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Cited by 67Sperm and Testicular FunctionSmoking Behavior and CessationHypothalamic control of reproductive hormones

Nicotine alters male reproductive hormones in male albino rats: The role of cessation

Open access
Oyeyipo, IbukunP, Raji, Yinusa, Bolarinwa, AdeyomboF·2013·Journal of Human Reproductive Sciences
DOI 10.4103/0974-1208.112380PMC PMC3713576
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Abstract

OBJECTIVES: The use of nicotine through smoking remains a serious health problem. It has been associated with reduced fertility, although the mechanism responsible is still unclear. The present study was designed to investigate whether nicotine-induced infertility is associated with altered male reproductive hormones in male albino rats. MATERIALS AND METHODS: Forty male rats were divided equally into five groups and treated orally for thirty days. Group I, which served as the control received 0.2 ml/kg normal saline, Group II and III received 0.5 mg/kg (low dose) and 1.0 mg/kg (high dose) body weight of nicotine, respectively. The fourth and fifth groups were gavaged with 0.5 mg/kg and 1.0 mg/kg body weight of nicotine but were left untreated for another 30 days. These groups served as the recovery groups. Serum was analyzed for testosterone, luteinizing hormone (LH), follicle stimulating hormones (FSH), and prolactin using radioimmunoassay. RESULTS: Results showed that nicotine administration significantly decreased (P < 0.05) testosterone in the low and high treated groups and FSH in the high dose treated group when compared with the control group. There was a significant increase (P < 0.05) in mean LH and prolactin level in the high dose treated group when compared with the control. However, the values of the recovery groups were comparable with the control. CONCLUSION: The findings in this study suggest that nicotine administration is associated with distorted reproductive hormones in male rats although ameliorated by nicotine cessation. It is plausible that the decreased testosterone level is associated with testicular dysfunction rather than a pituitary disorder.

AI snapshot

Written from the paper’s full text.

TL;DR

In male Sprague-Dawley rats, 30-day oral nicotine at 0.5 and 1.0 mg/kg altered serum reproductive hormones, with testosterone and FSH decreased and LH/prolactin increased at the high dose; 30-day cessation restored values comparable to control. The authors suggest nicotine-induced low testosterone reflects testicular dysfunction rather than a pituitary disorder.

Key findings

  • Nicotine significantly decreased (P < 0.05) serum testosterone in both the 0.5 mg/kg and 1.0 mg/kg treated groups versus control; the decrease was dose dependent.
  • High-dose nicotine (1.0 mg/kg) significantly increased (P < 0.05) mean LH and prolactin and significantly decreased (P < 0.05) FSH versus control; low-dose and recovery groups generally showed insignificant changes (P > 0.05) for LH and FSH.
  • Recovery groups given nicotine for 30 days then left untreated for another 30 days had values comparable with control, suggesting the effects were ameliorated by nicotine cessation.
  • The authors conclude the decreased testosterone is plausibly associated with testicular dysfunction rather than a pituitary disorder.

Methods

  • Forty male Sprague-Dawley rats, average weight 150–180 g and 2–2.5 months old, were divided into five equal groups with ad libitum rat chow and water, maintained at 12:12-hour light-dark and room temperature.
  • Groups received oral/gavage treatment for 30 days: control 0.2 ml/kg normal saline; 0.5 mg/kg nicotine; 1.0 mg/kg nicotine; and two recovery groups given 0.5 or 1.0 mg/kg nicotine for 30 days then left untreated for another 30 days.
  • Serum was analyzed for testosterone, LH, FSH, and prolactin. The abstract states radioimmunoassay, while the methods state tube-based enzyme immunoassay (EIA) using a kit from Immunometrics Limited, UK, meeting WHO standards. Results were analyzed with one-way ANOVA followed by Duncan’s multiple range post hoc test using SPSS.

Limitations

  • The paper states no explicit limitations section.
  • Evident from the text: findings are from male rats only, with small groups (n = 8 per group) and only 30-day treatment plus 30-day recovery periods; no exact hormone concentrations are reported in the text, and the figures are not included in the provided text.
  • Evident from the text: there is an assay-method inconsistency (abstract says radioimmunoassay; methods say enzyme immunoassay) and some P-value reporting inconsistencies, such as recovery testosterone described as an “insignificant decrease (P < 0.05)” and recovery prolactin as an “insignificant increase (P < 0.05).”

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.4103/0974-1208.112380

Cites

26 of 26 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

2 of 9 cited sources checked · 1 supported · 0 flagged · accuracy not yet measured

  • Premisecitation

    Hyperprolactinemia in men typically leads to hypogonadism resulting in decreased libido, erectile dysfunction, and abnormal semen quality.

    “Hyperprolactinemia in men typically leads to hypogonadism resulting in decreased libido, erectile dysfunction, and abnormal semen quality.[22]”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [22] Corsello, 2003, Clin Endocrinol (Oxf) source

      The Patients section reports libido and potency failure in 8 of 10 men with giant prolactinomas. The treatment-effects section reports improvement in libido and potency alongside hormonal changes, and improved sperm number and motility in one patient. This supports the sexual-symptom and semen-quality components, but the study does not establish that hyperprolactinemia in men generally or typically causes hypogonadism and abnormal semen quality. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
  • Interpretationcitation

    Nicotine-induced decrease in serum testosterone may be caused by disruption of testicular cytoarchitecture, adversely affecting Leydig cell number and function.

    “This might have been caused by the disruption of testicular cytoarchitecture by nicotine also observed in previous studies; consequently, adversely affected Leydig cell number and functioning leading to decrease serum testosterone level since Leydig cells secrete testosterone.[8]”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [8] Oyeyipo, 2010, Niger J Physiol Sci
    • Rests on an assumption: The hormone assay kit designed for human reproduction is valid for measuring rat serum hormones.
  • Findingown data

    The decrease in serum testosterone caused by nicotine was dose dependent.

    “The observed decrease is dose dependent as shown in Figure 1.”
    • Also stated in: § CONCLUSION · plain
      “However, the effects of nicotine on reproductive hormones were dose dependent and the observed effects were ameliorated with withdrawal.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The hormone assay kit designed for human reproduction is valid for measuring rat serum hormones.
  • Findingown data

    Nicotine administration at 1.0 mg/kg body weight for 30 days significantly increased mean serum LH in male rats compared with control.

    “There was a significant increase (P < 0.05) in mean LH and prolactin level in the high dose treated group when compared with the control.”
    • Also stated in: § Effect of nicotine on mean hormone levels · plain
      “The results showed that there was a significant increase (P < 0.05) in the mean serum LH level of rats that received 1.0 mg/kg B.W. nicotine daily for four weeks when compared with their control.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The hormone assay kit designed for human reproduction is valid for measuring rat serum hormones.
  • Findingown data

    Nicotine administration at 1.0 mg/kg body weight for 30 days significantly decreased mean serum FSH in male rats compared with control.

    “Results showed that nicotine administration significantly decreased (P < 0.05) testosterone in the low and high treated groups and FSH in the high dose treated group when compared with the control group.”
    • Also stated in: § Effect of nicotine on mean hormone levels · plain
      “The mean FSH level of rats that received 1.0 mg/kg BW nicotine daily for four weeks was significantly decreased (P < 0.05) when compared with the control group.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The hormone assay kit designed for human reproduction is valid for measuring rat serum hormones.
  • The quote only partly states this claim. 2
  • May combine two claims. 5
  • Classified as probably not a substantial claim. 4

  • The quote only partly states this claim.

    Findingown data

    In the recovery groups (30 days after cessation of nicotine), serum hormone values were comparable to control (not significantly different).

    “However, the values of the recovery groups were comparable with the control.”
    • Also stated in: § DISCUSSION · hedged
      “The recovery groups showed comparable values with the control indicating that the effect of nicotine on testosterone can be ameliorated by nicotine cessation.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The hormone assay kit designed for human reproduction is valid for measuring rat serum hormones.

  • The quote only partly states this claim.

    Findingown data

    Low dose nicotine (0.5 mg/kg) and recovery groups did not significantly change mean serum prolactin compared with control.

    “However, 0.5 mg/kg B.W. group and the recovery groups showed an insignificant increase (P < 0.05) when compared with the recovery group as shown in Figure 4.”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: The hormone assay kit designed for human reproduction is valid for measuring rat serum hormones.

  • May combine two claims.

    Premisecitation

    Hyperprolactinemia impairs male gonadal functions by decreasing GnRH pulse generator activity and/or decreasing LH and FSH secretion, and may inhibit testosterone secretion at Leydig cells.

    “Hyperprolactinemia impairs male gonadal functions by acting at various levels, possibly by decreasing GnRH pulse generator activity and/or by decreasing LH and FSH secretion, and might be inhibiting testosterone secretion at the level of Leydig cells as well.[23]”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [23] Horseman ND, Gregerson KA. Prolactin. In: DeGroot LJ, Jameson JL, editors. Endocrinology. Philadelphia: Elsevier Saunders; 2006. pp. 309-21.

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Classified as probably not a substantial claim.

    Premisecitation

    Testosterone is associated with FSH, which acts on the seminiferous tubules to initiate and maintain spermatogenesis.

    “Testosterone is associated with FSH, which acts on the seminiferous tubules to initiate and maintain spermatogenesis. Sexual maturation in male rat is related with an increase in FSH secretion since FSH binds within the seminiferous tubules to facilitate spermatogenesis.[13]”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [13] Ojeda SR, Urbanski HF. Puberty in rat. In: Knobil E, Neil JE, editors. The Physiology of Reproduction. 2 nd ed. New York II: Raven Press; 1994. p. 363-409.

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    Testosterone production by Leydig cells is primarily under the control of LH, and stimulation of LH is usually followed by stimulation of testosterone.

    “It is well-known that testosterone production by Leydig cell is primary under the control of LH and stimulation of LH is usually followed by stimulation of testosterone.[14]”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [14] Huthaniemi IT, Toppari J. Endocrine, paracrine, and autocrine regulation of testicular steroidogenesis. In: Mukhopadhya AK, Raizada MK, editors. Tissue Renin Angiotensin System. New York: Plenum Press; 1995. p. 33-53. source

  • May combine two claims.

    Interpretationcitation

    Abnormalities in sperm quality and decreased libido observed in a previous study can be attributed to the increased serum prolactin, since hyperprolactinemia impairs germ cell function due to low FSH and decreased intra-testicular testosterone.

    “Hence, abnormalities in sperm quality and decreased libido observed in the previous study can also be attributed to the increased in serum prolactin since hyperprolactinemia is attributed to impaired germ cell function due to low FSH and decreased intra-testicular testosterone.[25]”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [25] Molitch ME. Prolactin in human reproduction. In: Strauss JF III, Barbieri RL, editors. Yen and Jaffe′s Reproductive Endocrinology: Physiology, Pathophysiology, and Clinical Management. 6 th ed. Philadelphia, PA: Elsevier Inc; 2009. p. 57-78. source
    • Rests on an assumption: The hormone assay kit designed for human reproduction is valid for measuring rat serum hormones.

  • May combine two claims.

    Premisecitation

    Prolactin receptors are present in spermatogonia, seminiferous epithelium, and spermatocytes, suggesting prolactin may have a role in normal spermatogenesis.

    “Prolactin receptors have been demonstrated in the spermatogonia, seminiferous epithelium, and spermatocytes, suggesting that prolactin might have a role to play in normal spermatogenesis.[24]”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [24] Hondo, 1995, Biol Reprod source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    The hormone analysis used a tube-based enzyme immunoassay (EIA) protocol that met World Health Organization (WHO) standards in research programme for human reproduction.

    “The analysis was carried via the tube-based enzyme immunoassay (EIA) method. The protocol used for the hormone was according to the method described for the kit (Immunometrics Limited, UK) and meet the World Health Organization (WHO) standards in research programme for human reproduction.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationreasoning

    The decrease in FSH observed with nicotine treatment may be due to increased release of inhibin by Sertoli cells, inhibiting FSH release from the anterior pituitary and possibly inhibiting GnRH secretion.

    “Decrease in FSH observed with nicotine treatment could be due to increase release of inhibin by the sertoli cell thus inhibiting the release of FSH from the anterior pituitary and possibly also a negative effect on the hypothalamus to inhibit the secretion of GnRH.”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: The hormone assay kit designed for human reproduction is valid for measuring rat serum hormones.

  • Classified as probably not a substantial claim.

    Study design and conductreasoning

    To minimize the effect of diurnal fluctuation, all blood samples were obtained in baseline conditions between 8:00 A.M. and 9:30 A.M.

    “In order to minimize the effect of diurnal fluctuation, all samples were obtained in baseline conditions between 8:00 A.M. and 9:30 A.M.”
    Quote in the paperSubstantial claim
10 of 10

  • The paper relies on this without support.

    The mechanism by which nicotine causes male infertility is poorly understood.

    “However, the mechanism by which nicotine causes male infertility is poorly understood.”

  • The paper relies on this without support.

    No study has documented the effect of nicotine withdrawal on male reproductive hormones in male rats.

    “However, to the best of our knowledge no study has documented the effect of nicotine withdrawal on male reproductive hormones in male rats.”

  • The paper relies on this without support.

    The hormone assay kit designed for human reproduction is valid for measuring rat serum hormones.

    “The protocol used for the hormone was according to the method described for the kit (Immunometrics Limited, UK) and meet the World Health Organization (WHO) standards in research programme for human reproduction.”
3 of 3

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Hormone assay method is described inconsistently

    Major

    The abstract says the serum hormones were measured by radioimmunoassay, whereas the methods specify enzyme immunoassay.

  • Testosterone recovery result is called insignificant despite P < 0.05

    Minor

    The recovery-group testosterone decrease is described as insignificant with P < 0.05, but the paper uses P < 0.05 to denote a significant difference.

  • Prolactin result is called insignificant despite P < 0.05

    Minor

    The prolactin increase is described as insignificant with P < 0.05, contradicting the paper's stated significance threshold.

3 of 3

Cites

Flagged first, then by citations

2 of the 28 references couldn’t be matched to a known paper.

Research works printed but not linked: 4

  1. Langgassner, 1996, Rauchgewohnheiten der österreichischen Bevölkerung, Statistische Nachrichten, 319
  2. Henningfield JE, Goldberg SR. Pathophysiology of tobacco dependence. In: Bloom FE, Kupfer DJ, editors. Psychopharmacology: The fourth Generation of Progress. New York: Raven Press; 1983. p. 1715-29.
  3. Ojeda SR, Urbanski HF. Puberty in rat. In: Knobil E, Neil JE, editors. The Physiology of Reproduction. 2 nd ed. New York II: Raven Press; 1994. p. 363-409.
  4. Horseman ND, Gregerson KA. Prolactin. In: DeGroot LJ, Jameson JL, editors. Endocrinology. Philadelphia: Elsevier Saunders; 2006. pp. 309-21.

Cited by

Sorted by citations

Related

Authors
Oyeyipo, I., Raji, Y., & Bolarinwa, A.
Affiliations
University of Ibadan (NG)
Venue
Journal of Human Reproductive Sciences
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2013
Volume
6
Issue
1
Pages
40
ISSN
0974-1208 (ISSN-L)
DOI
10.4103/0974-1208.112380
PMC
PMC3713576
OpenAlex
W1981695960
Cited by
67
References
28
Citations by year
2026: 3 · 2025: 2 · 2024: 5 · 2023: 7 · 2022: 7 · 2021: 7 · 2020: 8 · 2019: 7 · 2018: 8 · 2017: 4 · 2015: 7 · 2014: 1 · 2013: 1
FWCI
3.27
Type
journal article
Language
en
Open access
Licence
cc-by-nc-sa
Locations
  • Journal of Human Reproductive Sciences (publishedVersion, cc-by-nc-sa)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Health Sciences › Medicine › Reproductive Medicine › Sperm and Testicular Function
  • Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
  • Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
Keywords
nicotine, male infertility, reproductive hormones, testosterone, luteinizing hormone, follicle-stimulating hormone, prolactin, nicotine cessation, recovery, testicular dysfunction, smoking, rats

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-11-05.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-11-05.

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Statistics and arithmetic are recomputed, not judged.

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