Chronic cigarette smoking impairs erectile function through increased oxidative stress and apoptosis, decreased nNOS, endothelial and smooth muscle contents in a rat model

Yun Ching Huang, Chih Chien Chin, Chih Shou Chen, Alan W Shindel, Dong Ru Ho, Ching Shwun Lin, Chung Sheng Shi

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Cigarette use is an independent risk factor for the development of erectile dysfunction (ED). While the association between chronic smoking and ED is well established, the fundamental mechanism(s) of cigarette-related ED are incompletely understood, partly due to no reliable animal model of smoking-induced ED. The present study was designed to validate an in vivo rat model of chronic cigarette-induced ED. Forty 12-week old male Sprague-Dawley rats were divided into 4 groups. Ten rats served as control group and were exposed only to room air. The remaining 30 rats were passively exposed to cigarette smoke (CS) for 4 weeks (n = 10), 12 weeks (n = 10), and 24 weeks (n = 10). At the 24-week time point all rats were assessed with intracavernous pressure (ICP) during cavernous nerve electrostimulation. Blood and urine were collected to measure serum testosterone and oxidative stress, respectively. Corporal tissue was assessed by Western blot for neuronal nitric oxide synthase (nNOS). Penile tissues were subjected to immunohistochemistry for endothelial, smooth muscle, and apoptotic content. Mean arterial pressure (MAP) was significantly higher in 24-week cigarette exposed animals compared to the control animals. Mean ICP/MAP ratio and cavernosal smooth muscle/endothelial contents were significantly lower in the 12- and 24-week rats compared to control animals. Oxidative stress was significantly higher in the 24-week cigarette exposed group compared to control animals. Mean nNOS expression was significantly lower, and apoptotic index significantly higher, in CS-exposed animals compared to control animals. These findings indicate that the rat model exposure to CS increases apoptosis and oxidative stress and decreases nNOS, endothelial and smooth muscle contents, and ICP in a dose dependent fashion. The rat model is a useful tool for further study of the molecular and cellular mechanisms of CS-related ED.

Original languageEnglish (US)
Article numbere0140728
JournalPLoS One
Volume10
Issue number10
DOIs
StatePublished - Oct 22 2015

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Nitric Oxide Synthase Type I
Oxidative stress
smoking (habit)
cigarettes
Tobacco Products
smooth muscle
Smooth Muscle
Muscle
Rats
Oxidative Stress
oxidative stress
apoptosis
animal models
Smoking
Erectile Dysfunction
Apoptosis
Animals
smoke
Smoke
rats

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

Chronic cigarette smoking impairs erectile function through increased oxidative stress and apoptosis, decreased nNOS, endothelial and smooth muscle contents in a rat model. / Huang, Yun Ching; Chin, Chih Chien; Chen, Chih Shou; Shindel, Alan W; Ho, Dong Ru; Lin, Ching Shwun; Shi, Chung Sheng.

In: PLoS One, Vol. 10, No. 10, e0140728, 22.10.2015.

Research output: Contribution to journalArticle

Huang, Yun Ching ; Chin, Chih Chien ; Chen, Chih Shou ; Shindel, Alan W ; Ho, Dong Ru ; Lin, Ching Shwun ; Shi, Chung Sheng. / Chronic cigarette smoking impairs erectile function through increased oxidative stress and apoptosis, decreased nNOS, endothelial and smooth muscle contents in a rat model. In: PLoS One. 2015 ; Vol. 10, No. 10.
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abstract = "Cigarette use is an independent risk factor for the development of erectile dysfunction (ED). While the association between chronic smoking and ED is well established, the fundamental mechanism(s) of cigarette-related ED are incompletely understood, partly due to no reliable animal model of smoking-induced ED. The present study was designed to validate an in vivo rat model of chronic cigarette-induced ED. Forty 12-week old male Sprague-Dawley rats were divided into 4 groups. Ten rats served as control group and were exposed only to room air. The remaining 30 rats were passively exposed to cigarette smoke (CS) for 4 weeks (n = 10), 12 weeks (n = 10), and 24 weeks (n = 10). At the 24-week time point all rats were assessed with intracavernous pressure (ICP) during cavernous nerve electrostimulation. Blood and urine were collected to measure serum testosterone and oxidative stress, respectively. Corporal tissue was assessed by Western blot for neuronal nitric oxide synthase (nNOS). Penile tissues were subjected to immunohistochemistry for endothelial, smooth muscle, and apoptotic content. Mean arterial pressure (MAP) was significantly higher in 24-week cigarette exposed animals compared to the control animals. Mean ICP/MAP ratio and cavernosal smooth muscle/endothelial contents were significantly lower in the 12- and 24-week rats compared to control animals. Oxidative stress was significantly higher in the 24-week cigarette exposed group compared to control animals. Mean nNOS expression was significantly lower, and apoptotic index significantly higher, in CS-exposed animals compared to control animals. These findings indicate that the rat model exposure to CS increases apoptosis and oxidative stress and decreases nNOS, endothelial and smooth muscle contents, and ICP in a dose dependent fashion. The rat model is a useful tool for further study of the molecular and cellular mechanisms of CS-related ED.",
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