Santanu Banerjee | University of Calcutta (original) (raw)

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Papers by Santanu Banerjee

Molecular Biology Research Communications, 2020

NAD(P)H: quinone oxidoreductase 1 (NQO1) is an endogenous cellular defence mechanism against seve... more NAD(P)H: quinone oxidoreductase 1 (NQO1) is an endogenous cellular defence mechanism against several carcinogenic quinones derived from cigarette smoke. NQO1 C609T polymorphism is a strong determinant of NQO1 structure and function. The people with mutant allele for this polymorphism has significantly reduced NQO1 activity. In this study, we tried to evaluate the risk of lung cancer associated with this polymorphism in male current smokers of the Eastern India. Using PCR-RFLP method, we compared the NQO1 C609T genotype distribution in male current smokers with (n=150) and without (n=200) lung cancer. We observed significant variation of genotypic distribution between these two groups. The allele frequency of the variant C609T allele were 40.3% and 32.7% in smokers with and without lung cancer, respectively. From the genotypic comparison between the two smoker groups, it was found that a higher risk (OR=1.64, 95% CI: 1.05-2.55, P<0.05) of lung cancer was associated with NQO1 C609T...

Toxicology Reports, 2016

Cigarette smoke (CS) is an important source of morbidity and early mortality worldwide. Besides c... more Cigarette smoke (CS) is an important source of morbidity and early mortality worldwide. Besides causing various life-threatening diseases, CS is also known to cause hypoxia. Chronic hypoxia would induce early aging and premature death. Continuation of smoking during pregnancy is a known risk for the unborn child. Although carbon monoxide (CO) is considered to be a cause of hypoxia, the effect of other component(s) of CS on hypoxia is not known. Here we show by immunoblots and mass spectra analyses that in smoker's blood p-benzoquinone (p-BQ) derived from CS forms covalent adducts with cysteine 93 residues in both the ␤ chains of hemoglobin (Hb) producing Hb-p-BQ adducts. UV-vis spectra and CD spectra analyses show that upon complexation with p-BQ the structure of Hb is altered. Compared to nonsmoker's Hb, the content of ␣-helix decreased significantly in smoker's Hb (p = 0.0224). p-BQ also induces aggregation of smoker's Hb as demonstrated by SDS-PAGE, dynamic light scattering and atomic force microscopy. Alteration of Hb structure in smoker's blood is accompanied by reduced oxygen binding capacity. Our results provide the first proof that p-BQ is a cause of hypoxia in smokers. We also show that although both p-BQ and CO are responsible for causing hypoxia in smokers, exposure to CO further affects the function over and above that produced by Hb-p-BQ adduct.

International Journal of Chronic Obstructive Pulmonary Disease, 2017

Background and objective: Identification of smokers having predisposition to COPD is important fo... more Background and objective: Identification of smokers having predisposition to COPD is important for early intervention to reduce the huge global burden of the disease. Using a guinea pig model, we have shown that p-benzoquinone (p-BQ) derived from cigarette smoke (CS) in the lung is a causative factor for CS-induced emphysema. p-BQ is also derived from CS in smokers and it elicits the production of anti-p-BQ antibody in humans. We therefore hypothesized that anti-p-BQ antibody might have a protective role against COPD and could be used as a predictive biomarker for COPD in smokers. The objective of this study was to compare the serum anti-p-BQ antibody level between smokers with and without COPD for the evaluation of the hypothesis. Methods: Serum anti-p-BQ antibody concentrations of current male smokers with (n=227) or without (n=308) COPD were measured by an indirect enzyme-linked immunoabsorbent assay (ELISA) developed in our laboratory. COPD was diagnosed by spirometry according to Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines. Results and discussion: A significant difference was observed in the serum anti-p-BQ antibody level between smokers with and without COPD (Mann-Whitney U-test =4,632.5, P=0.000). Receiver operating characteristic (ROC) curve analysis indicated that the ELISA had significant precision (area under the curve [AUC] =0.934, 95% confidence interval [CI]: 0.913-0.935) for identifying smokers with COPD from their low antibody level. The antibody cutoff value of 29.4 mg/dL was constructed from the ROC coordinates to estimate the risk for COPD in smokers. While 90.3% of smokers with COPD had a low antibody value (#29.4 mg/dL), the majority (86.4%) of smokers without COPD had a high antibody value (.29.4 mg/dL); 13.6% of current smokers without COPD having an antibody level below this cutoff value (odds ratio [OR] =59.3, 95% CI: 34.15-101.99) were considered to be at risk for COPD. Conclusion and future directions: Our results indicate that serum anti-p-BQ antibody level may be used as a biomarker to identify asymptomatic smokers at risk for COPD for early intervention of the disease.

International Journal of Chronic Obstructive Pulmonary Disease

Cigarette smoke (CS) is an important source of morbidity and early mortality worldwide. Besides c... more Cigarette smoke (CS) is an important source of morbidity and early mortality worldwide. Besides causing various life-threatening diseases, CS is also known to cause hypoxia. Chronic hypoxia would induce early aging and premature death. Continuation of smoking during pregnancy is a known risk for the unborn child. Although carbon monoxide (CO) is considered to be a cause of hypoxia, the effect of other component(s) of CS on hypoxia is not known. Here we show by immunoblots and mass spectra analyses that in smoker's blood p-benzoquinone (p-BQ) derived from CS forms covalent adducts with cysteine 93 residues in both the chains of hemoglobin (Hb) producing Hb-p-BQ adducts. UV–vis spectra and CD spectra analyses show that upon complexation with p-BQ the structure of Hb is altered. Compared to nonsmoker's Hb, the content of-helix decreased significantly in smoker's Hb (p = 0.0224). p-BQ also induces aggregation of smoker's Hb as demonstrated by SDS-PAGE, dynamic light scattering and atomic force microscopy. Alteration of Hb structure in smoker's blood is accompanied by reduced oxygen binding capacity. Our results provide the first proof that p-BQ is a cause of hypoxia in smokers. We also show that although both p-BQ and CO are responsible for causing hypoxia in smokers, exposure to CO further affects the function over and above that produced by Hb-p-BQ adduct.

Background and objective: Identification of smokers having predisposition to COPD is important f... more Background and objective:
Identification of smokers having predisposition to COPD is important for early intervention to reduce the huge global burden of the disease. Using a guinea pig model, we have shown that p-benzoquinone (p-BQ) derived from cigarette smoke (CS) in the lung is a causative factor for CS-induced emphysema. p-BQ is also derived from CS in smokers and it elicits the production of anti-p-BQ antibody in humans. We therefore hypothesized that anti-p-BQ antibody might have a protective role against COPD and could be used as a predictive biomarker for COPD in smokers. The objective of this study was to compare the serum anti-p-BQ antibody level between smokers with and without COPD for the evaluation of the hypothesis.
Methods: Serum anti-p-BQ antibody concentrations of current male smokers with (n=227) or without (n=308) COPD were measured by an indirect enzyme-linked immunoabsorbent assay (ELISA) developed in our laboratory. COPD was diagnosed by spirometry according to Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines.
Results and discussion: A significant difference was observed in the serum anti-p-BQ antibody level between smokers with and without COPD (Mann–Whitney U-test =4,632.5, P=0.000). Receiver operating characteristic (ROC) curve analysis indicated that the ELISA had significant precision (area under the curve [AUC] =0.934, 95% confidence interval [CI]: 0.913–0.935) for identifying smokers with COPD from their low antibody level. The antibody cutoff value of 29.4 mg/dL was constructed from the ROC coordinates to estimate the risk for COPD in smokers. While 90.3% of smokers with COPD had a low antibody value (< or =29.4 mg/dL), the majority (86.4%) of smokers without COPD had a high antibody value (>29.4 mg/dL); 13.6% of current smokers without COPD having an antibody level below this cutoff value (odds ratio [OR] =59.3, 95% CI: 34.15–101.99) were considered to be at risk for COPD.
Conclusion and future directions: Our results indicate that serum anti-p-BQ antibody level may be used as a biomarker to identify asymptomatic smokers at risk for COPD for early intervention of the disease.

Molecular Biology Research Communications, 2020

Toxicology Reports, 2016

International Journal of Chronic Obstructive Pulmonary Disease, 2017

International Journal of Chronic Obstructive Pulmonary Disease

Cigarette smoke (CS) is an important source of morbidity and early mortality worldwide. Besides c... more Cigarette smoke (CS) is an important source of morbidity and early mortality worldwide. Besides causing various life-threatening diseases, CS is also known to cause hypoxia. Chronic hypoxia would induce early aging and premature death. Continuation of smoking during pregnancy is a known risk for the unborn child. Although carbon monoxide (CO) is considered to be a cause of hypoxia, the effect of other component(s) of CS on hypoxia is not known. Here we show by immunoblots and mass spectra analyses that in smoker's blood p-benzoquinone (p-BQ) derived from CS forms covalent adducts with cysteine 93 residues in both the chains of hemoglobin (Hb) producing Hb-p-BQ adducts. UV–vis spectra and CD spectra analyses show that upon complexation with p-BQ the structure of Hb is altered. Compared to nonsmoker's Hb, the content of-helix decreased significantly in smoker's Hb (p = 0.0224). p-BQ also induces aggregation of smoker's Hb as demonstrated by SDS-PAGE, dynamic light scattering and atomic force microscopy. Alteration of Hb structure in smoker's blood is accompanied by reduced oxygen binding capacity. Our results provide the first proof that p-BQ is a cause of hypoxia in smokers. We also show that although both p-BQ and CO are responsible for causing hypoxia in smokers, exposure to CO further affects the function over and above that produced by Hb-p-BQ adduct.