title: Ultrastructural changes, increased oxidative stress, inflammation, and altered cardiac hypertrophic gene expressions in heart tissues of rats exposed to incense smoke.
abstract: Incense smoke exposure has recently been linked to cardiovascular disease risk, heart rate variability, and endothelial dysfunction. To test the possible underlying mechanisms, oxidative stress, and inflammatory markers, gene expressions of cardiac hypertrophic and xenobiotic-metabolizing enzymes and ultrastructural changes were measured, respectively, using standard, ELISA-based, real-time PCR, and transmission electron microscope procedures in heart tissues of Wistar rats after chronically exposing to Arabian incense. Malondialdehyde, tumor necrosis alpha (TNF)-α, and IL-4 levels were significantly increased, while catalase and glutathione levels were significantly declined in incense smoke-exposed rats. Incense smoke exposure also resulted in a significant increase in atrial natriuretic peptide, brain natriuretic peptide, β-myosin heavy chain, CYP1A1 and CYP1A2 messenger RNAs (mRNAs). Rats exposed to incense smoke displayed marked ultrastructural changes in heart muscle with distinct cardiac hypertrophy, which correlated with the augmented hypertrophic gene expression as well as markers of cardiac damage including creatine kinase-myocardial bound (CK-MB) and lactate dehydrogenase (LDH). Increased oxidative stress, inflammation, altered cardiac hypertrophic gene expression, tissue damage, and architectural changes in the heart may collectively contribute to increased cardiovascular disease risk in individuals exposed to incense smoke. Increased gene expressions of CYP1A1 and CYP1A2 may be instrumental in the incense smoke-induced oxidative stress and inflammation. Thus, incense smoke can be considered as a potential environmental pollutant and its long-term exposure may negatively impact human health.
authors: Center of Excellence in Biotechnology Research, College of Science, King Saud University, AB3, Building 5, Riyadh, 11451, Saudi Arabia.
authors: Omar S
authors: OS
authors: Al-Attas
authors: Tajamul
authors: T
authors: Hussain
authors: Mukhtar
authors: M
authors: Ahmed
authors: Nasser
authors: N
authors: Al-Daghri
authors: Arif A
authors: AA
authors: Mohammed
authors: Edgard
authors: E
authors: De Rosas
authors: Dikshit
authors: D
authors: Gambhir
authors: Terrance S
authors: TS
authors: Sumague
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D019363:Cytochrome P-450 CYP1A1 / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D005978:Glutathione / Q000378:metabolism; D007249:Inflammation; D015847:Interleukin-4 / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D009206:Myocardium / Q000648:ultrastructure*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D060888:Real-Time Polymerase Chain Reaction; D012906:Smoke; D014026:Nicotiana / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D012333:RNA, Messenger; D012906:Smoke; D014409:Tumor Necrosis Factor-alpha; D015847:Interleukin-4; D008315:Malondialdehyde; D002374:Catalase; D019363:Cytochrome P-450 CYP1A1; D005978:Glutathione