the weight of epididymis and vas deferens in both drug treated groups. The total cholesterol content is increased while protein, DNA and RNA contents and the epididymal sperm count were decreased. The acid phosphatase content is also decreased, whereas alkaline phosphatase is increased. The surface epithelial cell height of these ducts is decreased and secretory activity is reduced with the disruption of epithelial cell projections. These changes may be due to non-availability of androgens in nicotine treated rats.
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PMID:Nicotine induced inhibition of the activities of accessory reproductive ducts in male rats. 961 35

The objective of this study was to determine the effect of in utero and lactational exposure to nicotine on the male reproductive tract. Dams were randomly assigned to receive saline or nicotine bitartrate (1mg/kg-d s.c.) daily for two weeks prior to mating until weaning (postnatal day 21). Male offspring were sacrificed at 7 (peri-pubertal) and 26 (adult) weeks of age. Nicotine-exposure resulted in retention of spermatids after stage VIII, tubular vacuolation, degeneration of pachytene and round spermatids at stage VII in the testes; and lymphocyte infiltration, germ cell exfoliation, and hypospermia in epididymides, at 7 weeks of age. Nicotine-exposure had no effect on testis or epididymal morphology, daily sperm production, epididymal sperm reserve, sperm viability at 26 weeks of age, and circulating testosterone levels at either age examined. We conclude that maternal nicotine-exposure during pregnancy and lactation can induce transient structural changes in the testis and epididymis of male offspring.
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PMID:Effect of in utero and lactational nicotine exposure on the male reproductive tract in peripubertal and adult rats. 2118 33

Many studies have revealed the hazardous effects of cigarette smoking and nicotine exposure on male fertility, but the actual, underlying molecular mechanism remains relatively unclear. To evaluate the detrimental effects of nicotine exposure on the sperm maturation process, two-dimensional gel electrophoresis and mass spectrometry analyses were performed to screen and identify differentially expressed proteins from the epididymal tissue of mice exposed to nicotine. Data mining analysis indicated that 15 identified proteins were mainly involved in the molecular transportation process and the polyol pathway, indicating impaired epididymal secretory functions. Experiments in vitro confirmed that nicotine inhibited tyrosine phosphorylation levels in capacitated spermatozoa via the downregulated seminal fructose concentration. Sord, a key gene encoding sorbitol dehydrogenase, was further investigated to reveal that nicotine induced hyper-methylation of the promoter region of this gene. Nicotine-induced reduced expression of Sord could be involved in impaired secretory functions of the epididymis and thus prevent the sperm from undergoing proper maturation and capacitation, although further experiments are needed to confirm this hypothesis.
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PMID:Protein profile screening: reduced expression of Sord in the mouse epididymis induced by nicotine inhibits tyrosine phosphorylation level in capacitated spermatozoa. 2664 19

Nicotine is a pharmacologically active component of the tobacco that adversely affects the male reproductive system and fertility. Nicotine administration in experimental animals was found to affect spermatogenesis, epididymal sperm count, motility and the fertilizing potential of sperms. The goal of this work is to assess the protective or ameliorative effect of Eruca Sativa seed oil against testicular damage induced by oral administration of nicotine in rats. Male adult Sprague-Dawley rats were used and divided into three groups; control, nicotine treated and nicotine and Eruca seed oil treated groups. After three weeks of treatment, the rats were weighed and sacrificed where testes were removed and weighed then calculating relative testis weights. The testes were processed for routine paraffin embedding and staining and the sections were examined for different morphometric and histopathological changes. The results show that nicotine administration had an effect on the body and testis weight and various morphometric parameters of the testis. It also induced varying degrees of structural damage to the seminiferous tubules, with shrinkage and absence of mature spermatids. Disorganized, vacuolization and loss of germinal cells were noticed in the basement membrane. The co-administration of Eruca Sativa seed oil led to improvement in the morphometric and histopathological changes of the seminiferous tubules. In conclusion, Eruca Sativa seed oil treatment in this study had a protective role by reversing, almost completely, all morphometric and histological changes in the testis induced by nicotine administration.
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PMID:Protective effect of Eruca sativa seed oil against oral nicotine induced testicular damage in rats. 2728 44

Nicotine (NIC) adversely influences male reproductive system. Achillea millefolium (Achm) as a medicinal plant is highly regarded for its antioxidant and anti-inflammatory properties. The present study was conducted to assess whether Achm inflorescences alcoholic extract could serve as a protective agent against reproductive toxicity in NIC-exposed male rats. Adult male rats were randomly divided into six groups. Two groups received NIC at doses of 0.20 and 0.40 mg kg-1 per day in 0.50 mL sterile distilled water for 48 days intraperitoneally, respectively. The further two groups received NIC at doses of 0.20 and 0.40 mg kg-1 per day in 0.50 mL sterile distilled water for intraperitoneally along with Achm extract at a dose of 1.20 g kg-1 per day in 1 mL sterile distilled water orally for 48 days, respectively. A vehicle treated control group and an Achm-only treated group were also included. The NIC-exposed groups showed significant reductions in epididymal sperm count, motility, viability and serum levels of FSH, LH and testosterone as well as testicular antioxidant capacity. Moreover, the incidence of apoptosis and abnormality in spermatozoa along with testicular malondialdehyde and total nitrite levels were significantly higher in NIC-treated rats. The above-mentioned parameters were restored to near normal levels by Achm co-administration. These findings indicated that Achm may partially be protective against NIC-induced testicular toxicity.
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PMID:Ameliorative effects of Achillea millefolium inflorescences alcoholic extract on nicotine-induced reproductive toxicity in male rat: Apoptotic and biochemical evidences. 2878 83