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Evaluation of the subacute systemic thrombotic and organ toxicity of nicotine in mice
Author(s) -
Fahim Mohamed Abdelmonem,
Nemmar Abderrahim,
AlSalam Suhail,
Dhanasekaran Subramanian,
Shafiullah Mohamed,
Yasin Javed,
Hasan Mohamed Yousif
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.902.2
Subject(s) - nicotine , medicine , toxicity , superoxide dismutase , inflammation , pharmacology , platelet , oxidative stress , pathology , histopathology , necrosis
Nicotine is involved in the pathogenesis of hematological and cardiopulmonary diseases. However, the mechanisms underlying these effects are unclear. Presently, we have investigated the effect of nicotine on cerebral microvessel thrombosis, systemic and organs toxicity. Mice were injected with nicotine (1mg/kg, i.p), once a day for 7 days. Briefly, a photo insult of surgically exposed cerebral microvessel, after bolus intravenous injection with fluorescein, were done. The changes in platelet aggregation in microvessels were analysed. In conjunction, superoxide dismutase (SOD), LDH, liver enzymes, creatinine, BUN and histopathology were carried out. Our results revealed a significant reduction in the time required for platelet aggregation following nicotine exposure. Significant decrease in SOD and increase in LDH levels were observed. The liver enzyme showed substantial rise in the AST and ALT levels. The increase in LDH levels emphasizes an induction of systemic inflammation and reduction in SOD levels indicating the oxidative stress involvement in the tissue damages induced by nicotine. Lungs and liver histology showed intra‐vascular hemorrhagic infarction with necrosis and macrophages infiltration with inflammation. We conclude that the sub acute nicotine exposure causes systemic, hepatic and pulmonary toxicity and increases thrombotic event damage in cerebral microvessels.