title: Induction of CYP1A1, CYP1A2, CYP1B1, increased oxidative stress and inflammation in the lung and liver tissues of rats exposed to incense smoke.
abstract: Incense smoke is increasingly being recognized as a potential environmental contaminant and is linked to malignant and non-malignant respiratory diseases. The detoxification of environmental contaminants including polycyclic aromatic hydrocarbons (PAHs) involves the induction of cytochrome P-450 family enzymes (CYPs) by PAHs. However, the detoxification of PAHs also results in the generation of reactive and unstable intermediary metabolites which are implicated in the oxidative stress, DNA damage, and inflammation. It is unclear whether CYPs are similarly induced by incense smoke, which incidentally contains substantial amounts of PAHs. Here, we examined the impact of long-term incense smoke exposure on the induction of CYPs in male Wister Albino rats. Incense smoke exposure significantly induced the expression of CYP1A1, CYP1A2, and CYP1B1 mRNAs in both lung and liver tissues. The extent of CYP1A1 and CYP1B1 induction was significantly higher in the liver compared to that in the lung, while that of CYP1A2 was greater in the lung than in liver. Incense smoke exposure also increased malondialdehyde and reduced glutathione levels in lung and liver tissues, and the catalase activity in the liver tissues to significant levels. Furthermore incense smoke exposure led to a marked increase in TNF-α and IL-4 levels. The data demonstrate for the first time the capacity of incense smoke to induce CYP1 family enzymes in the target and non-target tissues. Induction of CYPs increased oxidative stress and inflammation appear to be intimately linked to promote the carcinogenesis and health complications in people chronically exposed to incense smoke.
authors.affiliation: Center of Excellence in Biotechnology Research, College of Science, King Saud University, AB3, Building 5, Riyadh, 11451, Saudi Arabia, thussain@ksu.edu.sa.
authors.forename: Tajamul
authors.initials: T
authors.lastname: Hussain
authors.forename: Omar S
authors.initials: OS
authors.lastname: Al-Attas
authors.forename: Nasser M
authors.initials: NM
authors.lastname: Al-Daghri
authors.forename: Arif A
authors.initials: AA
authors.lastname: Mohammed
authors.forename: Edgard
authors.initials: E
authors.lastname: De Rosas
authors.forename: Shebl
authors.initials: S
authors.lastname: Ibrahim
authors.forename: Benjamin
authors.initials: B
authors.lastname: Vinodson
authors.forename: Mohammed G
authors.initials: MG
authors.lastname: Ansari
authors.forename: Khaled I Alam
authors.initials: KI
authors.lastname: El-Din
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D019363:Cytochrome P-450 CYP1A1 / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D019388:Cytochrome P-450 CYP1A2 / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D065633:Cytochrome P-450 CYP1B1 / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D004781:Environmental Exposure / Q000009:adverse effects; D004790:Enzyme Induction; D007249:Inflammation / Q000201:enzymology* / Q000473:pathology; D015847:Interleukin-4 / Q000378:metabolism; D008099:Liver / Q000201:enzymology* / Q000473:pathology; D008168:Lung / Q000201:enzymology* / Q000473:pathology; D008297:Male; D009928:Organ Specificity / Q000235:genetics; D018384:Oxidative Stress / Q000235:genetics; D010476:Perfume / Q000009:adverse effects; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D017208:Rats, Wistar; D012906:Smoke / Q000009:adverse effects*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D015415:Biomarkers; D010476:Perfume; D012333:RNA, Messenger; D012906:Smoke; D014409:Tumor Necrosis Factor-alpha; D015847:Interleukin-4; D019363:Cytochrome P-450 CYP1A1; D019388:Cytochrome P-450 CYP1A2; D065633:Cytochrome P-450 CYP1B1