Effect of Nicotine on the Proestrous Ovulatory Surge of LH in the Rat1

Blake, Charles A.; Scaramuzzi, R. J.; Norman, Reid L.; Kanematsu, Shigeto; Sawyer, Charles H.

doi:10.1210/endo-91-5-1253

Cited by 37 publications

(17 citation statements)

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“…This finding is the same as those in previous reports showing that a single nicotine iv or sc injection does not totally abolish the LH and PRL surge but causes an acute reduction in both LH and PRL concentrations after the injecton [1][2][3][4]. Taking the present finding that icy nicotine injection did not cause any changes in the surge secretion of these hormones, all of these studies seem to suggest that nicotine injected systemically causes the effects by acting on certain sites(s) other than the central nervous system, in other words the site of action of nicotine is not on the GnRH surge generator, which is presumably in the preoptic area.…”

Section: Discussionsupporting

confidence: 92%

“…IT WAS early found that, in female rats, nicotine injected subcutaneously (sc), i.e., systemically, delayed the preovulatory surge of both LH and PRL secretion on the day of proestrus [1][2][3][4], although tobacco smoke delayed only the LH surge [5]. The LH surge advanced by progesterone injection in the morning of proestrus was also inhibited by nicotine injected intraperitonearly (ip) [6].…”

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confidence: 99%

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Nicotine Given Intracerebroventricularly Does Not Inhibit the Preovulatory Surge of LH and PRL Secretion in Female Rats.

et al. 1998

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Abstract. To determine the effect of nicotine on LH and PRL secretion, nicotine bitartrate (nicotine) dissolved in saline was administered at 1400 h, just before the critical period for the preovulatory surge of LH and PRL secretion, either intracerebroventricularly (icy) or intravenously (iv) in female rats in proestrus.Nicotine neither at a dose of 5 µg nor at a dose of 10 µg injected icy at 1400 h caused significant changes in the surge of LH and PRL secretion. When nicotine was given iv at a dose of 100 µg, a significant decrease in LH and PRL concentrations occurred immediately, lasting for 2 h. After 1700 h, LH and PRL concentrations as high as that observed after 1700 h in saline-injected control rats were recovered, just as if nicotine caused a transient deficit of the surge secretion of these hormones. The results indicate that nicotine does not inhibit the preovulatory surge of LH and PRL secretion by acting at the hypothalamic level accessible via the third ventricle, but inhibits it by acting at certain other site(s).

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Section: Discussionsupporting

confidence: 92%

mentioning

confidence: 99%

Nicotine Given Intracerebroventricularly Does Not Inhibit the Preovulatory Surge of LH and PRL Secretion in Female Rats.

et al. 1998

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“…Nicotine has been reported to inhibit the release of GH, an hormone of the anterior pituitary gland ( (Morgan et al, 2004). Other studies have shown that subcutaneous injection of nicotine on the day of proestrous delay the usual surge of LH and also decrease the peak level when compared with the control (Blake et al, 1972).…”

Section: Pituitarymentioning

confidence: 99%

Effect Of Nicotine Administration On Weight And Histology Of Some Vital Visceral Organs In Female Albino Rats

Iranloye¹,

Bolarinwa²

2009

Nig. J. Phys Sci

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Summary: It has been emphasized that cigarette smoking is not always synonymous with nicotine administration but the toxic effect of cigarette has often been associated with the nicotine content in cigarette. Epidemiologic studies have clearly indicated that cigarette smoking have many deleterious effects on visceral tissues in women. However it is not certain whether this effect is produced entirely by nicotine as cigarettes contain other toxic substances. Using an animal model the direct effect of nicotine administration on viscera tissues in female albino rats was investigated. Twenty-four female rats with regular oestrous cycle in the same phase of the cycle were divided into two equal groups with each group receiving 0.5mg/kg nicotine and 0.9% normal saline S.C. daily respectively. Six rats from each group were killed by cervical dissociation after 30 and 60 days treatment. The ovary, uterus, brain, kidney, heart, adrenal, pituitary and the liver were removed weighed and histological study carried out. Weights of the ovary, kidney, pituitary and uterus were significantly reduced (P< 0.05) following nicotine treatment while weights of the heart and liver increased with 60days treatment with the appearance of cartilaginous cells in the heart and deposition of adipose around the portal vein in the liver. Necrosis, congestion, fibrosis, follicular and endometrial degeneration were observed in the brain, pituitary, kidney, ovary and uterus respectively. No significant difference between the weekly growth rates in nicotine treated (5.13 ± .29) and control (5.25 ± 0.18) animals. Nicotine has deleterious effects on some vital visceral organs with observations similar to those reported in women smokers.

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“…From the study of laboratory animals, nicotine affects normal functioning of accessory reproductive organs in male albino rats (Patil et al 1999). Although nicotine's mechanism of action is not clearly understood, it inhibits the release of pituitary follicle-stimulating hormone and luteinizing hormone through its action on the hypothalamohypophyseal axis (Blake et al 1972, Blake 1974, 1978.…”

Section: Introductionmentioning

confidence: 99%

Folding, activity and import of steroidogenic acute regulatory protein into mitochondria changed by nicotine exposure

Bose¹,

Debnath²,

Chen³

et al. 2007

Journal of Molecular Endocrinology

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Nicotine, a pharmacologically active constituent of tobacco smoke, decreases sex steroid production and impairs reproductive function. The rate-limiting step in steroid hormone biosynthesis is the transport of substrate cholesterol from the outer to inner mitochondrial membrane by the steroidogenic acute regulatory protein (StAR). StAR is a 37 kDa cytoplasmic phosphoprotein processed as a 32 kDa intermediate to a mature 30 kDa inactive mitochondrial protein.StAR's cholesterol transport capacity is proportional to its residency time at the outer mitochondrial membrane (OMM). Nonsteroidogenic COS-1 cells transfected with StAR/F2, steroidogenic MA-10 cells induced with cAMP or transfected with StAR or the isolated steroidogenic mitochondria preincubated with nicotine reduced StAR expression, import and activity. Mitochondria isolated from steroidogenic tissues or cells, pretreated with nicotine, also reduced the association of StAR with the OMM, but had no effect on the import of signal sequence substituted SCC/N-62StAR. The fluorescence emission maximum of StAR was unchanged with nicotine, but StAR's free energy of unfolding and the surface area (m) increased in the presence of nicotine. Nicotine also blocked StAR from proteolysis with trypsin, suggesting that nicotine partially stabilised protein conformation by insertion into the molten globule conformation of StAR.

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Effect of Nicotine on the Proestrous Ovulatory Surge of LH in the Rat1

Cited by 37 publications

References 0 publications

Nicotine Given Intracerebroventricularly Does Not Inhibit the Preovulatory Surge of LH and PRL Secretion in Female Rats.

Nicotine Given Intracerebroventricularly Does Not Inhibit the Preovulatory Surge of LH and PRL Secretion in Female Rats.

Effect Of Nicotine Administration On Weight And Histology Of Some Vital Visceral Organs In Female Albino Rats

Folding, activity and import of steroidogenic acute regulatory protein into mitochondria changed by nicotine exposure

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