Home FOR AUTHORS General Physiology and Biophysics 2014 General Physiology and Biophysics Vol.33, No.3, p.345–355, 2014

Journal info


Founded: 1982
ISSN 1338-4325 (online)
ISSN 0231-5882 (print)
Published in English,
6 times per year

Aims and Scope
Editorial Info
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

General Physiology and Biophysics Vol.33, No.3, p.345–355, 2014

Title: Thromboembolic injury and systemic toxicity induced by nicotine in mice
Author: Mohamed A. Fahim, Abderrahim Nemmar, Suhail Al-Salam, Subramanian Dhanasekaran, Mohamed Shafiullah, Javed Yasin, Mohamed Y. Hasan

Abstract: Nicotine is involved in the pathogenesis of hematological and cardiopulmonary diseases. However, the understanding of the pathophysiological mechanisms underlying these undesirable effects is  unclear. Cigarette smoking, nicotine gums and patches are common sources for nicotine ingestion. We have investigated the nicotine’s effect on cerebral microvessel thrombosis and systemic toxicity. Mice received either nicotine (1 mg/kg, i.p.) or saline (control), once a day for 21 days. Briefly, after bolus intravenous fluorescein injection, a photo insult of cerebral microvessel was done. The platelet aggregation in microvessels was video recorded and analyzed. In conjunction, the plasma levels of superoxide dismutase (SOD), lactate dehydrogenase (LDH), liver enzymes, creatinine and blood urea nitrogen (BUN), and histopathological studies were carried out. Our results revealed a significant prothrombotic effect following nicotine exposure. Significant decrease in SOD indicates the occurrence of oxidative stress involved in the tissue damages and increase in the LDH emphasize the systemic toxicity. Substantial rise in the liver aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were observed. Lungs histology showed intra-vascular hemorrhagic infarction with necrosis, macrophage and neutrophils infiltration. Liver histology showed intravascular thrombosis and portal inflammation. We conclude that the sub-acute nicotine exposure causes an increase in thrombosis in cerebral microvessels and systemic, hepatic and pulmonary toxicity.

Keywords: Nicotine — Thrombosis — Systemic toxicity — Liver function — Histopathology
Published online: 08-Jul-2014
Year: 2014, Volume: 33, Issue: 3 Page From: 345, Page To: 355
doi:10.4149/gpb_2014012


download file



© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.