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.

3-D nasal cultures: Systems toxicological assessment of a candidate modified-risk tobacco product

“…CS exposure is linked to the increased CYP1A1/CYP1B1 activity (Hukkanen et al, 2002;Hussain et al, 2014). However, our results indicated that the prominent 3R4F (0.25)-induced toxicity (thinning of the nasal epithelium cultures and increased cytotoxicity level) also impacted the metabolic capacity of the cultures, i.e., the capacity to metabolize nitrosamines and polycyclic aromatic hydrocarbons, which are abundant in CS, via CYP1A1 and CYP1B1 (Hukkanen et al, 2002).…”

Aquilaria spp. (agarwood) as source of health beneficial compounds: A review of traditional use, phytochemistry and pharmacology

“…However, both studies showed decreased plasma testosterone levels. In contrast, chronic exposure resulted in increased levels of oxidative stress and inflammation markers, as well as marked ultrastructural changes in the heart muscle (Al-Attas et al, 2015;Alokail et al, 2011;Hussain et al, 2014). Considering the potential health risks of the emission from agarwood smoke, more refined studies are warranted to ensure the safety of indoor agarwood burning for human health.…”

Oxygen Metabolism in the Lung

“…Nevertheless, aryl hydrocarbon hydroxylase activity can be induced up to 15-fold in rat lung by treatment with 3-methylcholanthrene (Matsubara et al, 1974) and its induction is associated with exposure-related mitochondrial dysfunction (Bansal et al, 2014). The inducible aryl hydrocarbon hydroxylase activity of the lung may be particularly important in the formation of carcinogens from cigarette smoke components, and polymorphisms in these enzymes may be a risk factor for the development of lung cancer (Hussain et al, 2014;Hussein et al, 2014;Kim et al, 2004). The lung-specific activity for metabolism of some inhaled agents, particularly benzene and pxylene, exceeds the activity in the liver (Philpot and Smith, 1984) and is critical to the bioactivation of a range of pulmonary toxicants (Kartha and Yost, 2008).…”