Short-term systemic effects of nose-only cigarette smoke exposure in mice: Role of oxidative stress

Abderrahim Nemmar, Haider Raza, Deepa Subramaniyan, Javed Yasin, Annie John, Badreldin H. Ali, Elsadig E. Kazzam

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

Background/Aims: Long-term cigarette smoking (CS) is a major risk factor for respiratory and cardiovascular diseases, and is also known to adversely affect other organs. However, data on the systemic effects of short-term CS exposure (STCSE) are scarce. Presently, using a nose-only exposure system, we evaluated the systemic effects of STCSE in mice. Methods: We assessed the effects of CS generated by 9 consecutive cigarettes per day for 4 days in a nose-only exposure system on cardiovascular, hepatic and renal endpoints evaluated on day 5 in mice. Control mice were exposed to air only. Results: CS significantly increased systolic blood pressure and decreased total nitric oxide plasma concentration. Circulating platelets and erythrocyte numbers were also increased. However, STCSE did not significantly increase thrombosis in pial arterioles and venules. STCSE significantly raised plasma alanine aminotransferase and gamma glutamyl transpeptidase activities, but did not affect urea or creatinine concentrations. Interestingly, while STCSE enhanced the production of reactive oxygen species in heart and kidney and lipid peroxidation in heart, liver and kidneys, it also enhanced the antioxidant activity of superoxide dismutase, probably indicating that STCSE causes adaptive reactions to counterbalance the potentially damaging action of oxygen radicals induced by STCSE. Conclusion: These results suggest that STCSE causes blood pressure increase, hepatotoxicity and oxidative stress in the heart, liver and the kidneys. These data provide information on the initial steps leading to the systemic effects of STCSE, a stage at which the diseases may likely be reversed.

Original languageEnglish
Pages (from-to)15-24
Number of pages10
JournalCellular Physiology and Biochemistry
Volume31
Issue number1
DOIs
Publication statusPublished - 2013

Fingerprint

Nose
Smoke
Tobacco Products
Oxidative Stress
Smoking
Kidney
Blood Pressure
Liver
Reactive Oxygen Species
Erythrocyte Count
Venules
gamma-Glutamyltransferase
Arterioles
Cardiovascular System
Alanine Transaminase
Platelet Count
Lipid Peroxidation
Superoxide Dismutase
Urea
Creatinine

Keywords

  • Cigarette smoke
  • Liver enzymes
  • Nose-only exposure, short-term exposure
  • Oxidative stress
  • Systolic blood pressure
  • Thrombosis

ASJC Scopus subject areas

  • Physiology

Cite this

Short-term systemic effects of nose-only cigarette smoke exposure in mice : Role of oxidative stress. / Nemmar, Abderrahim; Raza, Haider; Subramaniyan, Deepa; Yasin, Javed; John, Annie; Ali, Badreldin H.; Kazzam, Elsadig E.

In: Cellular Physiology and Biochemistry, Vol. 31, No. 1, 2013, p. 15-24.

Research output: Contribution to journalArticle

Nemmar, Abderrahim ; Raza, Haider ; Subramaniyan, Deepa ; Yasin, Javed ; John, Annie ; Ali, Badreldin H. ; Kazzam, Elsadig E. / Short-term systemic effects of nose-only cigarette smoke exposure in mice : Role of oxidative stress. In: Cellular Physiology and Biochemistry. 2013 ; Vol. 31, No. 1. pp. 15-24.
@article{efccd15b9ca04a61a5c2276aa2eb6c83,
title = "Short-term systemic effects of nose-only cigarette smoke exposure in mice: Role of oxidative stress",
abstract = "Background/Aims: Long-term cigarette smoking (CS) is a major risk factor for respiratory and cardiovascular diseases, and is also known to adversely affect other organs. However, data on the systemic effects of short-term CS exposure (STCSE) are scarce. Presently, using a nose-only exposure system, we evaluated the systemic effects of STCSE in mice. Methods: We assessed the effects of CS generated by 9 consecutive cigarettes per day for 4 days in a nose-only exposure system on cardiovascular, hepatic and renal endpoints evaluated on day 5 in mice. Control mice were exposed to air only. Results: CS significantly increased systolic blood pressure and decreased total nitric oxide plasma concentration. Circulating platelets and erythrocyte numbers were also increased. However, STCSE did not significantly increase thrombosis in pial arterioles and venules. STCSE significantly raised plasma alanine aminotransferase and gamma glutamyl transpeptidase activities, but did not affect urea or creatinine concentrations. Interestingly, while STCSE enhanced the production of reactive oxygen species in heart and kidney and lipid peroxidation in heart, liver and kidneys, it also enhanced the antioxidant activity of superoxide dismutase, probably indicating that STCSE causes adaptive reactions to counterbalance the potentially damaging action of oxygen radicals induced by STCSE. Conclusion: These results suggest that STCSE causes blood pressure increase, hepatotoxicity and oxidative stress in the heart, liver and the kidneys. These data provide information on the initial steps leading to the systemic effects of STCSE, a stage at which the diseases may likely be reversed.",
keywords = "Cigarette smoke, Liver enzymes, Nose-only exposure, short-term exposure, Oxidative stress, Systolic blood pressure, Thrombosis",
author = "Abderrahim Nemmar and Haider Raza and Deepa Subramaniyan and Javed Yasin and Annie John and Ali, {Badreldin H.} and Kazzam, {Elsadig E.}",
year = "2013",
doi = "10.1159/000343345",
language = "English",
volume = "31",
pages = "15--24",
journal = "Cellular Physiology and Biochemistry",
issn = "1015-8987",
publisher = "S. Karger AG",
number = "1",

}

TY - JOUR

T1 - Short-term systemic effects of nose-only cigarette smoke exposure in mice

T2 - Role of oxidative stress

AU - Nemmar, Abderrahim

AU - Raza, Haider

AU - Subramaniyan, Deepa

AU - Yasin, Javed

AU - John, Annie

AU - Ali, Badreldin H.

AU - Kazzam, Elsadig E.

PY - 2013

Y1 - 2013

N2 - Background/Aims: Long-term cigarette smoking (CS) is a major risk factor for respiratory and cardiovascular diseases, and is also known to adversely affect other organs. However, data on the systemic effects of short-term CS exposure (STCSE) are scarce. Presently, using a nose-only exposure system, we evaluated the systemic effects of STCSE in mice. Methods: We assessed the effects of CS generated by 9 consecutive cigarettes per day for 4 days in a nose-only exposure system on cardiovascular, hepatic and renal endpoints evaluated on day 5 in mice. Control mice were exposed to air only. Results: CS significantly increased systolic blood pressure and decreased total nitric oxide plasma concentration. Circulating platelets and erythrocyte numbers were also increased. However, STCSE did not significantly increase thrombosis in pial arterioles and venules. STCSE significantly raised plasma alanine aminotransferase and gamma glutamyl transpeptidase activities, but did not affect urea or creatinine concentrations. Interestingly, while STCSE enhanced the production of reactive oxygen species in heart and kidney and lipid peroxidation in heart, liver and kidneys, it also enhanced the antioxidant activity of superoxide dismutase, probably indicating that STCSE causes adaptive reactions to counterbalance the potentially damaging action of oxygen radicals induced by STCSE. Conclusion: These results suggest that STCSE causes blood pressure increase, hepatotoxicity and oxidative stress in the heart, liver and the kidneys. These data provide information on the initial steps leading to the systemic effects of STCSE, a stage at which the diseases may likely be reversed.

AB - Background/Aims: Long-term cigarette smoking (CS) is a major risk factor for respiratory and cardiovascular diseases, and is also known to adversely affect other organs. However, data on the systemic effects of short-term CS exposure (STCSE) are scarce. Presently, using a nose-only exposure system, we evaluated the systemic effects of STCSE in mice. Methods: We assessed the effects of CS generated by 9 consecutive cigarettes per day for 4 days in a nose-only exposure system on cardiovascular, hepatic and renal endpoints evaluated on day 5 in mice. Control mice were exposed to air only. Results: CS significantly increased systolic blood pressure and decreased total nitric oxide plasma concentration. Circulating platelets and erythrocyte numbers were also increased. However, STCSE did not significantly increase thrombosis in pial arterioles and venules. STCSE significantly raised plasma alanine aminotransferase and gamma glutamyl transpeptidase activities, but did not affect urea or creatinine concentrations. Interestingly, while STCSE enhanced the production of reactive oxygen species in heart and kidney and lipid peroxidation in heart, liver and kidneys, it also enhanced the antioxidant activity of superoxide dismutase, probably indicating that STCSE causes adaptive reactions to counterbalance the potentially damaging action of oxygen radicals induced by STCSE. Conclusion: These results suggest that STCSE causes blood pressure increase, hepatotoxicity and oxidative stress in the heart, liver and the kidneys. These data provide information on the initial steps leading to the systemic effects of STCSE, a stage at which the diseases may likely be reversed.

KW - Cigarette smoke

KW - Liver enzymes

KW - Nose-only exposure, short-term exposure

KW - Oxidative stress

KW - Systolic blood pressure

KW - Thrombosis

UR - http://www.scopus.com/inward/record.url?scp=84872803708&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84872803708&partnerID=8YFLogxK

U2 - 10.1159/000343345

DO - 10.1159/000343345

M3 - Article

C2 - 23343613

AN - SCOPUS:84872803708

VL - 31

SP - 15

EP - 24

JO - Cellular Physiology and Biochemistry

JF - Cellular Physiology and Biochemistry

SN - 1015-8987

IS - 1

ER -