Cigarette smoke induced oxidative insult in local population of Pokhara

Jay Chandra Jha, B. R. Maharjan, D. Adhikari, P. Vishwanath, Akila, T. Nagamma, S. Azhari, P. P. Singh

Research output: Contribution to journalArticle

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Abstract

Objectives: To assess the effect of cigarette smoking on lipid peroxidation induced oxidative stress, antioxidants, uric acid and blood sugar in normal subjects. Methods: The study included 61 normal subjects with regular smoking habit and 57 never-smokers normal subjects matched in respect to socio-economic status, age and BMI. Information regarding smoking habit and other personal details were collected by oral questionnaire. Total antioxidant activity (TAA), reduced glutathione (GSH), α-tocopherol (α-T), ascorbic acid (AA), uric acid (UA), plasma and urinary thiobarbituric acid reactive substances (TBARS), fasting blood sugar (FBS) and urinary creatinine (Cr) were estimated by standard procedures in both the groups. Ferric Reducing Antioxidant Power (FRAP) procedure is used to estimate TAA which measures total dietary antioxidants. Statistical analysis was done with SPSS version 10. Results: The mean pack years smoked by smokers was 14.4 ± 15.8. The plasma TBARS level in smokers and never-smokers was 2.6 ± 0.8 and 2.5 ± 0.6 μmol/L respectively. The respective figure for urinary TBARS level was 4.6 ± 2.7 and 3.7 ± 1.4 μmol/gmCr. Smokers did not show any significant difference from never-smokers with respect to GSH, α-T, AA, plasma TBARS and FBS. However, the smokers had significantly lower levels of TAA (p<0.05) and raised level of urinary TBARS (p<0.05) and uric acid (p<0.01) as compared to never-smokers. Conclusion: Our study suggests that smoking induces mild lipid peroxidation but the body is able to compensate for it by removing its adducts. Importantly it also indicates enhanced oxidation of purines which are essential components of both DNA and RNA. Dietary antioxidants are consumed to scavenge free radicals (FR) and other reactive species (RS) in smoke. Female smokers are more prone to oxidative insult than male smokers. In summary RS present in smoke induce mild lipid peroxidation but are not the major contributors of redox imbalance in smoke induced toxicity in the selected subjects.

Original languageEnglish
Pages (from-to)511-517
Number of pages7
JournalKathmandu University Medical Journal
Volume5
Issue number20
Publication statusPublished - 01-12-2007
Externally publishedYes

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Smoke
Tobacco Products
Thiobarbituric Acid Reactive Substances
Antioxidants
Population
Uric Acid
Smoking
Lipid Peroxidation
Blood Glucose
Ascorbic Acid
Habits
Fasting
Purines
Tocopherols
Oxidation-Reduction
Free Radicals
Glutathione
Creatinine
Oxidative Stress
Economics

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Jha, J. C., Maharjan, B. R., Adhikari, D., Vishwanath, P., Akila, Nagamma, T., ... Singh, P. P. (2007). Cigarette smoke induced oxidative insult in local population of Pokhara. Kathmandu University Medical Journal, 5(20), 511-517.
Jha, Jay Chandra ; Maharjan, B. R. ; Adhikari, D. ; Vishwanath, P. ; Akila, ; Nagamma, T. ; Azhari, S. ; Singh, P. P. / Cigarette smoke induced oxidative insult in local population of Pokhara. In: Kathmandu University Medical Journal. 2007 ; Vol. 5, No. 20. pp. 511-517.
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Jha, JC, Maharjan, BR, Adhikari, D, Vishwanath, P, Akila, , Nagamma, T, Azhari, S & Singh, PP 2007, 'Cigarette smoke induced oxidative insult in local population of Pokhara', Kathmandu University Medical Journal, vol. 5, no. 20, pp. 511-517.

Cigarette smoke induced oxidative insult in local population of Pokhara. / Jha, Jay Chandra; Maharjan, B. R.; Adhikari, D.; Vishwanath, P.; Akila, ; Nagamma, T.; Azhari, S.; Singh, P. P.

In: Kathmandu University Medical Journal, Vol. 5, No. 20, 01.12.2007, p. 511-517.

Research output: Contribution to journalArticle

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AU - Jha, Jay Chandra

AU - Maharjan, B. R.

AU - Adhikari, D.

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AU - Akila,

AU - Nagamma, T.

AU - Azhari, S.

AU - Singh, P. P.

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N2 - Objectives: To assess the effect of cigarette smoking on lipid peroxidation induced oxidative stress, antioxidants, uric acid and blood sugar in normal subjects. Methods: The study included 61 normal subjects with regular smoking habit and 57 never-smokers normal subjects matched in respect to socio-economic status, age and BMI. Information regarding smoking habit and other personal details were collected by oral questionnaire. Total antioxidant activity (TAA), reduced glutathione (GSH), α-tocopherol (α-T), ascorbic acid (AA), uric acid (UA), plasma and urinary thiobarbituric acid reactive substances (TBARS), fasting blood sugar (FBS) and urinary creatinine (Cr) were estimated by standard procedures in both the groups. Ferric Reducing Antioxidant Power (FRAP) procedure is used to estimate TAA which measures total dietary antioxidants. Statistical analysis was done with SPSS version 10. Results: The mean pack years smoked by smokers was 14.4 ± 15.8. The plasma TBARS level in smokers and never-smokers was 2.6 ± 0.8 and 2.5 ± 0.6 μmol/L respectively. The respective figure for urinary TBARS level was 4.6 ± 2.7 and 3.7 ± 1.4 μmol/gmCr. Smokers did not show any significant difference from never-smokers with respect to GSH, α-T, AA, plasma TBARS and FBS. However, the smokers had significantly lower levels of TAA (p<0.05) and raised level of urinary TBARS (p<0.05) and uric acid (p<0.01) as compared to never-smokers. Conclusion: Our study suggests that smoking induces mild lipid peroxidation but the body is able to compensate for it by removing its adducts. Importantly it also indicates enhanced oxidation of purines which are essential components of both DNA and RNA. Dietary antioxidants are consumed to scavenge free radicals (FR) and other reactive species (RS) in smoke. Female smokers are more prone to oxidative insult than male smokers. In summary RS present in smoke induce mild lipid peroxidation but are not the major contributors of redox imbalance in smoke induced toxicity in the selected subjects.

AB - Objectives: To assess the effect of cigarette smoking on lipid peroxidation induced oxidative stress, antioxidants, uric acid and blood sugar in normal subjects. Methods: The study included 61 normal subjects with regular smoking habit and 57 never-smokers normal subjects matched in respect to socio-economic status, age and BMI. Information regarding smoking habit and other personal details were collected by oral questionnaire. Total antioxidant activity (TAA), reduced glutathione (GSH), α-tocopherol (α-T), ascorbic acid (AA), uric acid (UA), plasma and urinary thiobarbituric acid reactive substances (TBARS), fasting blood sugar (FBS) and urinary creatinine (Cr) were estimated by standard procedures in both the groups. Ferric Reducing Antioxidant Power (FRAP) procedure is used to estimate TAA which measures total dietary antioxidants. Statistical analysis was done with SPSS version 10. Results: The mean pack years smoked by smokers was 14.4 ± 15.8. The plasma TBARS level in smokers and never-smokers was 2.6 ± 0.8 and 2.5 ± 0.6 μmol/L respectively. The respective figure for urinary TBARS level was 4.6 ± 2.7 and 3.7 ± 1.4 μmol/gmCr. Smokers did not show any significant difference from never-smokers with respect to GSH, α-T, AA, plasma TBARS and FBS. However, the smokers had significantly lower levels of TAA (p<0.05) and raised level of urinary TBARS (p<0.05) and uric acid (p<0.01) as compared to never-smokers. Conclusion: Our study suggests that smoking induces mild lipid peroxidation but the body is able to compensate for it by removing its adducts. Importantly it also indicates enhanced oxidation of purines which are essential components of both DNA and RNA. Dietary antioxidants are consumed to scavenge free radicals (FR) and other reactive species (RS) in smoke. Female smokers are more prone to oxidative insult than male smokers. In summary RS present in smoke induce mild lipid peroxidation but are not the major contributors of redox imbalance in smoke induced toxicity in the selected subjects.

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Jha JC, Maharjan BR, Adhikari D, Vishwanath P, Akila , Nagamma T et al. Cigarette smoke induced oxidative insult in local population of Pokhara. Kathmandu University Medical Journal. 2007 Dec 1;5(20):511-517.